Browse the corpus

Hematuria, defined as the abnormal presence of blood in urine, is classified into 2 primary categories: gross and microscopic. Gross hematuria refers to visible blood in urine, while microscopic hematuria indicates red blood cell (RBC) detection through microscopic urinalysis without apparent visual blood. Hematuria evaluations encompass a broad spectrum of etiologies, with malignancy being a critical consideration, especially in patients with predisposing or high-risk factors. This course reviews the thorough assessment of hematuria, including thorough history-taking, physical examination, appropriate imaging, laboratory testing, and diagnostic cystoscopy. Participants will also gain an understanding of risk stratification based on parameters such as age, smoking history, RBC count, and prior episodes of hematuria to guide optimal management. Risk-appropriate evaluations are also emphasized to ensure timely detection and management of underlying pathology, particularly urological malignancies. This activity for healthcare professionals is designed to enhance the learner's competence in the timely recognition of gross and microscopic hematuria, integrating updated AUA risk stratification criteria for microhematuria into clinical practice, and implementing an appropriate interprofessional approach when managing this condition. Objectives: Differentiate gross hematuria and microscopic hematuria. Implement evidence-based protocols for the evaluation of patients with gross and microscopic hematuria. Select optimal treatment strategies for patients with gross and microscopic hematuria. Collaborate with interprofessional healthcare teams to appropriately coordinate care for patients with gross and microscopic hematuria. Access free multiple choice questions on this topic.

Gross and Microscopic Hematuria Definitions Hematuria, defined as the abnormal presence of blood in the urine, ranks among the most commonly diagnosed urological disorders, accounting for over 20% of all urological evaluations.[1][2] While hematuria can be classified in multiple ways—eg, intermittent or constant, glomerular or nonglomerular, and symptomatic or asymptomatic—the most clinically useful distinction separates cases into gross (visible) and microscopic (invisible) hematuria. Microhematuria is defined as the detection of 3 or more urinary red blood cells (RBCs) per high-power field (HPF) on microscopic urinalysis without an apparent cause, while the urine’s visual appearance remains normal.[1][3][4][5] Urinary dipstick findings alone do not provide a definitive diagnosis of microscopic hematuria and require confirmation through one or more microscopic urinalyses.[1][5][6][7] Microscopic examination of urinary sediment must always accompany dipstick-positive findings to verify microhematuria.[1][5][6][7] The absence of microscopic RBCs in strongly dipstick-positive samples suggests alternative causes, eg, myoglobinuria, hemoglobinuria from lysed erythrocytes, or other forms of pseudohematuria.[6][8][9][10][11] Blood from recent urological procedures, urinary tract infections (UTIs), or contamination from rectal or vaginal bleeding must also be excluded. This approach addresses the relatively high incidence of false positives and negatives associated with dipstick testing alone.[1][5][6][8][12] Microscopic hematuria can be further categorized into symptomatic microhematuria, asymptomatic microhematuria with proteinuria—indicative of potential glomerular disease—and asymptomatic microhematuria without proteinuria, which raises concern for possible urothelial malignancy. Microscopic urinalysis can also detect urinary infections and abnormal urinary sediment not identified by dipstick, eg, crystals, casts, and dysmorphic RBCs, thereby supporting the diagnosis of the underlying pathology.[13][14][15] Enhancing primary care education on definitions of hematuria and initial diagnostic steps can reduce unnecessary testing and referrals while improving the management of patients with confirmed microhematuria.[1][2][5][8][12][14] Hematuria Evaluation and Referral

Microscopic hematuria can be further categorized into symptomatic microhematuria, asymptomatic microhematuria with proteinuria—indicative of potential glomerular disease—and asymptomatic microhematuria without proteinuria, which raises concern for possible urothelial malignancy. Microscopic urinalysis can also detect urinary infections and abnormal urinary sediment not identified by dipstick, eg, crystals, casts, and dysmorphic RBCs, thereby supporting the diagnosis of the underlying pathology.[13][14][15] Enhancing primary care education on definitions of hematuria and initial diagnostic steps can reduce unnecessary testing and referrals while improving the management of patients with confirmed microhematuria.[1][2][5][8][12][14] Hematuria Evaluation and Referral Renal or urothelial malignancy represents the most severe potential cause of hematuria.[16][17] Evidence indicates that many patients with true microhematuria are not evaluated appropriately or referred promptly to urology, potentially delaying cancer diagnosis and worsening outcomes.[8][12] One study found that only 41% of primary care patients with dipstick-diagnosed microscopic hematuria received confirmatory microscopic urinalysis, and of those, only 24% had 3 or more RBC/HPF, confirming microhematuria.[8] Another study found that 84% of patients with positive microscopic urinalysis were not further evaluated or tested, highlighting dangerous lapses in guideline implementation.[12] Addressing these gaps is critical to enable early diagnosis of life-threatening conditions and optimize patient outcomes. Multiple classifications stratify patients into low-, intermediate-, and high-risk categories. The most widely used and validated framework follows the updated 2025 American Urological Association Guideline on Microhematuria Risk Stratification.[5] Some sources advocate for a more stringent requirement of at least 2 or 3 confirmed microscopic findings before confirming hematuria.[6] In cases where only a single microscopic finding is present, periodic follow-up urinalyses for at least 1 year are recommended if no further workup is performed after the initial result.[6][18][19]

Genitourinary disorders primarily cause hematuria, although systemic diseases can manifest with blood in the urine. Hematuria is classified as glomerular or nonglomerular, although the cause in many cases is idiopathic or undetermined. In general, glomerular sources are often associated with proteinuria.[13][20] In infants and young children, hematuria may signal Wilms tumor, polycystic kidney disease, Alport syndrome, inherited nephritis, glomerulonephritis, hypercalciuria, urinary tract infections, and, in the Black population, sickle cell disease.[21][22][23][24][25][26][27] Persistent microhematuria in younger patients has been associated with a higher risk of kidney failure due to primary glomerular disease.[28][29][30] In older individuals, the most common causes are urinary tract infections, various urological malignancies (eg, kidney and bladder cancers), urolithiasis, postinfectious and other types of glomerulonephritis, trauma, prostatic enlargement, and urinary instrumentation. In about 50% of cases, a specific cause of the hematuria can be identified, meaning no definite etiology can be determined about half the time.[29] Gross hematuria is a common admitting diagnosis for nonagenarian patients.[31] In this extremely vulnerable group, geriatric assessment tools can help in clinical decision-making and discharge planning.[31] The use of frailty-based risk stratification and measures to diminish functional decline during hospitalizations is encouraged, but requires additional research.[31] When hematuria is accompanied by proteinuria, casts, or dysmorphic (i.e., malformed) RBCs, this usually signals glomerular pathology and at least moderate kidney disease.[13] Common Glomerular Etiologies of Hematuria Some common glomerular causes of hematuria include: Alport syndrome [23] Crescentic glomerulonephritis [32] Diffuse progressive glomerulonephritis [13] Focal segmental glomerulonephritis [13][33] Goodpasture syndrome [34] Hypercalciuria [25] IgA vasculitis (Henoch-Schönlein purpura) [35] IgA nephropathy (Berger disease) [36] Lupus nephritis [37] Membranous glomerulonephritis [13][38] Minimal change disease [13][39] Nephrotic syndrome [40] Polycystic kidney disease [22][24] Poststreptococcal (postinfectious) glomerulonephritis [13][41] Rapidly progressive (pauci-immune) glomerulonephritis [42] Thin basement membrane disease (formerly benign familial hematuria) [13][43] Tubulointerstitial nephritis [44]

Membranous glomerulonephritis [13][38] Minimal change disease [13][39] Nephrotic syndrome [40] Polycystic kidney disease [22][24] Poststreptococcal (postinfectious) glomerulonephritis [13][41] Rapidly progressive (pauci-immune) glomerulonephritis [42] Thin basement membrane disease (formerly benign familial hematuria) [13][43] Tubulointerstitial nephritis [44] Common Nonglomerular Etiologies of Hematuria Nonglomerular causes typically demonstrate normal RBCs on microscopic urinalysis without proteinuria or casts. Common nonglomerular causes of hematuria include: Bladder calculi [45] Bladder and urothelial cancer [16] Benign prostatic hyperplasia [46] Endometriosis of the urinary tract [47] Foreign bodies in the urinary tract (eg, stones, catheters, and stents) [48] Genitourinary mucosal injury by instrumentation, including biopsies [49][50][51] Hematological disorders like sickle cell anemia, thrombocytopenia, and coagulopathies [52][53] Hemorrhagic cystitis [54] Infections (eg, cystitis, urethritis, and prostatitis) [21][55] Malignancy (eg, renal cell carcinoma, bladder, and prostate cancer) [16][17][56] Medication-related (eg, cyclophosphamide, ifosfamide) [57][58] Nephrocalcinosis [59] Nephrolithiasis, urolithiasis [48][60][61][62] Nutcracker Syndrome [63] Radiation cystitis [64] Schistosomiasis (Africa and endemic regions) [65] Sickle cell disease (from papillary necrosis) [52][53] Strenuous exercise [66] Trauma involving the genitourinary tract [67][68][69]

Gross hematuria is a common presentation in outpatient clinics and emergency departments. Asymptomatic hematuria is thought to be much more prevalent than symptomatic hematuria and may persist for years before detection.[70][71] The evaluation of hematuria, especially microhematuria, is often delayed in women, which can result in poorer outcomes for bladder and other urological cancers in females.[5][6][72][73][74][75][76] The prevalence of hematuria varies widely according to the definition used and the availability of medical evaluation. In the United States (US), the prevalence of microscopic hematuria is estimated at 6.5% of the population.[3] The prevalence varies worldwide, depending on the population studied and the definition used.[1][3] One study in Japan, where annual health check-ups with urine dipstick are the standard of care, found that 5% to 10% of the population were dipstick-positive for hematuria.[77] Another meta-analysis showed that the prevalence of asymptomatic microhematuria varies from 0.19% to 16%.[78] Prevalence depends greatly on the age and population studied. Older men have an especially high prevalence of asymptomatic microhematuria, with some estimates as high as 21%.[78] A primary focus of an evaluation of hematuria is to identify and exclude any underlying malignancy. Hematuria (either gross or microscopic) is the presenting symptom in most bladder cancers and is often the earliest presenting sign of a renal neoplasm.[16][17] The overall incidence of discovering a genitourinary malignancy in patients with microscopic hematuria is approximately 3%.[3][6][79] With gross hematuria, the incidence rises to 10%-20%.[36] This risk is increased in some groups and is related to gender, age, smoking history, chemical exposures (eg, benzene, aromatic amines, Agent Orange), and the degree of hematuria.[28][80][81][82] Asymptomatic hematuria can be found in 4% of normal school-aged children, more often in girls than boys.[83]

