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Acute renal colic is a severe and sudden flank pain primarily caused by ureteral calculi obstructing the urinary tract. The pain typically originates at the costovertebral angle and radiates anteriorly and inferiorly toward the groin or testicle. Ureteral stones, which can occur anywhere along the path between the kidneys and the bladder, are the leading cause of this condition. Contributing factors to urolithiasis include aciduria, low urine volume, urinary infections, hypercalciuria, hyperoxaluria, hyperuricosuria, and hypocitraturia. Initial evaluation of acute renal colic involves detailed history-taking, physical examination, laboratory testing, urinalysis, and imaging studies. Appropriate imaging studies include ultrasonography with resistive index, a plain abdominal x-ray of the kidney, ureter, and bladder, and unenhanced (non-contrast) computed tomography scans. Initial management of acute renal colic focuses on pain control, IV hydration, and antiemetics, with antibiotics administered if an infection is present. Although many ureteral stones pass spontaneously, larger or obstructing stones may require elective surgical interventions, such as extracorporeal shockwave lithotripsy, ureteroscopy, or cystoscopy with double J stenting. In certain urgent clinical cases, such as sepsis due to obstructive pyelonephritis (pyonephrosis), immediate surgical drainage of the infected renal pelvis is critical. Preventive strategies, including 24-hour urine testing, are recommended for recurrent cases to improve quality of life. This activity reviews the evaluation and management of acute renal colic caused by ureterolithiasis. This activity also emphasizes the importance of interprofessional collaboration among healthcare providers and highlights their critical roles in delivering comprehensive patient care and effectively managing this condition. Objectives: Identify the clinical presentation of acute renal colic, including characteristic flank pain and radiation patterns. Assess the need for imaging studies such as ultrasound or non-contrast computed tomography to confirm the diagnosis and evaluate stone size and location. Apply appropriate antibiotic therapy for patients presenting with signs of urosepsis or infected stones.

Identify the clinical presentation of acute renal colic, including characteristic flank pain and radiation patterns. Assess the need for imaging studies such as ultrasound or non-contrast computed tomography to confirm the diagnosis and evaluate stone size and location. Apply appropriate antibiotic therapy for patients presenting with signs of urosepsis or infected stones. Collaborate with a nephrologist, urologist, primary care provider, and dietitian to develop individualized management plans for patients with recurrent urolithiasis. Access free multiple choice questions on this topic.

Acute renal colic is a severe and sudden flank pain that typically originates at the costovertebral angle and extends anteriorly and inferiorly toward the groin or testicle. This condition is usually caused by an acute urinary tract obstruction due to calculus and is often associated with nausea and vomiting. Urolithiasis, commonly known as kidney stones, is a prevalent condition affecting approximately 1 in 11 individuals in the United States at some point in their lives. Urolithiasis typically occurs when a crystal or crystalline aggregate travels from the kidney through the genitourinary system, becoming lodged and obstructing urinary flow, usually in the ureter. This obstruction leads to proximal ureteral and renal pelvic dilation (hydroureteronephrosis), which is the primary cause of the intense pain known as renal colic.[1][2][3][4] The intensity of pain is related to the degree of obstruction, rather than the size of the stone, although stone size can help predict the likelihood of spontaneous passage. Although kidney stones are not the only cause of flank pain, their prevalence and the severity of the pain they cause make ureterolithiasis the most likely presumptive diagnosis when sudden, severe flank pain occurs, particularly when associated with hematuria. The nature, onset, location, and severity of the pain vary depending on the underlying cause. However, for most patients, the pain typically peaks 1 to 2 hours after its initial onset. Underlying causes of urolithiasis include inadequate hydration, aciduria, chronic urinary infections, hypercalciuria, hyperoxaluria, hyperuricosuria, and hypocitraturia. The initial evaluation of a patient presenting with acute renal colic involves laboratory testing, urinalysis, and appropriate imaging studies.

The nature, onset, location, and severity of the pain vary depending on the underlying cause. However, for most patients, the pain typically peaks 1 to 2 hours after its initial onset. Underlying causes of urolithiasis include inadequate hydration, aciduria, chronic urinary infections, hypercalciuria, hyperoxaluria, hyperuricosuria, and hypocitraturia. The initial evaluation of a patient presenting with acute renal colic involves laboratory testing, urinalysis, and appropriate imaging studies. The immediate treatment of acute renal colic due to urolithiasis includes pain control, intravenous (IV) hydration, antiemetics, and antibiotics (if indicated). Patients with severe or refractory symptoms may require hospital observation or admission. In some cases, urgent surgical intervention is necessary, such as in obstructive pyelonephritis (pyonephrosis), where emergent drainage of the infected renal pelvis is required. Definitive treatment for obstructing ureteral stones may involve conservative or procedural approaches. Surgical options include cystoscopy with double J stenting, extracorporeal shockwave lithotripsy (ESWL), ureteroscopy with stone basketing, and laser therapy, as open surgery for ureteral stones is rarely necessary. Please see StatPearls' companion resource, "Ureterolithiasis," for more information. Quality of life scores typically decrease as the frequency of kidney stone attacks increases. This decline is most noticeable when a patient experiences 5 or more lifetime episodes of renal colic, indicating that preventive measures, such as 24-hour urine testing, should be considered at that point, if not earlier.[5]

Renal colic is caused by the dilation of the renal pelvis and ureteral segments. While colic usually results from acute obstruction, such as a ureteral calculus, it can also be caused by other issues, including ureteral spasms following double J stent removal or ureteroscopy. Chronic ureteral blockages, such as those caused by ureteropelvic junction obstructions, prostate cancer, cervical or pelvic cancer, ureteral scarring, or retroperitoneal fibrosis, typically do not result in acute pain or colic. Several predictors and risk factors commonly associated with kidney stone formation are mentioned below. Aciduria Aciduria is the most common cause of uric acid stone formation, accounting for 5% to 10% of all urinary calculi. This may result from excessive intake of animal protein, renal tubular acidosis, or metabolic acidosis. Please see StatPearls' companion resources, "Metabolic Acidosis" and "Renal Tubular Acidosis," for more information. Treatment usually involves potassium citrate to achieve a sustained urinary pH of 6.5. Sodium bicarbonate may also be used, although it delivers a significant sodium load. Please see StatPearls' companion resources, "Hyperuricosuria" and "Uric Acid Nephrolithiasis," for more information. Cystinuria Cystinuria is an autosomal recessive genetic disorder characterized by elevated urinary cystine levels. Cystine stones are highly resistant to shockwave therapy and typically require laser therapy for effective fragmentation. Preventive measures include aggressive hydration, aiming to produce at least 3000 mL of urine daily, and urinary alkalinization to a pH of 7.5 or higher, as cystine becomes significantly more soluble in alkaline urine. Please see StatPearls' companion resource, "Cystinuria," for more information. Hypercalciuria

Cystinuria is an autosomal recessive genetic disorder characterized by elevated urinary cystine levels. Cystine stones are highly resistant to shockwave therapy and typically require laser therapy for effective fragmentation. Preventive measures include aggressive hydration, aiming to produce at least 3000 mL of urine daily, and urinary alkalinization to a pH of 7.5 or higher, as cystine becomes significantly more soluble in alkaline urine. Please see StatPearls' companion resource, "Cystinuria," for more information. Hypercalciuria Hypercalciuria, the most common chemical promoter of nephrolithiasis, is defined as urinary calcium excretion of 250 mg or more per day. This often results from increased intestinal calcium absorption, elevated renal calcium excretion (renal calcium leak), excessive vitamin D intake, hyperparathyroidism, metabolic acidosis, or idiopathic causes. Treatment strategies include moderating dietary calcium intake, normalizing vitamin D levels, correcting phosphate deficiencies (which can elevate vitamin D levels), administering oral phosphate supplements, and using thiazide diuretics to reduce renal calcium excretion. Please see StatPearls' companion resource, "Hypercalciuria," for more information. Hyperoxaluria Hyperoxaluria is typically defined as urinary oxalate excretion of 40 mg or more per day, with optimal levels being 25 mg/d or less. Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information. Oxalate is a potent promoter of calcium oxalate urolithiasis; therefore, reducing elevated oxalate levels is critical, particularly in patients producing calcium oxalate stones. Dietary oxalate intake should be reduced by limiting high-oxalate foods such as spinach, rhubarb, and collard greens. Taking oral calcium citrate supplementation with meals can enhance intestinal oxalate binding, reducing absorption and lowering urinary oxalate levels. Although most cases of hyperoxaluria are secondary, specific medications are available for treating primary hyperoxaluria. Please see StatPearls' companion resource, "Hyperoxaluria," for more information. Hyperuricosuria