A primary focus of an evaluation of hematuria is to identify and exclude any underlying malignancy. Hematuria (either gross or microscopic) is the presenting symptom in most bladder cancers and is often the earliest presenting sign of a renal neoplasm.[16][17] The overall incidence of discovering a genitourinary malignancy in patients with microscopic hematuria is approximately 3%.[3][6][79] With gross hematuria, the incidence rises to 10%-20%.[36] This risk is increased in some groups and is related to gender, age, smoking history, chemical exposures (eg, benzene, aromatic amines, Agent Orange), and the degree of hematuria.[28][80][81][82] Asymptomatic hematuria can be found in 4% of normal school-aged children, more often in girls than boys.[83] The National Cancer Institute estimates that there will be about 84,870 new cases of bladder cancer in the US, approximately 65,080 in men and 19,790 in women, in 2025, with 17,420 deaths. They have also estimated the annual incidence of bladder cancer at 18.7 per 100,000 population. However, the overall incidence is slowly decreasing. For renal cancer, the estimated yearly incidence in the US is around 79,000, about 50,000 men and 29,000 women, with 14,000 mortalities. Worldwide, over 400,000 persons are estimated to be diagnosed with this disease yearly, with about 180,000 deaths annually.[84] The overall global incidence appears to be slowly increasing.[84] The overall incidence of glomerulonephritis has been reported as high as 134 per 100,000 patient years, but reliable worldwide statistics are difficult to obtain.[85] Nephrolithiasis rates vary by gender, ethnicity, and geographic region, with rates about twice as common in males as in females. The reported incidence of urolithiasis ranges from 7% to 13% in the US and Canada, 5% to 9% in Europe, and 1% to 5% in Asia.[86] UTIs have an overall estimated global prevalence of 0.7%. The main risk factors for UTI are increasing age, previous history of UTI, sexual activity, and diabetes.[87] Acute cystitis is far more common than pyelonephritis. For every case of pyelonephritis, 18 to 28 cases of acute cystitis are diagnosed.[88] While UTIs are a common cause of microhematuria, the resolution of microhematuria after treatment should be verified and documented, as malignancy and UTI may coexist.[36]

The overall incidence of glomerulonephritis has been reported as high as 134 per 100,000 patient years, but reliable worldwide statistics are difficult to obtain.[85] Nephrolithiasis rates vary by gender, ethnicity, and geographic region, with rates about twice as common in males as in females. The reported incidence of urolithiasis ranges from 7% to 13% in the US and Canada, 5% to 9% in Europe, and 1% to 5% in Asia.[86] UTIs have an overall estimated global prevalence of 0.7%. The main risk factors for UTI are increasing age, previous history of UTI, sexual activity, and diabetes.[87] Acute cystitis is far more common than pyelonephritis. For every case of pyelonephritis, 18 to 28 cases of acute cystitis are diagnosed.[88] While UTIs are a common cause of microhematuria, the resolution of microhematuria after treatment should be verified and documented, as malignancy and UTI may coexist.[36] Benign prostatic hyperplasia (BPH) is extremely common, but most affected individuals initially demonstrate urinary symptoms other than hematuria. Half of men aged 50 or older show evidence of BPH.[89][90] This increases by about 2% to 2.5% per year with age.[91] In the US, the incidence of BPH in men aged 60 to 69 years is 70%, which rises to over 80% in men older than 70 years.[92] Polycystic kidney disease affects an estimated 4 to 7 million individuals worldwide and accounts for up to 15% of patients with end-stage kidney disease.[24] Approximately 5% of all traumas involve the kidney, with the majority coming from motor vehicle accidents, followed by sports injuries and falls.[68][93] Nutcracker syndrome, also known as left renal vein obstruction or entrapment, is a rare, sometimes symptomatic condition in which the left renal vein is obstructed as it enters the inferior vena cava, often by the superior mesenteric artery.[94] The incidence of this entity is unknown, but is most common in adults in the second and third decades. Please see StatPearls' companion reference resource, "Nutcracker Syndrome and Left Renal Vein Entrapment," for additional information.[63] Inherited illnesses that cause hematuria are relatively uncommon, including:

Nutcracker syndrome, also known as left renal vein obstruction or entrapment, is a rare, sometimes symptomatic condition in which the left renal vein is obstructed as it enters the inferior vena cava, often by the superior mesenteric artery.[94] The incidence of this entity is unknown, but is most common in adults in the second and third decades. Please see StatPearls' companion reference resource, "Nutcracker Syndrome and Left Renal Vein Entrapment," for additional information.[63] Inherited illnesses that cause hematuria are relatively uncommon, including: Alport syndrome: This condition is more common in the US, where the incidence is estimated at 1 in 5,000 population or up to 60,000 total affected individuals.[23] The incidence in Europe is lower, estimated at 1 in 50,000.[95] Approximately 3% of all children in the US with end-stage renal failure have Alport syndrome.[23] Autosomal dominant polycystic kidney disease: This inherited illness is found in roughly 1 in every 1,000 live births.[24] Goodpasture syndrome: The incidence of Goodpasture syndrome is fewer than 2 cases per 1 million population.[34] Thin basement membrane disease: This condition, formerly known as benign familial hematuria, affects at least 1% of the population worldwide.[43] Some patients previously thought to have thin basement membrane disease were found to have variations of Alport Syndrome.[95] Sickle cell disease: According to the Centers for Disease Control and Prevention, sickle cell disease affects about 100,000 Black Americans, or 1 out of every 365 Black Americans.[53][95] This can cause renal papillary necrosis or renal infarction, leading to sickle cell nephropathy and microscopic hematuria.[54] Sickle cell trait is found in 1 in 12 babies of African ancestry born in the US.[96] Furthermore, medications can cause hematuria or urinary discoloration due to pseudohematuria (ie, red, pink, or brown urine discoloration), kidney damage, urolithiasis, or hemorrhagic cystitis. Medications that can cause hematuria include: Allopurinol Anticoagulants (eg, warfarin or antiplatelet drugs) Captopril Cephalosporins Chlorpromazine Cyclophosphamide Dichlorphenamide Furosemide Hydralazine Ifosfamide Indinavir Metronidazole Minocycline Mirtazapine Nitrofurantoin Penicillin Phenazopyridine Phenolphthalein Propylthiouracil Rifampin Senna Sulfa drugs Thioridazine

Hematuria may result from structural alterations caused by injury, infection, or a mass anywhere in the genitourinary tract. Anticoagulation alone does not cause hematuria but may exacerbate this symptom. Patients on anticoagulants or antiplatelet therapy should receive the same evaluation as individuals not on such agents, as their risk of malignancy is the same.[1][97][98][99][100] Immunological or inflammatory processes may damage the integrity of the renal glomerular basement membrane, mesangium, or microvascular endothelium.[13] This usually presents as glomerular bleeding. Nonglomerular causes of bleeding, including nephrolithiasis, urolithiasis, certain drugs, nephrocalcinosis, genitourinary neoplasms, trauma-related urothelial mucosal damage, catheterization, urological biopsies or similar procedures, benign prostatic hyperplasia, radiation exposure, and various chemicals, may cause erosion or otherwise damage the urothelial surface somewhere in the urinary tract, leading to hematuria.

Hematuria can be classified in several ways, but the most clinically meaningful distinction is between gross and microscopic types. Gross Hematuria Gross hematuria refers to visible blood in the urine, which may appear reddish or pink. In some cases, urine may appear brown or tea-colored due to oxidation of heme pigments. Gross hematuria often indicates significant urological disease, regardless of the presence or absence of accompanying symptoms. A detailed patient history may reveal the underlying cause, such as recent urological surgery or instrumentation, a urinary tract infection, or passage of a kidney stone. When no clear explanation exists, gross hematuria typically warrants additional evaluation, including imaging studies, cytology, and cystoscopy, to rule out urological malignancy—particularly in individuals older than 35 years.[1][3][5] Clinicians should recognize that the presence of gross hematuria automatically places the patient in a high-risk category.[1][3][5] Microscopic Hematuria Evaluation of microscopic hematuria requires a comprehensive history and physical examination, including blood pressure assessment and measurement of serum creatinine levels, to identify potential risk factors for genitourinary malignancy. Such risk factors include a smoking history of 10 or more pack-years, a family history of Lynch syndrome, or exposure to carcinogenic chemicals. The assessment should also address possible medical renal, gynecologic, and nonmalignant genitourinary causes of microhematuria.[1][5] Patients receiving anticoagulant therapy require the same diagnostic approach as those not using blood-thinning medications, as anticoagulation does not exclude underlying pathology. Microscopic hematuria may be further classified into the following subtypes: Asymptomatic: This may be associated with bladder and other urological cancers. Typically, normal RBCs are seen microscopically. Requires further risk-stratified workup. Asymptomatic with proteinuria: Proteinuria in asymptomatic patients suggests glomerulonephritis. Dysmorphic, atypical RBCs are frequently observed on microscopic examination. A workup for glomerular disorders should be performed, which may require a renal biopsy.

Asymptomatic: This may be associated with bladder and other urological cancers. Typically, normal RBCs are seen microscopically. Requires further risk-stratified workup. Asymptomatic with proteinuria: Proteinuria in asymptomatic patients suggests glomerulonephritis. Dysmorphic, atypical RBCs are frequently observed on microscopic examination. A workup for glomerular disorders should be performed, which may require a renal biopsy. Symptomatic: This subtype is associated with urinary symptoms and is often suggestive of infection, prostatitis, BPH, or other urinary disorders. Further investigation should be performed with follow-up as warranted, including a repeat urinalysis with microscopic examination after the infection has been successfully and completely treated. Clinical Symptoms Associated with Hematuria A thorough history and focused physical examination can lead to proper evaluation, improved diagnosis, and optimal management. When obtaining a clinical history, other symptoms associated with hematuria should be noted, including: Active menstruation Back or flank pain Constitutional symptoms (eg, weight loss, anorexia, and cachexia) Fever (unexplained) Flank mass Flank pain Hearing loss Hemoptysis Joint pains, oral ulcers, rash Leg swelling Lower abdominal pain Passing urinary calculi Recent throat or skin infection Suprapubic pain Voiding and urinary symptoms, including: Dysuria Frequency Hesitancy Incomplete emptying Intermittent stream Passing clots Urgency Urinary retention Weak urinary stream Female patients during menstruation or with vaginal bleeding should either have a catheterized urine sample, use a tampon with cleaning of any residual blood before voiding, or be reevaluated when the gynecologic bleeding has resolved.[1][5] After a UTI, at least 6 weeks should elapse before a repeat urinalysis for hematuria. Patients should be asked about previous such episodes and any family history of hematuria. A detailed medical history, including any recent surgical procedures or biopsies, is essential for a proper evaluation. Medications should be carefully reviewed, particularly regarding any blood thinners. Certain medications can cause false positive dipstick readings, eg, peroxidases from organic sources, semen, metronidazole, and sodium hypochlorite.[6][101]

Female patients during menstruation or with vaginal bleeding should either have a catheterized urine sample, use a tampon with cleaning of any residual blood before voiding, or be reevaluated when the gynecologic bleeding has resolved.[1][5] After a UTI, at least 6 weeks should elapse before a repeat urinalysis for hematuria. Patients should be asked about previous such episodes and any family history of hematuria. A detailed medical history, including any recent surgical procedures or biopsies, is essential for a proper evaluation. Medications should be carefully reviewed, particularly regarding any blood thinners. Certain medications can cause false positive dipstick readings, eg, peroxidases from organic sources, semen, metronidazole, and sodium hypochlorite.[6][101] False-negative dipstick results are possible from extremely high urinary ascorbic acid levels.[6] Clinicians should also ascertain the patient's smoking history, as 10 pack-years or more is a significant risk factor for urothelial malignancies, eg, bladder cancer.[16] The risk is higher as the smoking history increases. Even after a full negative evaluation in a low-risk patient, persistent or recurrent microhematuria should reclassify that individual as either "intermediate" or "high-risk."[1][5][102] High-Risk Factors for Urothelial Cancers Clinical factors that are associated with a high risk for urothelial cancer include: Degree and persistence of microhematuria Family history of Lynch syndrome, urothelial malignancies, or any renal tumor-associated syndromes (Birt-Hogg-Dube, hereditary leiomyomatosis renal cell cancer, hereditary papillary renal cell cancer, tuberous sclerosis, or von Hippel-Lindau) History of pelvic radiation therapy History of unexplained gross hematuria Increasing age (especially older than 60 years) Indwelling catheters, suprapubic tubes Irritative lower urinary tract symptoms that are persistent and unexplained Male gender Occupational exposure to benzene, aromatic amines, Agent Orange, and similar chemicals Prior chemotherapy drug exposure (cyclophosphamide, ifosfamide) Significant smoking history [1][2] Physical Exam Findings A complete physical examination can contribute to making a valid differential diagnosis. Important signs to look for when assessing patients with hematuria include: Costovertebral angle tenderness Edema of the lower extremities Fever Flank mass or tenderness Gynecological abnormalities Hearing impairments

Significant smoking history [1][2] Physical Exam Findings A complete physical examination can contribute to making a valid differential diagnosis. Important signs to look for when assessing patients with hematuria include: Costovertebral angle tenderness Edema of the lower extremities Fever Flank mass or tenderness Gynecological abnormalities Hearing impairments Hypertension Joint swelling Lymphadenopathy Meatal blood, caruncles, or other abnormalities Palpable, enlarged, cystic kidneys Periorbital edema Presence of pallor, icterus, oral ulcers, or rashes Pubic or suprapubic tenderness/fullness Urethral or vaginal discharge, injuries, or tears Vaginal bleeding [1][2]

Evaluation of hematuria often remains deficient, inadequate, or incomplete.[1] More than half of patients identified with hematuria in primary care settings do not receive proper evaluation or timely referral to urology.[72] Cystoscopy remains substantially underutilized, as many clinicians rely too heavily on diagnostic imaging alone.[1][6] This practice creates significant concern, given that most cancer-related hematuria originates from bladder neoplasms, which are best and most reliably diagnosed through cystoscopy.[1][5][103][104][105][106] Many primary care practitioners order renal ultrasonography, despite the need for more detailed and accurate imaging, eg, a computed tomography (CT) urogram—an abdominal and pelvic CT scan performed with and without intravenous contrast—for higher-risk patients.[1][5][107] Studies consistently demonstrate that fewer than 20% of patients with hematuria undergo both appropriate urological imaging and cystoscopy, with variations influenced by gender and race.[1][5][103][104][105] Evaluation of hematuria, particularly microhematuria, frequently experiences delays in women, often due to assumptions that the cause involves a urinary tract infection, menstrual contamination, or vaginal bleeding. Such delays contribute to delays in diagnosis and poorer outcomes in females with bladder and other urological malignancies.[6] Urinalysis Urinalysis is the initial and most useful test to detect hematuria. Although urine dipsticks are widely available and can be performed quickly, they can give false-positive or false-negative results and require microscopic analysis to confirm positive findings.[1][5][6][7] The presence of 3 or more RBCs per high-power field on microscopic examination of the urine sediment establishes the diagnosis, though no lower limit of hematuria is completely safe.[1][2][5] The finding of abnormal urine appearance or pH, proteinuria, white blood cells, positive nitrites, leukocyte esterase, bacteria, crystals, or casts outside the reference range helps identify possible sources of hematuria.[13][14][15][20][21] Nonglomerular Hematuria Evaluation

Urinalysis is the initial and most useful test to detect hematuria. Although urine dipsticks are widely available and can be performed quickly, they can give false-positive or false-negative results and require microscopic analysis to confirm positive findings.[1][5][6][7] The presence of 3 or more RBCs per high-power field on microscopic examination of the urine sediment establishes the diagnosis, though no lower limit of hematuria is completely safe.[1][2][5] The finding of abnormal urine appearance or pH, proteinuria, white blood cells, positive nitrites, leukocyte esterase, bacteria, crystals, or casts outside the reference range helps identify possible sources of hematuria.[13][14][15][20][21] Nonglomerular Hematuria Evaluation Nonglomerular hematuria is the finding of normal red blood cells without an apparent cause, including no evidence of infection, renal failure, or glomerular disease. The absence of an identifiable cause suggests possible BPH, urolithiasis, or a urinary tract malignancy and warrants further evaluation based primarily on the overall stratified urological cancer risk as outlined below.[1][5] Urinary tract infection: Infection is suspected as the source of the hematuria if the urinalysis shows significant white blood cells, positive nitrites, and leukocyte esterase, together with urinary symptoms of frequency, urgency, or dysuria.[108] A urine culture should be performed, and the infection treated appropriately.[21] After treating the infection and eliminating any abnormal urinary symptoms, a repeat urinalysis should be performed to verify that the hematuria has resolved. If the hematuria persists, a risk-stratified approach to management should be adopted.[1][5] Please see StatPearls' companion reference resource, "Uncomplicated Urinary Tract Infections," for additional information on acute cystitis management.[21] Bladder, ureteral, and renal malignancies: Cancers are the most potentially troubling etiologies of painless hematuria, especially if the blood is easily visible. A full diagnostic urological evaluation is primarily designed to detect such cancers, not necessarily to identify the source of the hematuria. Please see StatPearls' companion reference resources, "Renal Cancer" and "Bladder Cancer," for additional information on evaluating these conditions.[16][17]

Bladder, ureteral, and renal malignancies: Cancers are the most potentially troubling etiologies of painless hematuria, especially if the blood is easily visible. A full diagnostic urological evaluation is primarily designed to detect such cancers, not necessarily to identify the source of the hematuria. Please see StatPearls' companion reference resources, "Renal Cancer" and "Bladder Cancer," for additional information on evaluating these conditions.[16][17] Nephrolithiasis: Renal calculi are a common cause of hematuria. The urinalysis will often show crystals, but this alone is not diagnostic. Some patients may be asymptomatic, but others will have a history of chronic infection or develop symptoms of acute renal colic with severe abdominal or flank pain, nausea, and vomiting. Imaging studies, including a renal ultrasound, along with a kidney, ureter, and bladder x-ray, or a CT scan of the abdomen, are required for proper diagnosis and to demonstrate the urinary calculi.[109][60][48][61] Please see StatPearls' companion reference resources, "Renal Calculi, Nephrolithiasis" and "Urolithiasis."[48][61] Prostatic bleeding: In older male patients with known or suspected benign prostatic hyperplasia (BPH), a prostatic source should be considered a potential cause of hematuria.[46] Reliable confirmation cannot be achieved without a comprehensive diagnostic evaluation, which typically includes appropriate genitourinary imaging and cystoscopy to identify or exclude a prostatic etiology.[1] Please see StatPearls' companion reference resource, "Benign Prostatic Hyperplasia," for additional information.[46]

Prostatic bleeding: In older male patients with known or suspected benign prostatic hyperplasia (BPH), a prostatic source should be considered a potential cause of hematuria.[46] Reliable confirmation cannot be achieved without a comprehensive diagnostic evaluation, which typically includes appropriate genitourinary imaging and cystoscopy to identify or exclude a prostatic etiology.[1] Please see StatPearls' companion reference resource, "Benign Prostatic Hyperplasia," for additional information.[46] Traumatic urinary bleeding: Traumatic bleeding can be minimal or severe and potentially life-threatening, which is why evaluating hematuria in a trauma setting requires a more urgent approach. Unstable patients may require immediate surgical exploration without prior diagnostic imaging. Renal trauma should be suspected in any abdominal trauma case, particularly falls and motor vehicle accidents.[68] A possible urological injury should be suspected in all pelvic trauma cases until proven otherwise by appropriate imaging.[110][67] Blood at the urethral meatus or an inability to void is suggestive of a urethral or bladder injury, which should ideally be evaluated by retrograde urethrography before attempting Foley catheterization.[110][67] A cystogram with adequate bladder filling—typically at least 300 mL—will demonstrate any extravasation or abnormal leakage.[110][67] Potential renal trauma requires immediate CT imaging, if possible.[68][110][67] Please see StatPearls' companion reference resources, "Kidney Trauma" and "Lower Genitourinary Trauma."[68][67] The standard evaluation for hematuria traditionally comprised urine cytology, upper tract imaging with an intravenous pyelogram (now considered obsolete), a CT urogram consisting of a CT of the abdomen and pelvis with and without IV contrast, and a cystoscopy. Cystoscopy is 98% sensitive in detecting bladder cancer.[111] Urine cytology and similar biomarkers are not currently recommended in the initial workup for microhematuria, as they have not demonstrated substantial value and do not eliminate the need for a cystoscopy.[1][5] However, the occasional patient with carcinoma in situ of the bladder may have a negative cystoscopy and be detected only by a positive or suspicious cytology.[1][5][112] Patients with gross hematuria should still have a urine cytology.[3]