Hyperoxaluria is typically defined as urinary oxalate excretion of 40 mg or more per day, with optimal levels being 25 mg/d or less. Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information. Oxalate is a potent promoter of calcium oxalate urolithiasis; therefore, reducing elevated oxalate levels is critical, particularly in patients producing calcium oxalate stones. Dietary oxalate intake should be reduced by limiting high-oxalate foods such as spinach, rhubarb, and collard greens. Taking oral calcium citrate supplementation with meals can enhance intestinal oxalate binding, reducing absorption and lowering urinary oxalate levels. Although most cases of hyperoxaluria are secondary, specific medications are available for treating primary hyperoxaluria. Please see StatPearls' companion resource, "Hyperoxaluria," for more information. Hyperuricosuria Hyperuricosuria, characterized by excessive urinary uric acid, contributes to the formation of both uric acid and calcium oxalate stones. Patients with calcium stones and elevated urinary uric acid levels can benefit from dietary modifications, such as reducing excessive animal protein intake, or medical management with allopurinol or febuxostat. Most uric acid stones are effectively treated with potassium citrate and urinary alkalinization. The optimal urinary uric acid level is 600 mg daily or less. Please see StatPearls' companion resources, "Hyperuricosuria" and "Uric Acid Nephrolithiasis," for more information. Hypocitraturia Hypocitraturia is typically defined as urinary citrate excretion of 320 mg or less per day, although this threshold does not account for factors such as urinary pH, stone composition, volume, or concentration. Clinicians are advised to prioritize achieving optimal urinary citrate concentrations of approximately 300 mg/L of urine daily. In managing aciduria or uric acid stones, urinary pH is more critical than absolute citrate levels, with an optimal target pH of 6.5 or higher. Potassium citrate is the preferred oral citrate supplement, although sodium bicarbonate may also be. Please see StatPearls' companion resources, "Uric Acid Nephrolithiasis" and "Hypocitraturia and Renal Calculi," for more information. Relative Dehydration and Inadequate Urinary Volume

Hypocitraturia is typically defined as urinary citrate excretion of 320 mg or less per day, although this threshold does not account for factors such as urinary pH, stone composition, volume, or concentration. Clinicians are advised to prioritize achieving optimal urinary citrate concentrations of approximately 300 mg/L of urine daily. In managing aciduria or uric acid stones, urinary pH is more critical than absolute citrate levels, with an optimal target pH of 6.5 or higher. Potassium citrate is the preferred oral citrate supplement, although sodium bicarbonate may also be. Please see StatPearls' companion resources, "Uric Acid Nephrolithiasis" and "Hypocitraturia and Renal Calculi," for more information. Relative Dehydration and Inadequate Urinary Volume Relative dehydration and inadequate urinary volume, particularly levels below 1 L/d, significantly increase the concentration of solutes (indicated by urine osmolarity exceeding 600 mOsm/kg) and promote urinary stasis. This can result in solute supersaturation and subsequent stone formation. The optimal daily urine volume for individuals prone to kidney stones is 2500 mL, with 2000 mL as the minimum acceptable threshold.[6] Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information. The average daily urinary fluid volume in most individuals is approximately 1300 mL. Inadequate urinary fluid excretion is the most common single cause of urolithiasis. Urinary Tract Infections Urinary tract infections caused by urease-producing bacteria lead to ammoniagenesis and increased urinary pH, creating conditions that promote the formation of struvite (infection) or triple phosphate (magnesium, calcium, and ammonium) calculi. Staghorn stones are typically composed of this material. Treatment involves infection control and complete removal of all infected stone material. In selected cases, acetohydroxamic acid, a urease inhibitor, may be used.[6] Please see StatPearls' companion resource, "Struvite and Triple Phosphate Renal Calculi," for more information.

The annual incidence of urolithiasis in North America and Europe is 0.5%. Among those diagnosed with urolithiasis, 50% will experience a recurrent stone within 10 years or less if preventive measures are not implemented.[7] According to the National Institutes of Health, approximately 6% of women and 11% of men in the United States will experience a kidney stone attack at some point in their lives. Over 1.2 million emergency department visits a year in the United States are due to acute renal colic, with about 20% of patients requiring hospital admission.[8][9] Over the past 30 years, the global incidence of kidney stone disease has steadily increased and continues to rise.[10][11] Most kidney stones (over 70%) occur in individuals aged 20 to 50, with men being more affected than women at a ratio of approximately 2:1. However, the incidence in women is increasing.[10] Patients with obesity, hypertension, a family history of nephrolithiasis, irritable bowel syndrome, and diabetes have an increased risk of developing kidney stones.[12][13][14] Hispanics and Blacks have a lower overall risk of kidney stones compared to Whites, who have the highest risk.[15] This difference is likely attributed to cultural dietary preferences, geographical location (warmer climates), and socioeconomic factors rather than genetic differences.[10] New stone formers have a 26% median probability of at least one additional symptomatic renal colic attack within 5 years of their initial stone event.[16] The lifetime risk of at least one other stone ranges from approximately 60% to 80%.[17] The likelihood of a repeat episode of renal colic is increased in patients with the following risk factors: Bariatric surgery (especially Roux-en-Y gastric bypass) Cardiovascular disease Chronic renal failure Diabetes Enteric hyperoxaluria First stone at a younger age History of cystine or uric acid stones Hypertension Malabsorption Metabolic syndrome Obesity Positive family history of kidney stones Previous renal colic episodes or kidney stone surgery Primary hyperoxaluria Untreated hyperparathyroidism White ethnicity (compared to Black, Hispanic, or Asian) [18][19]

As a kidney stone moves through the renal collecting system, it can significantly disrupt urine flow in the genitourinary tract by causing either constant or intermittent obstruction and hydronephrosis of the ureter. This leads to urine backing up into the kidney, ureteral dilation, pyelolymphatic backflow, and stretching of the renal capsule, which triggers pain by releasing prostaglandins. Intermittent obstruction often causes more prolonged discomfort and pain than constant blockage, as compensatory mechanisms can partially offset the increased ureteral intraluminal pressure. Acute ureteral obstruction leads to a decrease in the glomerular filtration rate (GFR) of the affected kidney, while increasing urine excretion by the unaffected kidney, accompanied by severe, excruciating pain. Complete obstruction of the ureter can result in the eventual loss of renal function, with damage potentially becoming irreversible after just 1 to 2 weeks. Additionally, urinary flow obstruction for an extended interval carries the risk of renal calyx rupture, which can potentially lead to the development of a urinoma. A kidney stone generally does not cause pain or discomfort unless it becomes infected or causes urinary obstruction. The severity of pain is determined by the degree of ureteral obstruction, not the size of the stone. Consequently, a larger stone may pass without pain, while a small 2- to 3-mm stone can cause significant discomfort. Intermittent obstruction, where the stone blocks and releases as it moves, is also possible. Urinary calculi can become impacted at various points in the urinary tract, but they most commonly occur at the following 3 anatomical sites where the ureter is narrowest: The ureteropelvic junction, where the renal pelvis narrows abruptly to meet the ureter. Near the pelvic brim, where the ureter makes an acute posterior turn just distal to the iliac bifurcation. The ureterovesical junction, the narrowest portion of the ureter, where the ureter tunnels transversely through the muscular bladder wall. Please see StatPearls' companion resource, "Anatomy, Abdomen and Pelvis Ureter," for more information.

Near the pelvic brim, where the ureter makes an acute posterior turn just distal to the iliac bifurcation. The ureterovesical junction, the narrowest portion of the ureter, where the ureter tunnels transversely through the muscular bladder wall. Please see StatPearls' companion resource, "Anatomy, Abdomen and Pelvis Ureter," for more information. Pain arises from a combination of factors, including ureteral muscle spasms, increased proximal ureteral dilation, enhanced peristalsis driven by intrinsic ureteral pacemakers, localized inflammatory changes induced by the stone, renal swelling with capsular stretching, edema, and irritation. These processes activate submucosal stretch receptors in the ureter, renal pelvis, and capsule, triggering prostaglandin release, which directly causes pain. The stretching of the renal pelvis, peripelvic renal capsule, and renal calyces closely resembles the pain experienced by patients with renal colic. The immediate effect of a newly obstructing ureteral stone is an increase in proximal intraluminal pressure, leading to distension of the renal pelvis and heightened ureteral peristalsis. Peak renal pelvic pressure from a high-grade obstruction typically occurs within 2 to 5 hours of complete ureteral obstruction. Additional renal changes following complete ureteral obstruction include pyelolymphatic and pyelovenous backflow. Interstitial renal edema develops, significantly increasing lymphatic drainage from the affected kidney and stretching the renal capsule, which stimulates renal capsular stretch receptors and causes pain. Over time, a state of equilibrium is often achieved as proximal ureteral dilation increases, permitting some urine to bypass the obstruction. This, along with other compensatory mechanisms, typically alleviates pain and stabilizes the condition. Pain fibers primarily travel through preganglionic sympathetic nerves and the ascending spinothalamic tracts. When the stone reaches the intramural ureter, involvement of the nervi erigentes can lead to bladder symptoms such as frequency, urgency, dysuria, hesitancy, and difficulty voiding.[20] Please see StatPearls' companion resources, "Physiology, Bladder" and "Physiology, Urination," for more information.

Pain fibers primarily travel through preganglionic sympathetic nerves and the ascending spinothalamic tracts. When the stone reaches the intramural ureter, involvement of the nervi erigentes can lead to bladder symptoms such as frequency, urgency, dysuria, hesitancy, and difficulty voiding.[20] Please see StatPearls' companion resources, "Physiology, Bladder" and "Physiology, Urination," for more information. Renal blood flow increases for up to 90 minutes after the initial ureteral blockage before gradually diminishing. This is due to vasodilation of the afferent preglomerular arterial blood supply. Within 5 hours of the obstruction, renal blood flow and ureteral intraluminal pressures return to normal levels or even decrease further. Renal blood flow gradually decreases over time, dropping to approximately half of the usual baseline by day 3. This decline continues over time, and by 8 weeks, renal blood flow is only 12% of its normal baseline value. Despite this, dilation and hydroureteronephrosis often persist, while ureteral peristalsis nearly disappears. By this point, renal blood flow in the contralateral kidney has increased. Nausea and vomiting are commonly reported in more than half of patients with classic renal colic caused by acute obstructing ureteral calculi. This association arises from a shared embryological innervation pathway between the kidneys and the gastrointestinal tract, mediated by afferent fibers of the vagus nerve and the celiac axis. These symptoms can be exacerbated by the gastrointestinal adverse effects of nonsteroidal anti-inflammatory drugs (NSAIDs) and opioid medications. Notably, nausea and vomiting are not directly linked to pain intensity, as other highly painful conditions do not typically produce such adverse effects. The severity of the pain does not reliably correlate with stone size or the likelihood of spontaneous expulsion.[21] Fortunately, acute renal colic pain is self-limited and lasts around 24 hours. Subsequently, the blocked ureter usually ceases further stretching, and it reaches equilibrium. Severe pain or other symptoms persisting for more than 3 days are likely to require surgical intervention.

The severity of the pain does not reliably correlate with stone size or the likelihood of spontaneous expulsion.[21] Fortunately, acute renal colic pain is self-limited and lasts around 24 hours. Subsequently, the blocked ureter usually ceases further stretching, and it reaches equilibrium. Severe pain or other symptoms persisting for more than 3 days are likely to require surgical intervention. Studies have identified characteristics that may help predict which patients are more likely to fail conservative management of acute renal colic. A previous history of renal colic weakly correlates with a failure of conservative treatment; however, factors such as gender, degree of hydronephrosis, initial pain level, stone size, shape, or location cannot reliably predict the need for surgical intervention.[22] Generally, the larger and more proximal the stone, the greater the likelihood that surgical intervention will eventually be required.

Patients with renal colic typically present with an acute onset of flank pain radiating inferiolaterally to the lower abdomen, groin, or testicle. They often describe a dull, constant discomfort, which is interspersed with colicky episodes of intense, sharp pain. The constant discomfort is usually due to the stretching of the renal capsule from obstruction, while the colicky pain results from peristalsis of the ureteral smooth muscle. Many patients report associated nausea or vomiting, and most (85%) will exhibit gross or microscopic hematuria. As the kidney stone moves distally toward the bladder, the patient may experience increasing lower urinary tract symptoms, such as dysuria, urinary frequency, urgency, or difficulty urinating. Patients experiencing renal colic often present with severe, excruciating pain. These patients are typically unable to find a comfortable position and may be writhing or pacing constantly, in contrast to patients with an acute abdomen, who generally prefer to remain still. Please see StatPearls' companion resource, "Acute Abdomen," for more information. The physical exam typically reveals flank pain or discomfort and may also show abdominal pain. The skin may be cool or diaphoretic. A personal or family history of kidney stones, recent ureteroscopic surgery, or removal of a double-J stent is often noted. In cases of recent ureteroscopy or immediate post-removal of a double-J stent, the history alone can often provide the diagnosis. The pain in these instances is caused by ureteral spasm, which can mimic an obstruction and lead to proximal ureteral and renal dilation, even without a stone. While the pain can be as intense as that caused by an obstructing ureteral stone, it is typically self-limited and resolves over time. However, some patients may require a drainage procedure or the placement of a new double-J stent. Patients taking topiramate, protease inhibitors (such as atazanavir and indinavir), acetazolamide, sulphadiazine, ephedrine, and guaifenesin are at higher risk of developing drug-related urolithiasis.[23][24][25]

Diagnosis relies on a comprehensive approach that includes the patient's history, physical examination, laboratory tests, and imaging studies.[7] Urinalysis Urinalysis reveals microscopic or gross hematuria in 85% of stone patients and should also be assessed for crystalluria, pH levels, and signs of infection (such as white blood cells [WBCs] and bacteria). A urinary pH greater than 7.5 may suggest a urease-producing bacterial infection, while a pH below 5.5 may indicate the presence of uric acid calculi. If there are signs of infection, a urine culture should be obtained. Please see StatPearls' companion resources, "Uric Acid Nephrolithiasis" and "Struvite and Triple Phosphate Renal Calculi," for more information. Hematuria Hematuria is present in 85% of acute renal colic cases caused by calculi.[26] While the presence of hematuria suggests a stone, it is not definitive, and its absence does not conclusively rule out the presence of a stone.[26] Laboratory Studies Laboratory studies should include a basic metabolic panel with serum calcium and creatinine levels to assess renal function, dehydration, acid-base status, and electrolyte balance.[7] Serum uric acid should also be checked. A complete blood count (CBC) may be considered to evaluate for leukocytosis if there is concern for infection; however, a mild elevation in WBC count (up to 15,000 WBCs per microliter) is common due to WBC demargination and is not necessarily indicative of an infection.[7][27][28] A 24-hour urine collection for prophylactic testing should be considered for interested patients, particularly those at high risk or recurrent stone formers. However, all patients with a history of urolithiasis should be informed about this option.[7] Parathyroid Hormone Levels Parathyroid hormone levels should be obtained if hypercalcemia is present or if primary hyperparathyroidism is suspected. If possible, urine should be strained to capture stones for chemical analysis to help determine optimal preventive prophylactic measures.

A 24-hour urine collection for prophylactic testing should be considered for interested patients, particularly those at high risk or recurrent stone formers. However, all patients with a history of urolithiasis should be informed about this option.[7] Parathyroid Hormone Levels Parathyroid hormone levels should be obtained if hypercalcemia is present or if primary hyperparathyroidism is suspected. If possible, urine should be strained to capture stones for chemical analysis to help determine optimal preventive prophylactic measures. Further metabolic testing, including a 24-hour urine collection for volume, pH, calcium, oxalate, uric acid, citrate, sodium, magnesium, and potassium concentrations, should be considered for high-risk first-time, pediatric, or recurrent stone formers. In addition, it is highly recommended for nephrolithiasis patients with solitary and transplanted kidneys, renal failure, and gastrointestinal bypass (eg, Roux-en-Y) or those at high anesthesia risk. Renal Ultrasonography Renal ultrasonography can assess hydronephrosis, measure the resistive index, and track larger renal stones, particularly uric acid stones. However, it may miss stones smaller than 3 mm and is not a reliable imaging modality for visualizing ureteral calculi.[29][30] The degree of perinephric fluid can help predict the extent of obstruction.[3] While it is not always possible to visualize ureteral calculi with ultrasound, identifying ureteral jets in the bladder can aid in assessing obstruction. Obstruction of the ureter typically leads to a decrease in the frequency of ureteral jets compared to the contralateral side.[29] Ultrasound offers the advantage of not exposing patients to ionizing radiation, can visualize radiolucent stones, and can be performed quickly at the bedside by emergency department (ED) physicians or ultrasound technologists in radiology. Ultrasound is the recommended imaging modality for pregnant patients. However, if ultrasonography is inadequate or nondiagnostic, low-dose unenhanced computed tomography (CT) scanning may be considered during the second and third trimesters.[31]

Ultrasound offers the advantage of not exposing patients to ionizing radiation, can visualize radiolucent stones, and can be performed quickly at the bedside by emergency department (ED) physicians or ultrasound technologists in radiology. Ultrasound is the recommended imaging modality for pregnant patients. However, if ultrasonography is inadequate or nondiagnostic, low-dose unenhanced computed tomography (CT) scanning may be considered during the second and third trimesters.[31] Ultrasonography alone may be sufficient for diagnosis in select cases, particularly in patients with a history of recurrent ureterolithiasis.[32][33] In these instances, a flat abdominal x-ray of the kidney, ureter, and bladder (KUB) is typically recommended for tracking and follow-up. However, relying solely on ultrasound may result in incorrect management in about one-fifth of patients, as it provides insufficient information on stone size, shape, or location.[34] Renal resistive index: As determined by ultrasound, this index is a valuable tool for diagnosing ureteral obstructions. This index is calculated as (peak systolic velocity−end diastolic velocity)/peak systolic velocity, with normal values typically being 0.7 or less. Higher values indicate either obstruction or intrinsic renal disease.[35][36][37][38][39] A high resistive index in a single kidney in a patient with renal colic on that side strongly suggests acute ureteral obstruction, such as from ureterolithiasis.[35][37][38] Medical renal disease typically results in elevated but similar resistive index levels bilaterally. Ultrasound is the preferred modality for evaluating a pregnant patient with suspected renal colic. Studies have shown that using ultrasound as the primary imaging method does not increase complications compared to CT. Ultrasound is also effective for monitoring patients with uric acid renal calculi.[40] However, while ultrasound may be suggestive, a negative result does not definitively rule out a ureteral stone or renal colic. Abdominal x-Ray (KUB) A plain abdominal x-ray (KUB) can identify many stones, but 10% to 20% of renal calculi are radiolucent and not visible on plain films. The x-ray provides limited information on hydronephrosis, obstruction, or internal renal anatomy and is less useful in obese patients. Additionally, bowel gas, the bony pelvis, and abdominal organs may interfere with stone visualization.