The standard evaluation for hematuria traditionally comprised urine cytology, upper tract imaging with an intravenous pyelogram (now considered obsolete), a CT urogram consisting of a CT of the abdomen and pelvis with and without IV contrast, and a cystoscopy. Cystoscopy is 98% sensitive in detecting bladder cancer.[111] Urine cytology and similar biomarkers are not currently recommended in the initial workup for microhematuria, as they have not demonstrated substantial value and do not eliminate the need for a cystoscopy.[1][5] However, the occasional patient with carcinoma in situ of the bladder may have a negative cystoscopy and be detected only by a positive or suspicious cytology.[1][5][112] Patients with gross hematuria should still have a urine cytology.[3] Other biomarkers, such as fluorescence in situ hybridization (FISH) assays, are cumbersome and expensive to use but may help in borderline or equivocal cases, determine response to Bacillus Calmette-Guérin (BCG) therapy, and identify upper tract urothelial cancer that may be poorly visualized on imaging.[113] Therefore, there is a role for cytology and possibly other urine-based malignant biomarkers, such as FISH assays, in patients with persistent microhematuria who also have other high-risk factors for possible carcinoma in situ, e.g., unexplained irritative urinary symptoms, history of gross hematuria, or a significant (10 or more pack years) smoking history.[1][3][5][112] Cytology and urine-based malignant biomarkers are not recommended for the initial evaluation of patients with microhematuria.[1][5] The Updated 2025 American Urological Association Guideline on Microhematuria Risk Stratification Guide The current guideline recommendations for evaluating hematuria rely on a risk-stratification approach to avoid expensive, unnecessary, low-yield, and uncomfortable testing in lower-risk individuals.[1][5][80][114][115] Low-risk patients To be classified as low-risk, patients must meet all of the following criteria: Women younger than 60 years Men younger than 40 years Nonsmoker or less than 10 pack-years Number of RBC/HPF of 3 to 10 No prior episodes of microhematuria No other risk factors for urothelial cancer Estimated cancer risk of less than 1% (0.0%-0.4%) [5][116][117][118] The following management protocol is recommended:

To be classified as low-risk, patients must meet all of the following criteria: Women younger than 60 years Men younger than 40 years Nonsmoker or less than 10 pack-years Number of RBC/HPF of 3 to 10 No prior episodes of microhematuria No other risk factors for urothelial cancer Estimated cancer risk of less than 1% (0.0%-0.4%) [5][116][117][118] The following management protocol is recommended: A repeat urinalysis should be performed within 6 months. If the result is negative, a second microscopic urinalysis may be considered after another 6 months, following shared decision-making with the patient. A positive urinalysis requires reclassification of the patient as either intermediate- or high-risk, followed by management based on the appropriate risk category.[5] Intermediate-Risk Patients To be classified as intermediate-risk, patients must meet any of the following criteria: [5] Women aged 60 years or more Men aged 40 to 59 years Smoker for 10 to 30 pack-years Number of RBCs/HPF of 11 to 25 One or more additional high-risk factors (Refer to "High-Risk Factors for Urothelial Cancers" in the History and Physical section for more details on specific risk factors.) Does not meet criteria for either low-risk or high-risk patient classification A previous episode of low-risk hematuria, which was not evaluated, AND 3 to 25 RBC/HPF on repeat microscopic urinalysis Estimated cancer risk of 0.2% to 3.1% [5][116][117][118] In intermediate-risk patients, evaluation with a renal ultrasonography and a cystoscopy is recommended and should generally be performed. The following treatments, based on the results from the diagnostic studies, are recommended: Positive findings: Treat accordingly. Negative findings: Repeat microscopic urinalysis within 12 months. Negative findings with persistent hematuria: Consider CT urogram or bilateral retrograde pyelograms.[5]

In intermediate-risk patients, evaluation with a renal ultrasonography and a cystoscopy is recommended and should generally be performed. The following treatments, based on the results from the diagnostic studies, are recommended: Positive findings: Treat accordingly. Negative findings: Repeat microscopic urinalysis within 12 months. Negative findings with persistent hematuria: Consider CT urogram or bilateral retrograde pyelograms.[5] Patients who receive appropriate counseling and choose to avoid cystoscopy, while accepting the associated risks, may elect ongoing monitoring through regular urine cytology or urine-based tumor marker testing.[5] When cystoscopy is deferred, a repeat microscopic urinalysis should be completed within 1 year. Persistent microhematuria warrants cystoscopic evaluation at that point. Patients should also undergo renal and bladder ultrasonography as part of their follow-up. This approach does not apply to high-risk patients, who require direct cystoscopic evaluation. Cytology and urine-based tumor markers should not be used during the initial evaluation of patients presenting with microscopic hematuria, but cytology is recommended in patients with gross hematuria.[3] High-Risk Patients To be classified as high-risk, patients must meet any of the following criteria: Men aged 60 years or older (Women are not categorized as high-risk based on age alone) Smoker of more than 30 pack-years More than 25 RBCs per HPF History of gross hematuria Prior episodes of hematuria that have not previously been evaluated by cystoscopy or imaging Does not meet criteria for low or intermediate risk categories One or more additional risk factors (Refer to "High-Risk Factors for Urothelial Cancers" in the History and Physical section for more details on specific risk factors.) Estimated cancer risk of 1.3% to 6.3% [5][116][117][118] High-risk patients require evaluation with a CT scan of the abdomen and pelvis performed both without and with intravenous contrast (CT urogram), along with cystoscopy.[5] Urine cytology is recommended when carcinoma in situ is suspected or when a history of gross hematuria is present.[3] Management strategies depend on the results of these studies. Based on the results, the following management therapies are recommended:

High-risk patients require evaluation with a CT scan of the abdomen and pelvis performed both without and with intravenous contrast (CT urogram), along with cystoscopy.[5] Urine cytology is recommended when carcinoma in situ is suspected or when a history of gross hematuria is present.[3] Management strategies depend on the results of these studies. Based on the results, the following management therapies are recommended: Positive findings: Treatment should be directed toward the identified condition. When a nonmalignant cause is identified, a repeat microscopic urinalysis should be performed after treatment to confirm resolution. Equivocal cystoscopy findings or persistent microhematuria with irritative urinary symptoms: Follow-up urine cytology evaluations may be appropriate to assess for underlying malignancy or ongoing pathology. Negative findings with persistent hematuria: Further evaluation for glomerular bleeding should be considered. Continued observation may be appropriate based on shared decision-making between the clinician and patient. Negative findings: A repeat urinalysis should be performed within 12 months. If the result remains negative, the patient can return to routine surveillance. Follow-up urine cytology evaluations may be considered in individuals with risk factors for carcinoma in situ.[5] Patients who experience a significant increase in microscopic hematuria, develop unexplained gross hematuria, or develop new urologic symptoms should be considered for further evaluation after shared decision-making. Patients with persistent or recurrent microscopic hematuria who were previously evaluated only with ultrasonography should have additional upper urinary tract imaging, e.g., a CT urogram.[5] Patients with microhematuria who have a family history of renal cell malignancies, suspicion of Lynch syndrome, or any other known genetic renal tumor syndrome (Birt-Hogg-Dube, hereditary leiomyomatosis renal cell cancer, hereditary papillary renal cell cancer, tuberous sclerosis, or von Hippel-Lindau) should have upper tract imaging performed regardless of other factors or their risk category.[5]

Patients with microhematuria who have a family history of renal cell malignancies, suspicion of Lynch syndrome, or any other known genetic renal tumor syndrome (Birt-Hogg-Dube, hereditary leiomyomatosis renal cell cancer, hereditary papillary renal cell cancer, tuberous sclerosis, or von Hippel-Lindau) should have upper tract imaging performed regardless of other factors or their risk category.[5] Magnetic resonance imaging (MRI) urography may be substituted if a CT urogram cannot be performed. If neither is possible, a noncontrast CT scan, an ultrasound of the abdomen and pelvis, and a bilateral retrograde pyelogram may be performed.[1] Upper tract imaging should be done regardless of risk category in patients with hematuria and a family history of renal cell carcinoma or any genetic predisposition to renal malignancies.[1] Initial imaging during pregnancy should be limited to ultrasonography. Blue light cystoscopy and other enhanced visualization techniques may be useful in patients previously diagnosed with bladder cancer, but their role in evaluating patients with microscopic hematuria remains unclear.[1][5] Patients with microscopic hematuria whose initial evaluations are negative have been found to have an ultimate urologic malignancy rate of less than 1% and, therefore, do not generally require follow-up urological evaluations unless they develop gross hematuria.[119] Nevertheless, the guidelines recommend a follow-up urinalysis in 12 months.[1][5] The patient's primary care physician can perform this. Patients with persistent microscopic hematuria have a higher risk of malignancy than those who test negative on follow-up examinations and, therefore, should be reclassified as intermediate-risk or high-risk.[1][5][102] Cytology and Urinary Biomarkers