A plain abdominal x-ray (KUB) can identify many stones, but 10% to 20% of renal calculi are radiolucent and not visible on plain films. The x-ray provides limited information on hydronephrosis, obstruction, or internal renal anatomy and is less useful in obese patients. Additionally, bowel gas, the bony pelvis, and abdominal organs may interfere with stone visualization. A KUB is recommended in all kidney stone cases when an unenhanced CT scan is positive, and the exact location of the stone is known. This helps identify stones that can be tracked with follow-up KUB, potentially making them amenable to lithotripsy. The KUB also provides a more accurate depiction of the stone's shape and offers valuable surgical orientation. Cost-Effective Imaging With Renal Ultrasound and Abdominal x-Ray (KUB) Combining renal ultrasonography with a KUB offers a cost-effective and efficient alternative to CT scans by reducing costs, limiting radiation exposure, and maintaining good diagnostic efficacy.[40][41] Renal ultrasound: This technique effectively demonstrates hydronephrosis, measures the resistive index to indicate obstruction, and identifies radiolucent renal calculi. However, it is less reliable for detecting ureteral calculi or stones smaller than 3 mm. Abdominal x-ray (KUB): The KUB is sensitive for detecting urinary calcifications but cannot visualize radiolucent stones or provide information on renal function, hydronephrosis, or ureteral obstruction. Symptomatic stones are likely to cause hydronephrosis or obstruction, be visible on ultrasound, or be directly identified on the KUB.[40][41] Combining KUB radiography with renal ultrasonography achieves a reported diagnostic accuracy of 90% for obstructing stones, with a specificity of 93% and a sensitivity of 88%.[42] N on-Contrast or Helical Computed Tomography Scans Unenhanced CT scans (non-contrast or helical CT) are the gold standard for diagnosing suspected renal colic, offering a sensitivity of 98%, specificity of 100%, and a negative predictive value of 97%.[43][44][45][46][47][48] This imaging modality provides rapid identification of stones, determines their location and size, and identifies associated findings such as hydroureter, hydronephrosis, or ureteral edema. Additionally, it can help detect alternative causes of pain, such as an abdominal aortic aneurysm or malignancy.[40]

Unenhanced CT scans (non-contrast or helical CT) are the gold standard for diagnosing suspected renal colic, offering a sensitivity of 98%, specificity of 100%, and a negative predictive value of 97%.[43][44][45][46][47][48] This imaging modality provides rapid identification of stones, determines their location and size, and identifies associated findings such as hydroureter, hydronephrosis, or ureteral edema. Additionally, it can help detect alternative causes of pain, such as an abdominal aortic aneurysm or malignancy.[40] CT scans are recommended for patients with acute renal colic and no prior history of nephrolithiasis to guide management. However, CT scans tend to underestimate stone size by approximately 12% compared to IV pyelography or KUB radiography.[49] CT scans using low-dose and ultra-low-dose radiation protocols are highly recommended for pediatric and pregnant patients to minimize radiation exposure while maintaining diagnostic efficacy for urolithiasis detection.[50][51][52][53] Low-dose CT delivers approximately half the radiation of a standard scan, and ultra-low-dose protocols further reduce exposure by an additional 55%.[50][51][54][55] The positive predictive value of low-dose CT in these cases is 95.8%.[56][57] While most urinary stones, including the relatively radiolucent cystine, dihydroxyadenine, xanthine, and uric acid calculi, are visible on CT scans, some stone compositions may not be detected. These include stones formed from antiviral protease inhibitors and their metabolites,[58][59] such as atazanavir and indinavir.[60][61][62][63][64][65] A contrast study is required when these stones are suspected.[59][64] However, CT scans expose patients to significant radiation and can be costly. In some patients with a history of renal colic who present with pain similar to previous episodes of obstructing urolithiasis, ultrasonography may be sufficient. Although ultrasound is less sensitive (60% to 76%) than CT for detecting calculi smaller than 5 mm, it can reliably identify hydronephrosis and other signs of ureteral obstruction, such as an increased resistive index in the affected kidney and unilateral blocked ureteral jets. If the stone passes before imaging can be performed, residual inflammation may still be present and identifiable, such as hydronephrosis, stranding, or pain, even if no stone is specifically or definitively identified.

In some patients with a history of renal colic who present with pain similar to previous episodes of obstructing urolithiasis, ultrasonography may be sufficient. Although ultrasound is less sensitive (60% to 76%) than CT for detecting calculi smaller than 5 mm, it can reliably identify hydronephrosis and other signs of ureteral obstruction, such as an increased resistive index in the affected kidney and unilateral blocked ureteral jets. If the stone passes before imaging can be performed, residual inflammation may still be present and identifiable, such as hydronephrosis, stranding, or pain, even if no stone is specifically or definitively identified. The American College of Obstetricians and Gynecologists (ACOG) and the American Urological Association (AUA) now support the selective and judicious use of low-dose, non-contrast CT imaging during pregnancy in cases where ultrasound is diagnostically insufficient.[56][66] Magnetic Resonance Pyrography Magnetic resonance pyelography has a lower positive predictive value (80%) for identifying urinary stones compared to CT, but it does not use ionizing radiation. Magnetic resonance urography may be indicated for patients who have a contraindication to ionizing radiation but an inadequate ultrasound evaluation for urinary stones. [56][57][67][68] The European Association of Urology (EAU) recommends it as a second-line imaging modality after ultrasound in equivocal clinical situations. This offers an alternative to ureteroscopic surgery and provides a safer option than CT scanning during pregnancy.[56][67][68] Ureteroscopic Surgery Ureteroscopic surgery with laser lithotripsy and double J stent placement is a reasonable option when the clinical presentation strongly suggests urolithiasis, especially if symptoms such as pain are prolonged or difficult to control.[56] Ureteroscopic surgery can be safely performed in pregnant patients with urolithiasis, yielding good outcomes and a negative ureteroscopy rate of only 14%.[57][69][70][71] Urosepsis

Ureteroscopic surgery with laser lithotripsy and double J stent placement is a reasonable option when the clinical presentation strongly suggests urolithiasis, especially if symptoms such as pain are prolonged or difficult to control.[56] Ureteroscopic surgery can be safely performed in pregnant patients with urolithiasis, yielding good outcomes and a negative ureteroscopy rate of only 14%.[57][69][70][71] Urosepsis Urosepsis is a potentially life-threatening organ dysfunction caused by a dysregulated host response to an infection originating from a urological source.[72][73] Urosepsis is characterized by symptoms such as hypotension, tachycardia (>90 beats/min), tachypnea (>20 breaths/min), pyuria, and leukocytosis (>12,000/μL [12 × 109/L]).[74] Mild leukocytosis, up to 15,000/μL (15 × 109/L), can be common in acute renal colic without infection.[7][27][28] Acidosis (serum pH <7.35) may also be present.[75] Patients with renal colic who also have a fever of 100°F (37.8°C) or higher, significant leukocytosis (>15,000 WBCs/mm³), pyuria, hypotension, or unexplained tachycardia should be considered at risk for urosepsis and obstructive pyelonephritis, especially if they have diabetes. Please see StatPearls' companion resource, "Urosepsis," for more information. The recommended treatment for patients with acute renal colic caused by an obstructing ureteral stone and signs of systemic infection, sepsis, or obstructive pyelonephritis is urgent drainage of the renal pelvis, either through cystoscopy with double J stenting or via percutaneous nephrostomy. Please see StatPearls' companion resource, "Complicated Urinary Tract Infections," for more information. As it is not possible to clinically distinguish acute pyelonephritis from obstructive pyelonephritis, imaging is necessary when the diagnosis is uncertain, especially in diabetic patients or those at increased surgical or anesthesia risk. Ultrasonography is typically sufficient for this purpose, but an unenhanced CT scan may be considered definitive if the results are uncertain or equivocal. Various urosepsis serum biomarkers have significant potential to identify septic patients earlier.[76] Please see StatPearls' companion resources, "Urosepsis," "Bacterial Sepsis," and "Laboratory Evaluation of Sepsis," for more information.

As it is not possible to clinically distinguish acute pyelonephritis from obstructive pyelonephritis, imaging is necessary when the diagnosis is uncertain, especially in diabetic patients or those at increased surgical or anesthesia risk. Ultrasonography is typically sufficient for this purpose, but an unenhanced CT scan may be considered definitive if the results are uncertain or equivocal. Various urosepsis serum biomarkers have significant potential to identify septic patients earlier.[76] Please see StatPearls' companion resources, "Urosepsis," "Bacterial Sepsis," and "Laboratory Evaluation of Sepsis," for more information. Urosepsis biomarkers for early diagnosis: The selection of biomarkers for diagnosing early urosepsis depends on factors such as cost, test availability, and physician familiarity with interpreting laboratory results. Below is a review of some clinically useful serum biomarkers. C-reactive protein: C-reactive protein (CRP) is an inexpensive and readily available laboratory indicator of infection and inflammation. CRP is slower to react to bacterial sepsis than procalcitonin, and it is not specific for bacterial infections. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[77][78] CRP is produced in the liver when serum interleukin-6 (IL-6) is stimulated.[78] The serum concentration of CRP begins to increase 6 hours after the initial inflammatory event, doubling every 8 hours, and peaks by 36 to 50 hours, approximately twice as long as procalcitonin.[78][79][80] A commonly used cutoff level of 50 mg/L is used to identify bacterial sepsis.[77] The half-life of CRP is 19 hours.[81] Please see StatPearls' companion resource, "C Reactive Protein," for more information. Interleukin-6: IL-6 may be a more effective biomarker for tracking disease progression than procalcitonin, lactic acid, or CRP.[82][83][84][85] IL-6 is a proinflammatory cytokine intimately involved in host defense mechanisms and has been proposed as a laboratory biomarker for sepsis.[86] IL-6 is produced by immune and stromal cells, including endothelial cells, fibroblasts, endothelial cells, macrophages, monocytes, and T-lymphocytes.[83][87][88] A threshold level of 52.6 pg/mL or higher has been suggested for identifying sepsis.[83] IL-6 levels peak at around 12 hours, with a half-life of about 1 hour.[89][90]

IL-6 is produced by immune and stromal cells, including endothelial cells, fibroblasts, endothelial cells, macrophages, monocytes, and T-lymphocytes.[83][87][88] A threshold level of 52.6 pg/mL or higher has been suggested for identifying sepsis.[83] IL-6 levels peak at around 12 hours, with a half-life of about 1 hour.[89][90] Lactic acid (lactate): Lactic acid (lactate) levels in the serum are normally less than 2 mmol/L (18.2 mg/dL). Elevated levels indicate infection, and levels exceeding 4 mmol/L (36.4 mg/dL) are considered severe, often suggesting sepsis, particularly if they increase rapidly. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[91] Serum lactic acid levels reflect relative tissue hypoxia, but recent research suggests they also represent an adaptive chemical response to abnormal metabolism and serve as a marker of elevated endogenous catecholamine levels. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[92] A reduction in lactic acid levels is a good indicator of tissue recovery.[92] If lactate is initially elevated, a repeat measurement in 6 hours is recommended,[93] with some guidelines suggesting rechecking levels every 2 hours for critically ill patients initially.[94] Lactate and lactic acid levels are similar but not chemically equivalent, so the normal ranges in the specific laboratory should be verified. The half-life of serum lactate is approximately 20 minutes. Neutrophil-to-lymphocyte ratio: The neutrophil-to-lymphocyte (NLR) ratio is more elevated in patients with worsening sepsis and is also higher in older individuals.[95] Normal and abnormal thresholds for NLR have not been conclusively defined, but levels above 3.75 to 4 are commonly associated with sepsis and urosepsis.[95] This test has the advantages of being inexpensive, readily available, easily calculated, and immediately available.[95][96][97][98] Pentraxin-3: Pentraxin-3 (PTX3) is an inflammatory serum protein produced early in the inflammatory process by various cell types. PTX3 activates the complement immune system pathway, dendritic cells, and macrophages. The protein also promotes the identification of pathogenic bacteria and serves as an antibody precursor.[84][99][100]

Pentraxin-3: Pentraxin-3 (PTX3) is an inflammatory serum protein produced early in the inflammatory process by various cell types. PTX3 activates the complement immune system pathway, dendritic cells, and macrophages. The protein also promotes the identification of pathogenic bacteria and serves as an antibody precursor.[84][99][100] Several studies suggest that PTX3 could be a useful laboratory marker for sepsis and a prognostic indicator, comparable to IL-6.[83][84][101][102][103][104] PTX3 has a relatively short half-life of 1 to 4 hours.[105][106] Procalcitonin: Procalcitonin is a precursor of calcitonin and is a valuable marker for assessing the severity of bacterial infections and monitoring disease progression. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[92][107] Procalcitonin correlates well with the degree of leukocytosis and CRP levels for infection monitoring.[77][107] Procalcitonin is considered superior to CRP as a sepsis marker because it is more specific to bacterial infections; it rises earlier (peaking at 6-12 hours) and normalizes faster. Please see StatPearls' companion resource, "Procalcitonin," for more information.[107][108] Normal procalcitonin levels are typically below 0.1 μg/L, although patients with renal failure may have higher baseline levels.[107][109] A low or normal procalcitonin level does not completely rule out a bacterial infection. Please see StatPearls' companion resource, "Procalcitonin," for more information.[107] Procalcitonin has a half-life of about 24 hours.[107] Please see StatPearls' companion resource, "Procalcitonin," for more information.[107] Considerations for the Evaluation of Renal Colic in Pregnancy Pregnancy can complicate the diagnosis and management of renal colic. The pressure from the gravid uterus on surrounding structures can alter the flow of urine from the renal pelvis to the urinary bladder. Additionally, pregnant patients may excrete higher levels of calcium in their urine.[110]

Considerations for the Evaluation of Renal Colic in Pregnancy Pregnancy can complicate the diagnosis and management of renal colic. The pressure from the gravid uterus on surrounding structures can alter the flow of urine from the renal pelvis to the urinary bladder. Additionally, pregnant patients may excrete higher levels of calcium in their urine.[110] Ultrasound is the preferred first-line study for evaluating renal colic in pregnancy, as it poses no risk of ionizing radiation. However, the results may be nondiagnostic or equivocal.[56] Options for management include conservative measures and observation, low-dose CT imaging, magnetic resonance urography, or ureteroscopic surgery. Ureteroscopic surgery can be safely performed in pregnant patients with urolithiasis, with good outcomes and a negative ureteroscopy rate of only 14%.[57][69][70][71] Placement of a double J stent or performing a percutaneous nephrostomy is a less invasive method to temporize the clinical situation until after delivery, allowing more definitive diagnostic and therapeutic measures to be safely performed without jeopardizing the pregnancy. Surgical intervention is more likely and typically performed earlier in pregnant patients with acute renal colic who present with the following conditions: Anterior-posterior diameter of the renal pelvis of greater than 18 mm Abnormal ureteral anatomy Continuous pain lasting 4 or more days Difficulty controlling pain Elevated serum creatinine levels Extrarenal pelvis Fever Elevated leukocytosis High stone density (>700 Hounsfield units) High serum CRP levels Higher degree of hydronephrosis Higher NLR Increased fetal body weight Larger (≥8 mm) ureteral calculi Multiple previous stone surgical procedures Stone volume of 0.2 cc or more Ureteral stone length of 9 mm or more Ureteral wall thickness of more than 2 mm [111][112][113] Patients diagnosed with kidney stones during pregnancy should have close obstetrical follow-up, as those admitted for renal colic are at up to a 2-fold increased risk of preterm labor. This may be mediated by oxytocin release in response to maternal dehydration caused by nausea and vomiting.[114]

Management of Acute Renal Colic Symptoms Immediate management includes providing adequate analgesia, antiemetics, and IV hydration. Antibiotics should be administered if the patient presents with systemic signs of infection or has infected urine. NSAIDs and opioids are considered first-line therapies for analgesia. Nonsteroidal anti-inflammatory drugs: NSAIDs are typically the first-line treatment for pain relief, as they are often as effective as, or even more effective than, opioids, while avoiding the complications associated with opioid usage.[115][116][117][118][119][120] These medications reduce the production of arachidonic acid metabolites, which mediate pain receptor activation, thereby alleviating pain caused by renal capsule distension. Additionally, NSAIDs inhibit prostaglandin production, further decreasing pain receptor activity and reducing ureteral contractions. However, this inhibition may result in some degree of platelet dysfunction. Please see StatPearls' companion resources, "Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)" and "Ketorolac," for more information. Additionally, NSAIDs induce contraction of the efferent arterioles of the glomerulus, lowering the GFR and reducing hydrostatic pressure across the glomerulus. As patients with renal colic often cannot tolerate oral medications, parenteral options such as ketorolac (15-30 mg IV or intramuscular [IM]) or diclofenac (37.5 mg IV) are commonly used.[121][122][115] Please see StatPearls' companion resources, "Ketorolac" and "Diclofenac," for more information. Ketorolac, an injectable NSAID commonly used for renal colic, is generally considered equivalent to or superior to opioids in treating acute ureterolithiasis pain while being safer with fewer significant adverse effects.[115][116][117][123] As a result, ketorolac and similar NSAIDs are typically preferred for the initial management of pain in acute renal colic. Ketorolac can also be administered as a continuous IV infusion, usually at a rate of 3 to 5 mg/h.[124][125][126][127] Please see StatPearls' companion resources, "Ketorolac" and "Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)," for more information.

Ketorolac, an injectable NSAID commonly used for renal colic, is generally considered equivalent to or superior to opioids in treating acute ureterolithiasis pain while being safer with fewer significant adverse effects.[115][116][117][123] As a result, ketorolac and similar NSAIDs are typically preferred for the initial management of pain in acute renal colic. Ketorolac can also be administered as a continuous IV infusion, usually at a rate of 3 to 5 mg/h.[124][125][126][127] Please see StatPearls' companion resources, "Ketorolac" and "Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)," for more information. Ketorolac may be used in combination with IV acetaminophen, although this is generally not recommended for more than a few days, despite no specific negative interactions being noted. No published data support the efficacy of this combination for treating renal colic. Ketorolac (an FDA pregnancy category C drug) is contraindicated in patients with renal failure (GFR <30 mL/min), a history of gastrointestinal bleeding, an allergy to aspirin or NSAIDs, or in pregnant women. Please see StatPearls' companion resource, "Ketorolac," for more information. Additional steroidal medications, such as dexamethasone (8 mg IV), have been shown to improve pain relief in renal colic patients compared to ketorolac alone.[117][128] Opioid pain medications: Opioids such as morphine sulfate (0.1 mg/kg IV or IM) or hydromorphone (0.02 mg/kg IV or IM) can be effective for analgesia, particularly when other treatments, such as ketorolac, have failed or their maximum dose is insufficient. Please see StatPearls' companion resources, "Morphine" and "Hydromorphone," for more information. However, opioids carry risks of respiratory depression, reduced gastrointestinal motility, nausea, sedation, and dependence with prolonged use. There is also a risk of dependence associated with prolonged opiate use.[129] Please see StatPearls' companion resources, "Opioid Withdrawal" and "Opioid Use Disorder," for more information. The administration of IV morphine following ketorolac has demonstrated effectiveness in providing additional analgesia for patients with inadequate pain relief.[117]