Patients with microscopic hematuria whose initial evaluations are negative have been found to have an ultimate urologic malignancy rate of less than 1% and, therefore, do not generally require follow-up urological evaluations unless they develop gross hematuria.[119] Nevertheless, the guidelines recommend a follow-up urinalysis in 12 months.[1][5] The patient's primary care physician can perform this. Patients with persistent microscopic hematuria have a higher risk of malignancy than those who test negative on follow-up examinations and, therefore, should be reclassified as intermediate-risk or high-risk.[1][5][102] Cytology and Urinary Biomarkers Various biomarkers and cytology are not recommended for the initial evaluation of patients with microscopic hematuria due to their high false-negative rates and lack of proven benefit in large, well-designed, randomized trials.[1][5][120][121] Urinary cytology has a relatively low sensitivity for low-grade urothelial bladder malignancies.[120][121] Urine cytology remains the only biomarker to have gained consensus acceptance in guidelines, and even then, it is not recommended for the initial evaluation of asymptomatic patients with microscopic hematuria.[1][5] However, it is recommended for patients with gross hematuria, especially if they have a significant smoking history (10 or more pack years).[3][122] Various other biomarkers are available but lack verification from large prospective randomized studies.[120][121] If a urinary biomarker is done anyway and has a positive result, the patient should be treated as a higher risk, and follow-up studies are indicated.[120] The decision to perform a cystoscopy for a patient with microhematuria should not be based on the results of an initial urine cytology or urine-based tumor marker.[5] Urine cytology is most appropriate for patients with persistent or recurrent unexplained microscopic hematuria and irritative voiding symptoms, or for those presenting with other risk factors for carcinoma in situ.[1][5][16] Cytology and urine-based tumor markers are not recommended for patients with microscopic hematuria without risk factors for carcinoma in situ and a normal cystoscopy.[3][5] Glomerular Hematuria Evaluation

The decision to perform a cystoscopy for a patient with microhematuria should not be based on the results of an initial urine cytology or urine-based tumor marker.[5] Urine cytology is most appropriate for patients with persistent or recurrent unexplained microscopic hematuria and irritative voiding symptoms, or for those presenting with other risk factors for carcinoma in situ.[1][5][16] Cytology and urine-based tumor markers are not recommended for patients with microscopic hematuria without risk factors for carcinoma in situ and a normal cystoscopy.[3][5] Glomerular Hematuria Evaluation Glomerular hematuria is suggested by the presence of excessive urinary protein (>500 mg/24 hours), dysmorphic RBCs, or casts, especially red cell casts, particularly if associated with clinical findings, eg, hypertension, peripheral edema, and "frothy" or "foamy" urine.[123][124] Dysmorphic RBCs of more than 25% per HPF have a specificity greater than 96% and an excellent positive predictive value of 94.6%, but low sensitivity (20%) for glomerulonephritis.[125] RBC casts are rare but highly diagnostic and specific for glomerular pathology.[123] Such patients are usually referred to nephrology for further evaluation, but a risk-based urological evaluation should still be performed.[1][5] Glomerulonephritis describes several renal disorders characterized by damage to the glomerular basement membrane, capillary endothelium, or mesangium from abnormal immune system activity.[13] This damage tends to be progressive, resulting in increasing glomerular damage, tubulointerstitial fibrosis, and reduced plasma filtering ability, eventually resulting in sclerotic glomeruli and renal failure in many cases. This damage is also responsible for the hematuria, proteinuria, red cell casts, and renal dysfunction associated with the disorder.[13] Glomerulonephritis accounts for 10% to 15% of all patients with end-stage renal failure in the US, making it the third most common cause after diabetes and hypertension.[13] Further evaluation of glomerulonephritis generally includes: Antistreptolysin O titer Autoantibodies (eg, antinuclear, antineutrophil cytoplasmic, antiglomerular basement membrane, and anti-ds-DNA antibodies) C-reactive protein Complement (C3, C4 levels) Complete blood count (CBC) Cryoglobulins Immunoglobulins Liver function Renal function tests (eg, BUN and creatinine) Serology for HIV, hepatitis B, and hepatitis C

Antistreptolysin O titer Autoantibodies (eg, antinuclear, antineutrophil cytoplasmic, antiglomerular basement membrane, and anti-ds-DNA antibodies) C-reactive protein Complement (C3, C4 levels) Complete blood count (CBC) Cryoglobulins Immunoglobulins Liver function Renal function tests (eg, BUN and creatinine) Serology for HIV, hepatitis B, and hepatitis C Serum electrolytes Serum levels of free light chain immunoglobulins and serum immunofixation Sickle cell testing (eg, peripheral smear, solubility sickling tests, hemoglobin electrophoresis, isoelectric focusing, high-performance liquid chromatography, PCR-based testing, and genetic testing) Urine analysis ratios (eg, albumin to creatinine or protein to creatinine ratios) Urine collection over 24 hours for urea and creatinine clearance, as well as quantitative protein measurements. Urinary Bence-Jones proteins [13] Depending on the clinical evaluation and the results from the above, a renal biopsy may be considered.[13][126] Renal biopsies are often necessary for a definitive diagnosis of glomerulonephritis and related glomerular bleeding.[126] They are typically required when a glomerular source of hematuria appears likely. Although serious complications are rare, renal biopsy can have adverse effects, including life-threatening bleeding. A nephrologist or interventional radiologist usually performs the procedure.[126] Usually, only 2 or 3 biopsy cores are sufficient for diagnostic purposes. Standard light optical microscopy, electron microscopy, and immunofluorescence are performed to examine the glomerular structure for specific diagnosis. Glomerulonephritis leads to 10% to 15% of end-stage renal disease cases in the US.[13] In most instances, the disease becomes progressive without timely intervention, eventually leading to morbidity.[70] This makes chronic glomerulonephritis the third most common cause of end-stage renal disease in the US, following diabetes mellitus and hypertension, accounting for 10% of patients on dialysis.[13] The finding of hematuria, together with glomerular podocytopathies (e.g., focal segmental glomerulosclerosis, membranous nephropathy, and minimal change disease), is an independent, significant indicator of worse outcomes, more prolonged proteinuria, and an increased risk of progressive renal failure.[127] Please see StatPearls' companion reference resource, "Glomerulonephritis," for additional information.[13]

Glomerulonephritis leads to 10% to 15% of end-stage renal disease cases in the US.[13] In most instances, the disease becomes progressive without timely intervention, eventually leading to morbidity.[70] This makes chronic glomerulonephritis the third most common cause of end-stage renal disease in the US, following diabetes mellitus and hypertension, accounting for 10% of patients on dialysis.[13] The finding of hematuria, together with glomerular podocytopathies (e.g., focal segmental glomerulosclerosis, membranous nephropathy, and minimal change disease), is an independent, significant indicator of worse outcomes, more prolonged proteinuria, and an increased risk of progressive renal failure.[127] Please see StatPearls' companion reference resource, "Glomerulonephritis," for additional information.[13] Hematuria in Children In the pediatric population, gross and microscopic hematuria are relatively common findings with overlapping etiologies.[128] Normal children will have positive urine dipsticks for hematuria 1% to 4% of the time. Unlike adults, hematuria in children rarely occurs due to an underlying malignancy.[129] Family history can suggest an underlying hereditary etiology.[83] Asymptomatic, isolated microscopic hematuria is often idiopathic with no identifiable etiology.[128] Microscopic hematuria generally suggests an upper urinary tract source, while gross hematuria is more likely from the bladder or urethra.[83][129] When a specific cause is identified, the most common diagnoses are glomerulonephritis conditions (eg, poststreptococcal or infectious, IgA nephropathy, and thin basement membrane disease), urinary tract infections, or hypercalciuria.[128] The most common glomerulonephritis in children is poststreptococcal or infectious types.[128][129][130] Moreover, proteinuria, fluid overload, casts or dysmorphic RBCs on urinary microscopy, brown "cola"- colored hematuria, or hypertension suggest glomerular disease in the pediatric age group, as in adults.[128][129]

When a specific cause is identified, the most common diagnoses are glomerulonephritis conditions (eg, poststreptococcal or infectious, IgA nephropathy, and thin basement membrane disease), urinary tract infections, or hypercalciuria.[128] The most common glomerulonephritis in children is poststreptococcal or infectious types.[128][129][130] Moreover, proteinuria, fluid overload, casts or dysmorphic RBCs on urinary microscopy, brown "cola"- colored hematuria, or hypertension suggest glomerular disease in the pediatric age group, as in adults.[128][129] IgA vasculitis, also known as Henoch-Schönlein purpura, occurs infrequently, with approximately 10 to 20 cases per 100,000 children.[35] This immune-mediated glomerulonephritis primarily affects children younger than 10 years and may also involve the gastrointestinal tract, resulting in bleeding. Episodes of hematuria often follow an infection. Renal manifestations range from mild disease to severe crescentic glomerulonephritis.[35] Initial treatment typically includes corticosteroids, although angiotensin-converting enzyme inhibitors (ACEIs), immunosuppressants, and plasma exchange may also be indicated.[35] The condition generally resolves spontaneously, with only about 1% of patients progressing to end-stage renal failure.[35] Please see StatPearls' companion reference resource, "IgA Vasculitis (Henoch-Schönlein Purpura)," for further details.[35] Hemolytic uremic syndrome occurs predominantly in childhood and should be suspected in pediatric patients with hematuria accompanied by anemia, thrombocytopenia, or azotemia.[131][132][133][134] This disorder affects approximately 3 in 100,000 children and typically follows a bacterial infection linked to consumption of unpasteurized milk or undercooked beef. Gastrointestinal symptoms frequently accompany the illness, and management remains primarily supportive.[134] Please see StatPearls' companion reference resource, "Hemolytic Uremic Syndrome," for further information.