Opioid pain medications: Opioids such as morphine sulfate (0.1 mg/kg IV or IM) or hydromorphone (0.02 mg/kg IV or IM) can be effective for analgesia, particularly when other treatments, such as ketorolac, have failed or their maximum dose is insufficient. Please see StatPearls' companion resources, "Morphine" and "Hydromorphone," for more information. However, opioids carry risks of respiratory depression, reduced gastrointestinal motility, nausea, sedation, and dependence with prolonged use. There is also a risk of dependence associated with prolonged opiate use.[129] Please see StatPearls' companion resources, "Opioid Withdrawal" and "Opioid Use Disorder," for more information. The administration of IV morphine following ketorolac has demonstrated effectiveness in providing additional analgesia for patients with inadequate pain relief.[117] Intravenous acetaminophen: IV acetaminophen has shown comparable effectiveness to ketorolac in a meta-analysis. However, the available data are insufficient to recommend it over standard analgesics. IV acetaminophen can be safely used in combination with NSAIDs and opioids.[130][131] Intravenous lidocaine: IV lidocaine has been used effectively for pain relief in acute renal colic, with positive results reported.[132][133][134] The standard protocol involves injecting 100 to 120 mg of lidocaine in 100 mL of normal saline IV over 10 minutes. The drug is particularly effective for intractable renal colic unresponsive to standard therapy, typically providing relief within 3 to 5 minutes. No adverse events have been reported.[135] The benefit of adding lidocaine to patients who have already received ketorolac remains unclear, as studies on this are conflicting. However, salvage therapy with lidocaine has also been reported in some cases.[136]

Intravenous lidocaine: IV lidocaine has been used effectively for pain relief in acute renal colic, with positive results reported.[132][133][134] The standard protocol involves injecting 100 to 120 mg of lidocaine in 100 mL of normal saline IV over 10 minutes. The drug is particularly effective for intractable renal colic unresponsive to standard therapy, typically providing relief within 3 to 5 minutes. No adverse events have been reported.[135] The benefit of adding lidocaine to patients who have already received ketorolac remains unclear, as studies on this are conflicting. However, salvage therapy with lidocaine has also been reported in some cases.[136] Intradermal sterile water injection therapy: This has proven effective in relieving the pain of acute renal colic, showing results roughly equivalent to NSAIDs.[137][138][139][140][141][142][143] Pain relief is not achieved when normal saline is used in place of sterile water. The injections are administered directly into the flank at the point of greatest tenderness. The mechanism underlying this surprising result remains unclear. However, most experts suggest it involves diffuse noxious inhibitory control or a pain-gating mechanism.[142][144] In addition, it may also produce localized inflammation, triggering the cutaneous A-afferents, leading to endorphin release or working through physiological distraction.[144][145] The technique is simple, safe, inexpensive, and free of significant adverse effects, with the option for repetition as needed. This does not interfere with other pain management methods. Therefore, intradermal water injection therapy shows promise and warrants further investigation for potential clinical use in managing acute renal colic pain.

The technique is simple, safe, inexpensive, and free of significant adverse effects, with the option for repetition as needed. This does not interfere with other pain management methods. Therefore, intradermal water injection therapy shows promise and warrants further investigation for potential clinical use in managing acute renal colic pain. Antiemetics: Antiemetics should be used as needed for symptomatic relief in patients with acute renal colic. Data regarding the relative effectiveness of antiemetic drugs for controlling nausea and vomiting are limited in these patients. Please see StatPearls' companion resource, "Antiemetic Medications," for more information. Limited studies suggest that ondansetron (4-8 mg IV or PO) may be the preferred drug in these situations. Please see StatPearls' companion resource, "Antiemetics, Selective 5-HT3 Antagonists," for more information.[146][147] The use of additional agents to optimize symptom relief when ondansetron alone is insufficient remains unclear. Please see StatPearls' companion resource, "Ondansetron," for more information. Intravenous fluid hydration: Intravenous fluid hydration is recommended as an adjunct to the initial treatment of acute renal colic. Although no evidence suggests that empiric fluids can help "flush out" a stone, many patients who are dehydrated due to decreased oral intake, nausea, or vomiting benefit from supplemental IV hydration. Nerve blocks: Nerve blocks can be beneficial, particularly in cases of chronic flank pain.[148] An anesthetic injection is typically administered near the 11th or 12th intercostal nerve area. The reported efficacy of nerve blocks suggests a musculoskeletal or neuropathic etiology. Paravertebral, splanchnic, and intercostal nerve blocks have all demonstrated varying degrees of effectiveness in relieving flank pain.[149][150][151] Reported randomized clinical trials of alternative analgesic agents: Reported randomized clinical trials of alternative analgesic agents for pain relief in acute renal colic often use morphine and other opioid-based medications as rescue drugs, complicating the assessment of their reported relative effectiveness.[152] Future randomized controlled studies should define therapeutic success as achieving total or near-total pain relief rather than relying on unquantified pain relief.[152]

Reported randomized clinical trials of alternative analgesic agents: Reported randomized clinical trials of alternative analgesic agents for pain relief in acute renal colic often use morphine and other opioid-based medications as rescue drugs, complicating the assessment of their reported relative effectiveness.[152] Future randomized controlled studies should define therapeutic success as achieving total or near-total pain relief rather than relying on unquantified pain relief.[152] Kidney stone prophylaxis: Kidney stone prophylaxis through 24-hour urine testing should be considered for all urolithiasis patients, particularly those at high risk or with recurrent stones. This includes patients with solitary or horseshoe kidneys, renal failure, abnormal ureteral anatomy, pediatric patients, cystine stone formers, and those with high surgery or anesthesia risks. The success of 24-hour urine testing largely depends on the patient's commitment to long-term treatment recommendations and dietary modifications. The AUA guidelines recommend informing even first-time stone formers about 24-hour urine testing and prophylactic therapy.[7] Comprehensive guidelines for interpreting 24-hour urine tests and optimizing treatment selection are available for free download. Calcium loading tests for patients with hypercalciuria are no longer recommended. Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information.[7][153][154] Behavior modification, dietary adjustments, and general urolithiasis prevention strategies should be discussed with all kidney stone patients. Common recommendations include: Patients are advised to increase fluid intake to optimize urine output, aiming for at least 2000 mL, with an optimal goal of 2500 mL of urine daily. Patients with calcium stones and elevated urine calcium should limit sodium and meat protein intake while maintaining a moderate calcium intake of 1000 to 1200 mg daily. Thiazide diuretics and a salt-restricted diet are recommended for those with high urinary calcium to reduce the amount of urinary calcium. Individuals with calcium stones and low urinary citrate, or those with uric acid stones and high urinary uric acid, should increase their intake of fruits and vegetables while reducing their intake of nondairy animal protein.

Thiazide diuretics and a salt-restricted diet are recommended for those with high urinary calcium to reduce the amount of urinary calcium. Individuals with calcium stones and low urinary citrate, or those with uric acid stones and high urinary uric acid, should increase their intake of fruits and vegetables while reducing their intake of nondairy animal protein. Uric acid stone formers are typically treated with potassium citrate (a urinary alkalinizer) to achieve an optimal urinary pH of 6.5 or higher. Hyperuricosuric calcium stone formers may benefit from allopurinol or febuxostat. Patients with hyperoxaluria should be encouraged to reduce their intake of oxalate-rich foods (eg, spinach, nuts, chocolates, and green leafy vegetables), maintain a moderate calcium intake, or use calcium citrate supplementation with meals high in oxalates (usually lunch and dinner), and increase their fluid intake. Cystine stone formers require significant urine volumes of 3000 mL or more daily, along with a urine pH of 7.5 or higher, to optimize cystine solubility. Potassium citrate is the preferred urinary alkalinizer, and tiopronin or other thiol medications can help lower urinary cystine levels.[6] Please see StatPearls' companion resources, "Hyperuricosuria," "Hypercalciuria," "Hyperoxaluria," "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," "Hypocitraturia and Renal Calculi," "Struvite and Triple Phosphate Renal Calculi," and "Uric Acid Nephrolithiasis," for more information. Treatment of Ureterolithiasis Medical expulsive therapy: This is generally recommended, particularly for smaller stones in the distal ureter.[7][48] Alpha-1 adrenergic receptors are found in increasing concentrations in the distal ureter, and blocking these receptors with alpha-blocking medications (such as tamsulosin, alfuzosin, nifedipine, and silodosin) may assist in the expulsion of the stone by relaxing and dilating the distal ureter.[48][155][156][157][158][159][160][161]. However, data from randomized controlled trials regarding the effectiveness of these medications in improving spontaneous stone passage rates are somewhat mixed.[47][48][155][162]