Management depends on the underlying etiology. Observation may be a reasonable approach for asymptomatic intermittent hematuria associated with negative imaging, stable renal function, and absence of proteinuria. Overt gross hematuria needs prompt management. Hemodynamic stability should be assured first. Blood products, transfusions, or medications should be utilized to correct any underlying hematological abnormality. In rare instances, interventional radiology-guided embolization may be required to stop life-threatening bleeding from the renal vasculature or for hemorrhagic cystitis refractory to conventional treatments.[135][136] Immediate Management of Significant Gross Hematuria Significant gross hematuria, especially when associated with urinary difficulty, voiding of clots, clot retention, or severe blood loss, will require immediate treatment with a large (ie, ≥22 French) 3-way Foley catheter placement and continuous bladder irrigation (CBI). Evacuation of clots from the bladder by vigorous hand irrigation or transurethral surgical extraction may be required to control the hematuria. A large 30 cc balloon is not recommended except immediately after transurethral prostate resection.[137] Anticoagulant therapy should be stopped or reversed when possible. If all the clots in the bladder are not evacuated, the Foley catheter will likely become clogged, and the breakdown products of urokinase activity will act as natural anticoagulants, prolonging bleeding.[138] More invasive surgical options to control significant gross hematuria include nephrostomy tube placement for supravesical urinary diversion and interventional radiological superselective embolization of the prostatic artery or the anterior branch of the internal iliac artery.[139][140] The final treatment of last resort would be a cystectomy with urinary diversion.[141][142][143][144][145] Treatment selection typically starts with the least invasive therapy and progresses as necessary. Chemical thrombolysis The need to take a patient to the operating room for electrocautery or laser ablation with clot evacuation when initial manual irrigation is unsuccessful can sometimes be avoided by using chemical thrombolysis. The following techniques successfully soften and dissolve retained clots in the bladder,[146][147] allowing them to be evacuated through the catheter and avoiding surgical clot evacuation:

The need to take a patient to the operating room for electrocautery or laser ablation with clot evacuation when initial manual irrigation is unsuccessful can sometimes be avoided by using chemical thrombolysis. The following techniques successfully soften and dissolve retained clots in the bladder,[146][147] allowing them to be evacuated through the catheter and avoiding surgical clot evacuation: Administer limited palliative radiation therapy in selected cases of otherwise intractable hematuria if ionizing radiation has not been previously utilized.[148][149][150][151][152][153][154][155] Instill 30 to 50 mL of a hydrogen peroxide irrigation solution (1:5 mixture of 3% hydrogen peroxide and 0.9% saline) into the bladder and leave it there for 3 to 5 minutes. The bladder is then manually irrigated and evacuated.[147] The process is repeated with another installation of the hydrogen peroxide solution placed into the bladder.[147] Instill 40,000 units of chymotrypsin into 50 mL of 5% sodium bicarbonate solution using a large 22- to 24-French Foley catheter, and leave it in the bladder for 30 minutes.[146] Place a nephrostomy tube for supravesical urinary diversion and interventional radiological superselective embolization of the prostatic artery or the anterior branch of the internal iliac artery.[139][140] Superselectively embolize a vesicle branch of the hypogastric or prostatic artery in otherwise intractable cases.[139][140] Utilize urinary diversion with a cystectomy, which is the final treatment of last resort when nothing else has worked.[141][142][143][144][145] Hemorrhagic cystitis management Controlling bleeding from hemorrhagic cystitis can be particularly challenging, most often seen after pelvic irradiation (ie, radiation cystitis) or after chemotherapy, particularly with oxazaphosphorines (eg, cyclophosphamide, ifosfamide, and trofosfamide). Treatment selection typically starts with the least invasive therapy and progresses as necessary.

Controlling bleeding from hemorrhagic cystitis can be particularly challenging, most often seen after pelvic irradiation (ie, radiation cystitis) or after chemotherapy, particularly with oxazaphosphorines (eg, cyclophosphamide, ifosfamide, and trofosfamide). Treatment selection typically starts with the least invasive therapy and progresses as necessary. Bleeding from radiation cystitis can be managed with pentosan polysulfate, transurethral electrofulguration/laser treatment, and intravesical instillations (e.g., silver nitrate, formalin, or alum).[136][156][157][158] Of the intravesical instillations mentioned, formalin is the most toxic to the bladder mucosa and is therefore reserved as one of the final options.[156][159][160][161] Hyperbaric oxygen therapy with or without oral pentosan polysulfate can be used and is particularly helpful with radiation-induced hemorrhagic cystitis.[64][162] Severe hemorrhagic cystitis may need transurethral surgery with electrocautery or laser therapy.[136] Intractable cases of severe hemorrhagic or radiation cystitis may even require a cystectomy.[141][142][143][144][145] Please see StatPearls' companion reference resource, "Radiation Cystitis and Hyperbaric Management," for additional information on hyperbaric management of radiation cystitis.[64] Nonglomerular Hematuria Management The management approach selected depends on the underlying etiology and severity of the hematuria. Acute urinary tract infections Acute urinary tract infections are treated with 3 to 7 days of first-line antibiotics.[126] Complicated infections will take longer to resolve.[55] Bladder cancer and transitional cell (urothelial) carcinoma Bladder cancer may require transurethral resection, arterial embolization, palliative radiation, or even a cystectomy to control severe, intractable bleeding not responding to Foley catheterization, clot evacuation, irrigation, and intravesical therapies.[148][151][163][164]

Bladder cancer and transitional cell (urothelial) carcinoma Bladder cancer may require transurethral resection, arterial embolization, palliative radiation, or even a cystectomy to control severe, intractable bleeding not responding to Foley catheterization, clot evacuation, irrigation, and intravesical therapies.[148][151][163][164] Transitional cell carcinoma can occur anywhere in the genitourinary tract, but is most often found in the bladder.[16] Transurethral resection of the tumor and periodic cystoscopies are the standard recommended therapy. Invasive bladder cancers may require a cystectomy, and high-grade carcinoma-in-situ of the bladder will require intravesical Bacillus Calmette-Guerin (BCG) vaccine therapy.[16][165][166] Metastatic cancers will require staging and further individualized oncological treatment, including radiotherapy or surgical management. Genitourinary trauma Genitourinary trauma will require specific therapy depending on the hemodynamic stability of the patient and the severity and location of the injury. Most renal injuries can be managed conservatively if the patient is hemodynamically stable.[68] Ureteral trauma is uncommon and will often heal with stenting, but may require surgical repair.[110][67] Intraperitoneal bladder ruptures typically need immediate surgery, but extraperitoneal leakages will often heal with catheter drainage alone.[110][67] Urethral injuries may need to be surgically repaired, either immediately or after a reasonable delay of 2 to 3 months, using suprapubic drainage in the interim.[167] Postprocedural hematuria can usually be managed conservatively or with a Foley catheter and irrigation as appropriate. Please see StatPearls' companion reference resources, "Kidney Trauma" and "Lower Genitourinary Trauma," for additional information on the management of hematuria due to renal and genitourinary injuries.[29][68][67][64] Prostatic bleeding

Genitourinary trauma will require specific therapy depending on the hemodynamic stability of the patient and the severity and location of the injury. Most renal injuries can be managed conservatively if the patient is hemodynamically stable.[68] Ureteral trauma is uncommon and will often heal with stenting, but may require surgical repair.[110][67] Intraperitoneal bladder ruptures typically need immediate surgery, but extraperitoneal leakages will often heal with catheter drainage alone.[110][67] Urethral injuries may need to be surgically repaired, either immediately or after a reasonable delay of 2 to 3 months, using suprapubic drainage in the interim.[167] Postprocedural hematuria can usually be managed conservatively or with a Foley catheter and irrigation as appropriate. Please see StatPearls' companion reference resources, "Kidney Trauma" and "Lower Genitourinary Trauma," for additional information on the management of hematuria due to renal and genitourinary injuries.[29][68][67][64] Prostatic bleeding Prostatic bleeding can generally be controlled with a standard Foley catheter or a 3-way catheter with continuous bladder irrigation. If this is not adequate, transurethral fulguration, selective prostatic artery embolization, or even a brief course of palliative radiation therapy may be used.[139][140][148][149][150][151][152][153] Less severe hematuria from the prostate can often be managed with 5-alpha reductase inhibitors (eg, finasteride and dutasteride).[168][169] Severe bleeding from prostatic cancer may require transurethral electrocautery and possible resection, the initiation of hormone-ablative therapy, antiandrogens with a luteinizing hormone-releasing hormone antagonist (eg, degarelix), and palliative radiation therapy.[148][152][163][170] Renal cell carcinoma Renal cell carcinoma, other malignancies confined to the kidneys, and renal pelvic urothelial cancers will require surgery and possible nephrectomy or nephroureterectomy.[171] Palliative radiation therapy or selective renal arterial branch embolization for hematuria control can be considered in selected patients with bleeding from a kidney.[148][154][155] Various benign renal neoplasms (angiomyolipomas, oncocytomas) may also cause hematuria and require surgical ablation, medical therapy, embolization, or other surgery.[172][173] Urolithiasis

Renal cell carcinoma, other malignancies confined to the kidneys, and renal pelvic urothelial cancers will require surgery and possible nephrectomy or nephroureterectomy.[171] Palliative radiation therapy or selective renal arterial branch embolization for hematuria control can be considered in selected patients with bleeding from a kidney.[148][154][155] Various benign renal neoplasms (angiomyolipomas, oncocytomas) may also cause hematuria and require surgical ablation, medical therapy, embolization, or other surgery.[172][173] Urolithiasis Urolithiasis management is generally supportive, emphasizing pain control, preventing or treating infections, facilitating stone passage, and ensuring adequate hydration.[48] Stone size, symptoms, and location may warrant further management.[174] Approximately 90% of stones smaller than 4 mm will pass spontaneously. Larger symptomatic stones may require lithotripsy, ureteroscopy, or percutaneous surgery.[109][175] If complicated by a simultaneous urinary tract infection, preliminary drainage with a nephrostomy or double-J stent will most likely be required until the infection is eliminated and definitive stone treatment can be undertaken.[109][176][177] Severe bleeding from urolithiasis is rare. Glomerular Hematuria Management The management approach for glomerular hematuria also depends on the underlying cause and the effect on renal function. Some hereditary diseases, like Alport syndrome, thin basement membrane disease, and polycystic kidney disease, require regular monitoring of renal function and periodic follow-up examinations. Poststreptococcal glomerulonephritis requires supportive care, and IgA nephropathy treatment depends on the degree of proteinuria and renal function.[13] Relatively normal creatinine with minimal proteinuria may be managed conservatively.