Medical expulsive therapy: This is generally recommended, particularly for smaller stones in the distal ureter.[7][48] Alpha-1 adrenergic receptors are found in increasing concentrations in the distal ureter, and blocking these receptors with alpha-blocking medications (such as tamsulosin, alfuzosin, nifedipine, and silodosin) may assist in the expulsion of the stone by relaxing and dilating the distal ureter.[48][155][156][157][158][159][160][161]. However, data from randomized controlled trials regarding the effectiveness of these medications in improving spontaneous stone passage rates are somewhat mixed.[47][48][155][162] The consensus opinion and the recommendation from the AUA guidelines indicate that medical expulsive therapy is helpful for smaller stones in the lower or distal ureter and is generally recommended. However, such treatment will likely have limited benefits for larger stones in the proximal ureter.[47][155][163][164][165][166][167] Tamsulosin: This is the most frequently used agent, typically prescribed at a dose of 0.4 mg orally daily. While alfuzosin and tamsulosin were found to be roughly comparable, nifedipine appeared to be less effective overall than other agents used for medical expulsive therapy.[161] Mirabegron: This is a beta-3 adrenoceptor agonist usually used for bladder overactivity and has shown a beneficial effect on facilitating spontaneous ureteral stone passage. A recent systematic review and meta-analysis of randomized controlled trials found that the drug improved the spontaneous expulsion rate of ureteral calculi, particularly for smaller stones (less than 6 mm) located in the distal ureter.[168][169] However, mirabegron did not reduce the time for spontaneous expulsion or help with pain management.[169] Data on using mirabegron with alpha-blocker medications for medical expulsive therapy of ureteral calculi are unavailable. Tadalafil: This has been suggested as an agent for medical expulsive therapy, but the results of studies are conflicting, and it cannot be recommended as a standalone treatment.[170][171][172][173]

Mirabegron: This is a beta-3 adrenoceptor agonist usually used for bladder overactivity and has shown a beneficial effect on facilitating spontaneous ureteral stone passage. A recent systematic review and meta-analysis of randomized controlled trials found that the drug improved the spontaneous expulsion rate of ureteral calculi, particularly for smaller stones (less than 6 mm) located in the distal ureter.[168][169] However, mirabegron did not reduce the time for spontaneous expulsion or help with pain management.[169] Data on using mirabegron with alpha-blocker medications for medical expulsive therapy of ureteral calculi are unavailable. Tadalafil: This has been suggested as an agent for medical expulsive therapy, but the results of studies are conflicting, and it cannot be recommended as a standalone treatment.[170][171][172][173] Silodosin: This has been shown to be superior to both tamsulosin and alfuzosin in several recent systematic reviews, comparisons, and meta-analyses of agents used for medical expulsive therapy.[156][174][175][176] If silodosin is selected for medical expulsive therapy, the higher dose (8 mg) is recommended, as the 4 mg dose has been shown to be inferior, with reduced expulsion rates and increased pain.[177] Various combinations of medical expulsive drugs have been studied, such as tadalafil with either tamsulosin or silodosin, which appeared to be somewhat more effective than single agents or other combinations.[178][179] However, further high-quality studies are needed to determine the relative efficacy and optimal composition of such combination treatments for medical expulsive therapy of ureteral calculi.[178] Antibiotics: Antibiotic use in patients with acute renal colic should generally be reserved for patients with acute renal colic who have clinical or laboratory evidence of a urinary tract infection. A microscopic urinalysis showing at least 10 WBCs per high-power field (HPF) (or more WBCs than RBCs), bacteriuria, or positive nitrites on the urine dipstick would indicate the need for antibiotics.

Antibiotics: Antibiotic use in patients with acute renal colic should generally be reserved for patients with acute renal colic who have clinical or laboratory evidence of a urinary tract infection. A microscopic urinalysis showing at least 10 WBCs per high-power field (HPF) (or more WBCs than RBCs), bacteriuria, or positive nitrites on the urine dipstick would indicate the need for antibiotics. Systemic signs of infection include leukocytosis, fever, tachycardia, lactic acidosis, elevated procalcitonin, or other indicators of a possible urinary or systemic infection. Notably, patients with kidney stones may initially appear stable with typical vital signs but can rapidly develop urosepsis from obstructive pyelonephritis, becoming critically ill within hours. High-risk patients include older adults (who may not show signs of infection until sepsis is advanced), those with diabetes, those with solitary kidneys, and those with a history of urinary tract infections or who are immunocompromised. While inappropriate, unjustified, and excessive antibiotic use is discouraged, consideration should be given to administering antimicrobials in high-risk individuals, particularly those with diabetes presenting with acute renal colic who are not yet septic. Some of these patients may later develop urosepsis and obstructive pyelonephritis. Definitive surgical management of impacted ureteral stones: Definitive surgical management can be achieved through several procedures, including ESWL, which uses high-energy shock waves to fragment stones, ureteroscopy with stone basketing, laser or electrohydraulic stone fragmentation, or, in rare cases, open surgery.[47] Please see StatPearls' companion resources, "Ureterolithiasis," "Extracorporeal Shockwave Lithotripsy," and "Ureteroscopy," for more information. Laparoscopic and robotic surgery are alternative procedural options, typically reserved for complex or unusual clinical situations.[180][181][182] In the presence of infection, a double J stent or percutaneous nephrostomy may be used to facilitate urinary drainage of the affected renal unit, with definitive stone therapy deferred until the infection has resolved.[47][183][184] Indications for Surgical Intervention in Ureterolithiasis The indications for surgical intervention in ureterolithiasis causing renal colic depend on the following factors:

Laparoscopic and robotic surgery are alternative procedural options, typically reserved for complex or unusual clinical situations.[180][181][182] In the presence of infection, a double J stent or percutaneous nephrostomy may be used to facilitate urinary drainage of the affected renal unit, with definitive stone therapy deferred until the infection has resolved.[47][183][184] Indications for Surgical Intervention in Ureterolithiasis The indications for surgical intervention in ureterolithiasis causing renal colic depend on the following factors: Evidence of worsening kidney failure or renal damage from prolonged obstruction. Failure to pass ureteral stones after 4 to 6 weeks, with or without medical expulsive therapy. Intractable or persistent pain, nausea, or vomiting lasting more than 3 days. New onset of anuria that coincides with the ureteral obstruction. Likely or suspected obstructive pyelonephritis (pyonephrosis). Patient preference for intervention. Pregnant patients who have not responded to conservative management. Recurrent urinary tract infections related to the stone disease. The stone's size, shape, and position significantly influence the likelihood of spontaneous passage, as mentioned below. Larger, angular-shaped, and proximal ureteral calculi are less likely to pass spontaneously without intervention. Stones larger than 10 mm will generally require surgery. Stones exceeding 7 mm are much less likely to pass spontaneously and often necessitate surgery. Stones 4 mm or smaller have a 90% to 95% spontaneous passage rate and rarely require a procedure. Solitary kidney or simultaneous, bilateral ureteral obstruction. Presence of a urinary tract infection, where drainage procedures are performed until the infection is resolved.[47][185][186][187] Double J stent placement: Double J stent placement can promptly relieve pain and symptoms associated with ureteral obstruction, facilitate drainage of an infected renal unit until the infection is resolved, and dilate the ureter to aid subsequent ureteroscopy. However, routine preoperative use is generally discouraged unless infection is present, as it involves additional anesthesia and operating room procedures.

Double J stent placement: Double J stent placement can promptly relieve pain and symptoms associated with ureteral obstruction, facilitate drainage of an infected renal unit until the infection is resolved, and dilate the ureter to aid subsequent ureteroscopy. However, routine preoperative use is generally discouraged unless infection is present, as it involves additional anesthesia and operating room procedures. Obstructive pyelonephritis or pyonephrosis: Obstructive pyelonephritis or pyonephrosis is a potentially life-threatening condition in which an obstructed kidney, caused by a ureteral or renal calculus, becomes infected, leading to progressive urosepsis. Prompt surgical drainage of the renal pelvis is essential, as antibiotics alone are insufficient to resolve the condition.[183][188][189][190][191] Please see StatPearls' companion resource, "Complicated Urinary Tract Infections," for more information. Mortality from obstructive pyelonephritis remains significant, reported to be as high as 7.4%, even with treatment. The standard technique for draining the renal pelvis is placing a double J stent cystoscopically. However, a general anesthetic is needed. The procedure also requires manipulating a guide wire and stent past the obstructive stone, and it may not be successful in every case. Please see Statpearls' companion resource, "Double J Placement Methods Comparative Analysis," for more information. If the ureteral obstruction is significant or the patient is critically ill and too unstable for general anesthesia, percutaneous nephrostomy is the preferred method for renal drainage. This approach requires only minimal sedation and local anesthesia, minimizes manipulation of the infected renal unit, and eliminates the risk of unsuccessful bypass with a double J stent.[192][193][194][195][196][197][198] Details on the technique for percutaneous nephrostomy are available in other resources.[196][197] Please see StatPearls' companion resource, "Percutaneous Nephrostomy," for more information.

If the ureteral obstruction is significant or the patient is critically ill and too unstable for general anesthesia, percutaneous nephrostomy is the preferred method for renal drainage. This approach requires only minimal sedation and local anesthesia, minimizes manipulation of the infected renal unit, and eliminates the risk of unsuccessful bypass with a double J stent.[192][193][194][195][196][197][198] Details on the technique for percutaneous nephrostomy are available in other resources.[196][197] Please see StatPearls' companion resource, "Percutaneous Nephrostomy," for more information. Delays in the surgical decompression of obstructive pyelonephritis can increase the risk of death by approximately 30%.[199][200] These delays were often associated with minority patient populations, lower socioeconomic status, and weekend presentations, highlighting critical areas for improvement.[199] Delaying treatment, especially postponing drainage procedures beyond 2 days, significantly increases morbidity and mortality.[200] Evidence suggests that third-generation cephalosporins may be the preferred antibiotics in these cases, although surgical intervention remains the primary treatment.[201] Most patients with obstructive pyelonephritis who undergo timely drainage can safely proceed with definitive ureterolithiasis surgery within 1 to 2 weeks.[202] Risk Factors for Obstructive Pyelonephritis in Ureterolithiasis Risk factors for developing obstructive pyelonephritis in patients with ureterolithiasis include: Greater degree of hydronephrosis Diabetes Elevated CRP, lactic acid, procalcitonin, or NLR levels Increasing patient age Lower serum albumin Perinephric fat stranding on imaging Positive nitrites on urinalysis Pyuria Renal failure Size of obstructing stone larger than 5 mm Thrombocytopenia [203][204][205][206][207][208][209]

Numerous conditions can cause flank pain that may simulate renal colic, including: Abdominal aortic aneurysm dissection Acute mesenteric ischemia Angiomyolipomas Appendicitis Biliary colic Bowel obstruction Cholecystitis Costochondritis Dietl crisis Diverticulitis Double J stenting or removal Ectopic pregnancy Endometriosis Focal nephronia Hepatitis Herpes zoster Iliac aneurysms Irritable bowel syndrome Lobar pneumonia Local mass or growth Neurological disorders and neuropathic pain Nutcracker syndrome Musculoskeletal conditions Ovarian cyst torsion Pancreatitis Papillary necrosis Pelvic pain syndrome Perinephric abscess Peritonitis Pleural pain Polycystic kidney disease Post-ureteroscopy Prostatitis Pyelonephritis Referred pain from the back Renal abscess Renal hematoma Renal infarct Renal neoplasm Renal vein thrombosis Renovascular compromise Retroperitoneal disorders Retroperitoneal fibrosis Spinal disc disorders Spinal tumor or fracture Splenic infarction Ureteral compression (iatrogenic, neoplasms, and scarring) Ureteral spasms Ureteral stricture Ureteroceles Ureteropelvic junction obstruction Urinary tract infection Wunderlich syndrome (a rare condition with spontaneous renal subcapsular and/or retroperitoneal bleeding and hematoma formation)

The prognosis depends on the clinical situation, stone size and location, the patient’s anatomy, clinical history, and comorbidities. Smaller stones (<5 mm) located in the distal ureter are highly likely to pass spontaneously. However, the larger the stone size and the more proximal its location in the ureter, the less likely it is to pass without intervention. If the kidney becomes infected, urgent surgical intervention to drain the renal pelvis may be necessary to prevent urosepsis, embolic ischemia, limb amputations, and death. All patients with urinary calculi should be provided information about 24-hour urine testing for prophylactic treatment. This testing is especially recommended for children, patients with renal failure, solitary kidneys, recurrent stone formers, or those at high surgical or anesthetic risk.

Possible complications include: Embolic ischemia Failure of spontaneous stone passage Forniceal (calyceal) rupture with extravasation Hematuria Intractable pain, nausea, or vomiting Obstructive pyelonephritis (pyonephrosis) Pyelolymphatic backflow Renal failure or damage Sepsis Ureteral scarring or stricture Urinary tract infection

Patients should be informed about the possibility of identifying chemical risk factors for future stone formation through a 24-hour urine test. The analysis of these results can guide specific recommendations regarding dietary changes, lifestyle modifications, or medications to help reduce the risk of additional stones, although prevention is not always guaranteed. Testing is recommended for high-risk individuals, including those with significant comorbidities, solitary or horseshoe kidneys, recurrent stone formation, children, and patients with elevated surgical or anesthetic risks. The effectiveness of the preventive therapy program largely depends on patient motivation and discipline. Patients who are committed to minimizing their risk of future stones will benefit the most, as long-term compliance with the treatment is essential. Even without specific testing, general recommendations include increasing fluid intake to produce at least 2000 mL of urine daily, with an optimal goal of 2500 mL. Calcium intake should be moderate, as both insufficient and excessive amounts are discouraged. Dietary adjustments should include reducing excessive sodium, animal protein, and high-oxalate foods. Patients with cystine stones face a significantly high risk of recurrence and require specialized treatment to remain stone-free. Prophylactic measures include maintaining aggressive hydration to produce 3000 to 3500 mL of urine daily and alkalinizing the urine to achieve a pH of 7.5. Please see StatPearls' companion resource, "Cystinuria," for more information.

The size and location of the calculus, along with the patient's level of discomfort, help predict the likelihood of spontaneous stone passage. About 90% of stones smaller than 5 mm pass within 4 weeks, while up to 95% of stones larger than 8 mm are likely to become impacted and require intervention. Hospital admission is indicated for significant renal stones in a solitary kidney, severe kidney injury, infected renal stones, intractable pain or nausea, urinary extravasation, or sepsis. Patients with infected stones (eg, nephrolithiasis accompanied by evidence of a urinary tract infection) require urgent and specialized treatment. The infected stone is a nidus for infection, leading to urinary stasis and impairing the body's ability to manage the infection. In many cases, these stones must be completely removed through surgery to prevent recurrent infections and the formation of new stones. As it is not possible to clinically differentiate acute pyelonephritis (a medical condition treated with antibiotics) from pyonephrosis (obstructive pyelonephritis), a potentially life-threatening condition requiring urgent surgical intervention and drainage, imaging is essential in nearly all cases of acute flank pain. This is particularly important if patients admitted for pyelonephritis do not improve with medical therapy. Ultrasound may be sufficient but is not always definitive. If the results are equivocal, insufficient, or negative, a non-contrast CT may be necessary, as obstructive pyelonephritis can still be present even with a routine renal ultrasound. Intervention is recommended for a stone that has not moved or passed after 4 to 6 weeks, even if the patient remains asymptomatic. This is due to the risk of ureteral scarring and other complications. Convincing an asymptomatic patient to undergo surgery can be challenging, but explaining the need for the procedure early in the course of treatment can be effective. This allows patients to understand that the procedure is necessary to protect the kidneys and ureters from permanent damage if a stone or obstruction is stuck and not resolving on its own.

Intervention is recommended for a stone that has not moved or passed after 4 to 6 weeks, even if the patient remains asymptomatic. This is due to the risk of ureteral scarring and other complications. Convincing an asymptomatic patient to undergo surgery can be challenging, but explaining the need for the procedure early in the course of treatment can be effective. This allows patients to understand that the procedure is necessary to protect the kidneys and ureters from permanent damage if a stone or obstruction is stuck and not resolving on its own. An infected kidney or urinary tract infection with obstructing ureterolithiasis is considered an urgent surgical emergency. Please see StatPearls' companion resource, "Complicated Urinary Tract Infections," for more information.[188][189][190] In the most serious cases or when there is a significant ureteral stone burden, percutaneous renal drainage is preferred over double J stents.[192][193][194][195] All stone material should be collected and sent for chemical analysis. Urine tests collected over a 24-hour period are essential for long-term preventive therapy but require high levels of patient dedication and compliance for success. Despite this, they should be offered to all patients with nephrolithiasis. 24-Hour urine testing is particularly recommended in the following situations: Abnormal urinary tract anatomy Chronic diarrhea Family history of nephrolithiasis First stone before or at age 21 High anesthesia or surgical risk Irritable bowel syndrome Morbid obesity Nephrocalcinosis Preexisting renal failure Prior ureteral or urinary stone surgery Stone composition primarily other than calcium oxalate or struvite (cystine, calcium phosphate, and uric acid) Recurrent urinary tract infections Recurrent urolithiasis Reimplanted ureter(s) Renal failure (GFR<60 mL/min due to obstructive calculi) Solitary kidney Underlying predisposing condition (eg, bypass surgery, short-bowel syndrome, and enteric hyperoxaluria) Ureteropelvic junction obstruction Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information.[210]

The management of renal stones is most effective when conducted by an interprofessional healthcare team, which includes a nephrologist, ED physician, radiologist, urologist, dietitian or nutritionist, and primary care provider. Although most renal stones will pass spontaneously within 4 weeks, stones larger than 7 mm may require surgical intervention. Stones measuring 10 mm or larger typically necessitate surgery. Healthcare providers, including nurse practitioners who treat patients with kidney stones, should consult with a urologist when ureteral stones fail to pass after 4 to 6 weeks, with or without medical expulsive therapy. Urologic nurses play a key role in treatment by monitoring patients, offering ongoing support and education, and updating the team on any changes in patient status. Pharmacists ensure prescribed medications are dosed appropriately, check for potential drug interactions, and provide patient education. Ethical considerations are crucial when determining treatment options and respecting patient autonomy in decision-making. Responsibilities within the interprofessional team of healthcare providers should be clearly defined, with each member contributing their specialized knowledge and skills to optimize patient care. Effective interprofessional communication fosters a collaborative environment where information is shared, questions are encouraged, and concerns are addressed promptly. Lastly, care coordination is essential to ensure seamless and efficient patient care. Physicians, advanced practitioners, nurses, pharmacists, and other healthcare professionals must collaborate to streamline the patient's journey from diagnosis through treatment and follow-up. This coordination minimizes errors, reduces delays, and enhances patient safety, ultimately leading to improved outcomes and patient-centered care that prioritizes the well-being and satisfaction of individuals affected by nephrolithiasis.