The management approach for glomerular hematuria also depends on the underlying cause and the effect on renal function. Some hereditary diseases, like Alport syndrome, thin basement membrane disease, and polycystic kidney disease, require regular monitoring of renal function and periodic follow-up examinations. Poststreptococcal glomerulonephritis requires supportive care, and IgA nephropathy treatment depends on the degree of proteinuria and renal function.[13] Relatively normal creatinine with minimal proteinuria may be managed conservatively. High-risk features, including rising creatinine levels, persistent proteinuria (>1 g/day), and active disease on renal biopsy, warrant consideration of immunosuppressive therapy.[178] General treatment for most glomerulopathies includes angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin II receptor blockers (ARB), which help control hypertension, reduce proteinuria, and slow disease progression.[13] Nephrotic syndrome and other etiologies generally necessitate a nephrology consultation for further management. Please see StatPearls' companion reference resource, "Nephrotic Syndrome," for further details.[40] The following management approaches are recommended for these specific heritable or genetic glomerular disorders: Alport syndrome: A hereditary disorder of type IV collagen production that affects the renal glomerular basement membranes, eyes, and ears, characterized by progressive renal failure, bilateral sensorineural hearing loss, and eye abnormalities. Alport syndrome eventually produces proteinuria, hypertension, progressive azotemia, and end-stage renal disease.[23][179][180] In addition to ACEI or ARB medications, adding a statin and a non-dihydropyridine calcium channel blocker appears helpful. One study shows that ramipril can decrease disease progression in children by almost half.[181] The condition tends to be progressive and may eventually require dialysis or renal transplantation.[23] See our companion StatPearls reference article on "Alport Syndrome."[23] Pierson syndrome: This rare syndrome is very similar to Alport syndrome. Pierson syndrome mainly affects the eyes and kidneys, resulting in microcoria, visual problems, and congenital nephrotic syndrome, which is progressive. Hypotonic musculature and blindness may also develop.[182][183]

Alport syndrome: A hereditary disorder of type IV collagen production that affects the renal glomerular basement membranes, eyes, and ears, characterized by progressive renal failure, bilateral sensorineural hearing loss, and eye abnormalities. Alport syndrome eventually produces proteinuria, hypertension, progressive azotemia, and end-stage renal disease.[23][179][180] In addition to ACEI or ARB medications, adding a statin and a non-dihydropyridine calcium channel blocker appears helpful. One study shows that ramipril can decrease disease progression in children by almost half.[181] The condition tends to be progressive and may eventually require dialysis or renal transplantation.[23] See our companion StatPearls reference article on "Alport Syndrome."[23] Pierson syndrome: This rare syndrome is very similar to Alport syndrome. Pierson syndrome mainly affects the eyes and kidneys, resulting in microcoria, visual problems, and congenital nephrotic syndrome, which is progressive. Hypotonic musculature and blindness may also develop.[182][183] Polycystic kidney disease: Polycystic kidney disease (PKD) is the most common genetic cause of end-stage renal failure in the adult population and accounts for 6% to 8% of patients on dialysis.[24] Approximately 50% of patients will need kidney replacement therapy by the age of 60. Cyst aspiration with ultrasound or CT guidance can be used for pain from large cysts distorting the genitourinary system, but this treatment will not change the course of the disease. Laparoscopic surgical cyst fenestration may also help. Polycystic kidney disease has no specific treatment; if it progresses to end-stage renal failure, dialysis or renal transplantation can be performed. Nephrectomy is usually recommended at that point.[24] Approximately 20% of patients with polycystic kidney disease will develop nephrolithiasis.[24][22] Please see StatPearls' companion reference resources, "Polycystic Kidney Disease In Adults" and "Autosomal Dominant Polycystic Kidney Disease," for additional management details.[22][24][184]

Polycystic kidney disease: Polycystic kidney disease (PKD) is the most common genetic cause of end-stage renal failure in the adult population and accounts for 6% to 8% of patients on dialysis.[24] Approximately 50% of patients will need kidney replacement therapy by the age of 60. Cyst aspiration with ultrasound or CT guidance can be used for pain from large cysts distorting the genitourinary system, but this treatment will not change the course of the disease. Laparoscopic surgical cyst fenestration may also help. Polycystic kidney disease has no specific treatment; if it progresses to end-stage renal failure, dialysis or renal transplantation can be performed. Nephrectomy is usually recommended at that point.[24] Approximately 20% of patients with polycystic kidney disease will develop nephrolithiasis.[24][22] Please see StatPearls' companion reference resources, "Polycystic Kidney Disease In Adults" and "Autosomal Dominant Polycystic Kidney Disease," for additional management details.[22][24][184] Thin basement membrane disease: Formerly known as familial benign hematuria, this relatively common hereditary renal disorder may present in 5% to 9% of adults.[185][186][187] The finding of diffuse thinning of the glomerular basement membrane on electron microscopy of a renal biopsy is diagnostic. A history of familial hematuria is present in 30% to 50% of cases. This disorder is sometimes associated with focal segmental glomerulosclerosis.[188] Thin basement membrane disease may be a less severe form of Alport syndrome, as both involve thinning the glomerular basement membrane.[189][190] The diagnosis of thin basement membrane disease is usually suggested by a benign course, lack of proteinuria, and a positive family history of hematuria without renal failure. In the absence of proteinuria, hypertension, peripheral edema, or renal failure, a renal biopsy may not be required. No treatment is usually necessary as it typically has a benign course, although significant proteinuria and a family history of renal failure suggest a more guarded prognosis.[43][191] Close monitoring and follow-up examinations are suggested.[43][191] Please see StatPearls' companion reference resource, "Thin Basement Membrane Nephropathy," for additional information.[43]

The diagnosis of thin basement membrane disease is usually suggested by a benign course, lack of proteinuria, and a positive family history of hematuria without renal failure. In the absence of proteinuria, hypertension, peripheral edema, or renal failure, a renal biopsy may not be required. No treatment is usually necessary as it typically has a benign course, although significant proteinuria and a family history of renal failure suggest a more guarded prognosis.[43][191] Close monitoring and follow-up examinations are suggested.[43][191] Please see StatPearls' companion reference resource, "Thin Basement Membrane Nephropathy," for additional information.[43] In addition to ACE-I and ARB medications, autoimmune glomerular disorders often require additional therapies. Corticosteroids are used in some cases, especially if excessive proteinuria is noted.[13][192] Rituximab is a monoclonal immunosuppressive antibody that lyses B-lymphocytes.[193] Rituximab is most useful in membranoproliferative glomerulonephritis, lupus nephritis, and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides.[193][194] Cytotoxic agents (eg, cyclophosphamide and methotrexate) may be used, as well as plasma exchange and calcineurin inhibitors, which reduce T-cell activity.[13] Please see StatPearls' companion reference resource, "Glomerulonephritis," for further information.[13] The following management approaches are recommended for these autoimmune glomerular disorders: Antiglomerular basement membrane disease: Also known as Goodpasture syndrome, this condition significantly affects the lungs and kidneys. Although genetic predisposition contributes to disease development, an additional trigger—eg, drug exposure, medical procedures, or toxins—typically damages the alveolar capillaries and initiates the autoimmune response.[34] Anti-GBM disease accounts for approximately 10% to 20% of all cases of crescentic glomerulonephritis. Initial management includes prednisone, cyclophosphamide, and daily plasmapheresis, while steroids are used to control life-threatening alveolar hemorrhage.[34] Rituximab has also demonstrated benefit in some patients.[195] Please see StatPearls' companion reference resource, "Goodpasture Syndrome," for more information.[34]

Antiglomerular basement membrane disease: Also known as Goodpasture syndrome, this condition significantly affects the lungs and kidneys. Although genetic predisposition contributes to disease development, an additional trigger—eg, drug exposure, medical procedures, or toxins—typically damages the alveolar capillaries and initiates the autoimmune response.[34] Anti-GBM disease accounts for approximately 10% to 20% of all cases of crescentic glomerulonephritis. Initial management includes prednisone, cyclophosphamide, and daily plasmapheresis, while steroids are used to control life-threatening alveolar hemorrhage.[34] Rituximab has also demonstrated benefit in some patients.[195] Please see StatPearls' companion reference resource, "Goodpasture Syndrome," for more information.[34] Crescentic glomerulonephritis: Crescentic glomerulonephritis, or rapidly progressive glomerulonephritis, represents an autoimmune disorder characterized by extensive glomerular crescents in more than 50% of glomeruli, formed from infiltrating macrophages and proliferating epithelial cells of Bowman’s capsule.[191][32] The condition causes a rapid decline in renal function and may develop as a complication of other glomerulopathies. Initial therapy includes glucocorticoids with cyclophosphamide or, in selected patients, rituximab. Plasma exchange can provide additional benefit. Maintenance therapy may involve azathioprine, methotrexate, or rituximab.[191][32] Please see StatPearls' companion reference resource, "Crescentic Glomerulonephritis," for additional management information.[32] Diffuse proliferative glomerulonephritis: A condition often associated with lupus nephritis, its severity can vary widely.[37][196] Standard treatment includes ACEI or ARB plus statins due to the high rate of cardiovascular atherosclerosis.[196] More severe disease is treated with corticosteroids. If unresponsive to steroids, calcineurin inhibitors (eg, tacrolimus) can be added. Plasmapheresis, mycophenolate mofetil, and cyclophosphamide are used in selected cases.[196] Please see StatPearls' companion reference resources, "Diffuse Proliferative Glomerulonephritis" and "Lupus Nephritis" for additional information.[37][196]

Diffuse proliferative glomerulonephritis: A condition often associated with lupus nephritis, its severity can vary widely.[37][196] Standard treatment includes ACEI or ARB plus statins due to the high rate of cardiovascular atherosclerosis.[196] More severe disease is treated with corticosteroids. If unresponsive to steroids, calcineurin inhibitors (eg, tacrolimus) can be added. Plasmapheresis, mycophenolate mofetil, and cyclophosphamide are used in selected cases.[196] Please see StatPearls' companion reference resources, "Diffuse Proliferative Glomerulonephritis" and "Lupus Nephritis" for additional information.[37][196] Hepatitis-related nephropathy: This autoimmune glomerular disorder can present as membranoproliferative glomerulonephritis or mixed cryoglobulinemia. Treatment is similar to other autoimmune and postinfectious glomerulopathies, with the addition of appropriate antiviral therapy.[197][198][199][200][201] IgA nephropathy: IgA nephropathy, or Berger disease, represents one of the most frequent causes of microscopic hematuria worldwide. The disease commonly begins with painless, intermittent gross hematuria related to upper respiratory infections and may progress to persistent microhematuria.[36] The condition occurs slightly more often in males and White populations. Up to 20% of patients may progress to chronic renal failure, typically over a 10-year period following diagnosis.[36][202] Treatment involves ACE inhibitors or ARBs, with corticosteroids added when proteinuria is excessive.[13][36][202] Please see StatPearls' companion reference resource, "IgA Nephropathy (Berger Disease)" for additional management information.[36][202]

IgA nephropathy: IgA nephropathy, or Berger disease, represents one of the most frequent causes of microscopic hematuria worldwide. The disease commonly begins with painless, intermittent gross hematuria related to upper respiratory infections and may progress to persistent microhematuria.[36] The condition occurs slightly more often in males and White populations. Up to 20% of patients may progress to chronic renal failure, typically over a 10-year period following diagnosis.[36][202] Treatment involves ACE inhibitors or ARBs, with corticosteroids added when proteinuria is excessive.[13][36][202] Please see StatPearls' companion reference resource, "IgA Nephropathy (Berger Disease)" for additional management information.[36][202] Membranous glomerulonephritis: This condition, a leading cause of nephrotic syndrome worldwide, involves immune-complex deposition beneath the subepithelial podocytes of glomerular capillaries. The disorder results from an autoimmune reaction involving antibodies targeting podocytes. Approximately 12 million individuals in the United States receive a diagnosis of membranous glomerulopathy annually.[203] Systemic lupus erythematosus represents the most frequent cause of secondary membranous nephropathy, classified as type V lupus nephritis.[37] Patients typically exhibit nephrotic-range proteinuria, hematuria, and hypertension. Kidney biopsy findings include positive staining for IgG, IgM, IgA, C3, and C1q.[38] Treatment parallels that of other autoimmune glomerular diseases and begins with ACE inhibitors or ARBs. Additional therapies may include immunosuppressive agents, corticosteroids, cyclophosphamide, calcineurin inhibitors, or rituximab.[204] Please see StatPearls' companion reference resource, "Membranous Nephropathy," for additional management information.[38][38]

Membranous glomerulonephritis: This condition, a leading cause of nephrotic syndrome worldwide, involves immune-complex deposition beneath the subepithelial podocytes of glomerular capillaries. The disorder results from an autoimmune reaction involving antibodies targeting podocytes. Approximately 12 million individuals in the United States receive a diagnosis of membranous glomerulopathy annually.[203] Systemic lupus erythematosus represents the most frequent cause of secondary membranous nephropathy, classified as type V lupus nephritis.[37] Patients typically exhibit nephrotic-range proteinuria, hematuria, and hypertension. Kidney biopsy findings include positive staining for IgG, IgM, IgA, C3, and C1q.[38] Treatment parallels that of other autoimmune glomerular diseases and begins with ACE inhibitors or ARBs. Additional therapies may include immunosuppressive agents, corticosteroids, cyclophosphamide, calcineurin inhibitors, or rituximab.[204] Please see StatPearls' companion reference resource, "Membranous Nephropathy," for additional management information.[38][38] Poststreptococcal glomerulonephritis: This condition typically appears within 6 weeks of a streptococcal skin infection but only 1 to 2 weeks after a streptococcal sore throat. The inflammatory response to streptococcal infection triggers a significant autoimmune reaction, often leading to a rapid decline in renal function.[41] Symptoms may include gross hematuria (seen in 30%-50% of cases), oliguria, hypertension, peripheral edema found in 65% to 90% of cases, and proteinuria.[41] Skin infections are becoming a more common etiology, although the overall incidence of poststreptococcal glomerulonephritis is declining in developed countries. Even so, poststreptococcal glomerulonephritis remains the most common cause of glomerulonephritis in children, even in the US.[128] Please see StatPearls' companion reference resource, "Poststreptococcal Glomerulonephritis," for additional information.[41] Worldwide, 97% of cases are found in underdeveloped regions.[41] Treatment involves supportive therapy along with antibiotics. ACEI or ARBs are also recommended, and calcium channel blockers may be used if necessary.[41] Corticosteroids are reserved for patients who develop kidney failure or have crescents on renal biopsy, while immunosuppression does not appear to be helpful in this disorder.[41]

Worldwide, 97% of cases are found in underdeveloped regions.[41] Treatment involves supportive therapy along with antibiotics. ACEI or ARBs are also recommended, and calcium channel blockers may be used if necessary.[41] Corticosteroids are reserved for patients who develop kidney failure or have crescents on renal biopsy, while immunosuppression does not appear to be helpful in this disorder.[41] Dialysis is reserved for only the most severe cases. Furosemide is preferred over thiazides for controlling hypertension and edema, along with fluid and salt restriction.[41]

The differential diagnosis of hematuria includes etiologies that cause the appearance of discolored red, pink, brown, or yellow urine, including: Alkaptonuria Bile pigments in urine Drug effects False positive urine dipstick test not confirmed by microscopy Hemoglobinuria Hemolytic anemias Porphyria Rhabdomyolysis Phenazopyridine use Various foods (eg, beets, blackberries, and fava beans)

Children with isolated hematuria generally experience favorable outcomes; however, the coexistence of proteinuria, hypertension, or impaired renal function indicates a glomerular origin and often carries a more guarded prognosis. In adults, unexplained hematuria—particularly when gross—requires careful evaluation because it may indicate an underlying urinary tract malignancy. Nonglomerular hematuria typically has a favorable prognosis, as most causes respond well to targeted therapies. In contrast, genetic glomerulopathies present greater challenges, as available treatments offer limited efficacy and disease progression can ultimately lead to end-stage renal failure. Thin basement membrane disease, previously known as benign familial hematuria, has an excellent prognosis and does not require specific therapy.[43] Hematuria resulting from BPH, urinary tract infections, superficial bladder cancer, or urolithiasis generally responds well to treatment, yielding good overall outcomes. Prognosis for other causes depends on the type and severity of the underlying pathology. Prompt recognition and appropriate management remain essential to reduce complications and preserve renal function.

The following issues and complications can be associated with hematuria: False positives are common if microscopic urinalyses are not used to confirm positive dipstick findings for microhematuria. This causes costly, unnecessary evaluations and consultations. Failure to properly evaluate or treat hematuria may result in catastrophic or life-threatening disease. Some conditions may result in progressive loss of renal function, leading to end-stage renal failure. Even in these severe cases, patients can still be treated with dialysis or renal transplantation, which may result in associated postsurgical complications (eg, infection, wound dehiscence, and transplantation rejection).

Nephrology consultation should be considered if dysmorphic RBCs, cellular casts, especially red-cell casts, abnormal renal function, or significant proteinuria is noted. Urology should be involved in all cases of gross or unexplained microscopic hematuria, especially if associated with urinary symptoms suggestive of BPH, nephrolithiasis, or possible urinary tract neoplasms.

Hematuria is a common problem that may portend possible pathology, eg, urinary calculi or urinary tract malignancies. Most of the time, the evaluation is negative, which should be considered reassuring. The recommended criteria of 3 RBC/HPF or more on microscopic urinalysis must be followed after every unexplained positive dipstick hematuria result to avoid unnecessary testing and patient anxiety.

Key factors to bear in mind when managing gross and microscopic hematuria include the following: A dipstick evaluation of hematuria is not reliable for diagnosing microhematuria. However, an unexplained microscopic urinalysis of a properly obtained urine sample showing 3 or more RBC/HPF is sufficient to warrant further evaluation.[5] Patients on anticoagulants who develop hematuria still need a full and proper evaluation based on their risk-adjusted status.[5] Female patients with hematuria are the most likely to receive inadequate or incomplete evaluations, probably due to their high incidence of UTIs and potential contamination of the urine from vaginal bleeding. Performing follow-up microscopic urinalyses in such patients to identify those with persistent microhematuria requiring further evaluation is vital and possibly life-saving.[5] In patients who present with hematuria and a UTI, the resolution of hematuria, tested at least 6 weeks after antibiotic treatment, should be documented, as UTIs and malignancies can coexist.[1][5] The initial classification of hematuria should be as follows: Microscopic or gross hematuria Nonglomerular (normal RBCs on microscopic examination) or glomerular (proteinuria, dysmorphic RBCs, red-cell or other casts, azotemia, edema, and "cola-colored" or "frothy" urine). Symptomatic (suggestive of infection, urolithiasis, or BPH), or asymptomatic (suspicious for bladder cancer). To help guide the workup, nonglomerular microhematuria is further classified as low-, intermediate-, or high-risk based on associated risk factors and the degree of hematuria.[1][5] If a patient does not fit the risk-stratification categories, they should be treated as belonging to the next higher risk category.[1][5] Even if the initial impression is a glomerular cause, a urological risk-stratified evaluation should still be performed.[1][5] Cystoscopy, along with possible CT urogram or retrograde pyelogram, is the definitive testing protocol for bladder and urothelial cancer.[1][5] Consider adding a statin to patients with glomerular disease, such as glomerulonephritis, to help slow atherosclerosis progression. The development of unexplained gross hematuria automatically upgrades the patient to the high-risk category, even if previously evaluated with negative findings.[1][5]

Cystoscopy, along with possible CT urogram or retrograde pyelogram, is the definitive testing protocol for bladder and urothelial cancer.[1][5] Consider adding a statin to patients with glomerular disease, such as glomerulonephritis, to help slow atherosclerosis progression. The development of unexplained gross hematuria automatically upgrades the patient to the high-risk category, even if previously evaluated with negative findings.[1][5] Consider IgA vasculitis and hemolytic uremic syndrome for unexplained hematuria in children, primarily when associated with a predisposing infection, renal failure, anemia, or thrombocytopenia.[35][134] In managing urinary clot retention, consider using the intavesical chymotrypsin/sodium bicarbonate or diluted hydrogen peroxide irrigation solutions described earlier for thrombus dissolution.[146][147] These treatments may help prevent the need for surgical clot evacuation in the operating room. When more straightforward options are unsuccessful, consider intravesical treatments, selective arterial embolization, and palliative radiation therapy for the control of otherwise intractable hematuria.[136][139][140][148][149][150][151][152][153][154][155][156][157][158] Check a coagulation profile and platelet count for patients with unexplained hematuria who might have a coagulopathy.

Hematuria, the presence of blood in the urine, may originate from glomerular or nonglomerular causes and can indicate underlying renal or urological pathology. While many cases result from benign conditions such as infections, urolithiasis, or benign prostatic hyperplasia, persistent or unexplained hematuria, especially gross hematuria, may signal malignancy and requires prompt evaluation. Early diagnosis and appropriate management are essential to prevent renal impairment and ensure favorable outcomes. Effective management of hematuria requires collaboration among physicians, advanced practitioners, nurses, pharmacists, and allied health professionals. Given its multifactorial etiology, an interprofessional team led by primary care or emergency physicians spearheads the initial assessment. Referral to nephrologists or urologists should likely follow, dictated by the hematuria severity, likely etiology, and underlying risk factors. Clinicians must apply diagnostic accuracy through urinalysis, imaging, and cystoscopy while identifying risk factors such as age, smoking, chemical exposure, genetic factors, or family history of malignancy. Nurses play a critical role in patient education, follow-up, and monitoring, while pharmacists ensure safe medication use and renal protection. Interprofessional communication and coordinated care pathways enhance patient safety, streamline evaluations, prevent diagnostic delays, and promote patient-centered outcomes through timely and evidence-based interventions.