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The Kidney in Pregnancy Unless excessive, dietary calcium should not be restricted 200 mg/24 h in pregnant women. Values >300 mg/24 h are because this will increase oxalate absorption. Oxalate excre- considered abnormal. Prepartum proteinuria may also worsen tion can be decreased by limiting foods high in oxalate such during pregnancy, making pregnancy-related changes difficult as nuts, cocoa, spinach, rhubarb, and beets. Potassium citrate to distinguish from a flare of an underlying kidney disease or or potassium bicarbonate will increase urinary citrate excre- development of preeclampsia. tion, which helps prevent crystallization. An additional Because of increased renal vascular and interstitial vol- benefit of potassium citrate is a decrease in renal calcium ume, kidney size may increase by 1 to 1.5 cm. Physiologic excretion, possibly related to preventing calcium release hydronephrosis and hydroureter, due in part to external com- from bone. pression of the ureters, are common in pregnancy, increase as In patients with uric acid stones, management consists of pregnancy advances, and may take weeks to resolve postpar- increasing the solubility of uric acid by alkalinizing the urine tum. The dilated collecting system can lead to urinary stasis, with potassium citrate or bicarbonate; allopurinol can be ben- which increases the risk for pyelonephritis. Therefore, screen- eficial if uric acid excretion is elevated. ing for asymptomatic bacteriuria at least once in early preg- In patients with cystine stones, urine output should be nancy is recommended, and treatment is indicated. See maintained at >3000 mL/d to decrease solubility of urinary MKSAP 19 Infectious Disease for more information. cystine. Urinary cystine excretion can be further reduced by Chronic respiratory alkalosis due to progesterone-induced limiting sodium intake and by alkalizing the urine to a pH 57.0. hyperventilation commonly decreases Pco, to 27 to 32 mm Hg Struvite stones typically require urologic intervention. (3.6-4.3 kPa). Renal compensation results in decreased serum Before any surgical procedure, it is important that active infec- bicarbonate levels between 18 to 20 mEq/L (18-20 mmol/L), tion be treated with antibiotics to avert sepsis. To prevent with a serum pH of approximately 7.45. recurrent stone formation, all stone fragments must be Changes in antidiuretic hormone response to osmolality removed from the kidney. In patients unable to undergo sur- (reset osmostat) cause mild hyponatremia (decrease in serum gery, the urease inhibitor acetohydroxamic acid may reduce sodium of 4 to 5 mEq/L [4-5 mmol/L]) with a decrease in urine alkalinity and decrease stone growth; however, this is serum osmolality by 8 to 10 mOsm/kg H,O. No treatment is best used as an adjunct to urologic intervention. indicated. Rarely, transient gestational diabetes insipidus can develop due to excessive metabolism of antidiuretic hormone by placental vasopressinase. e Acute management of symptomatic nephrolithiasis includes pain management and facilitation of stone passage. e Pregnancy is associated with increased glomerular e Urologic intervention is required in all patients with filtration rate with decreased serum creatinine and

Unless excessive, dietary calcium should not be restricted 200 mg/24 h in pregnant women. Values >300 mg/24 h are because this will increase oxalate absorption. Oxalate excre- considered abnormal. Prepartum proteinuria may also worsen tion can be decreased by limiting foods high in oxalate such during pregnancy, making pregnancy-related changes difficult as nuts, cocoa, spinach, rhubarb, and beets. Potassium citrate to distinguish from a flare of an underlying kidney disease or or potassium bicarbonate will increase urinary citrate excre- development of preeclampsia. tion, which helps prevent crystallization. An additional Because of increased renal vascular and interstitial vol- benefit of potassium citrate is a decrease in renal calcium ume, kidney size may increase by 1 to 1.5 cm. Physiologic excretion, possibly related to preventing calcium release hydronephrosis and hydroureter, due in part to external com- from bone. pression of the ureters, are common in pregnancy, increase as In patients with uric acid stones, management consists of pregnancy advances, and may take weeks to resolve postpar- increasing the solubility of uric acid by alkalinizing the urine tum. The dilated collecting system can lead to urinary stasis, with potassium citrate or bicarbonate; allopurinol can be ben- which increases the risk for pyelonephritis. Therefore, screen- eficial if uric acid excretion is elevated. ing for asymptomatic bacteriuria at least once in early preg- In patients with cystine stones, urine output should be nancy is recommended, and treatment is indicated. See maintained at >3000 mL/d to decrease solubility of urinary MKSAP 19 Infectious Disease for more information. cystine. Urinary cystine excretion can be further reduced by Chronic respiratory alkalosis due to progesterone-induced limiting sodium intake and by alkalizing the urine to a pH 57.0. hyperventilation commonly decreases Pco, to 27 to 32 mm Hg Struvite stones typically require urologic intervention. (3.6-4.3 kPa). Renal compensation results in decreased serum Before any surgical procedure, it is important that active infec- bicarbonate levels between 18 to 20 mEq/L (18-20 mmol/L), tion be treated with antibiotics to avert sepsis. To prevent with a serum pH of approximately 7.45. recurrent stone formation, all stone fragments must be Changes in antidiuretic hormone response to osmolality removed from the kidney. In patients unable to undergo sur- (reset osmostat) cause mild hyponatremia (decrease in serum gery, the urease inhibitor acetohydroxamic acid may reduce sodium of 4 to 5 mEq/L [4-5 mmol/L]) with a decrease in urine alkalinity and decrease stone growth; however, this is serum osmolality by 8 to 10 mOsm/kg H,O. No treatment is best used as an adjunct to urologic intervention. indicated. Rarely, transient gestational diabetes insipidus can develop due to excessive metabolism of antidiuretic hormone by placental vasopressinase. e Acute management of symptomatic nephrolithiasis includes pain management and facilitation of stone passage. e Pregnancy is associated with increased glomerular e Urologic intervention is required in all patients with filtration rate with decreased serum creatinine and evidence of infection, acute kidney injury, intractable increased proteinuria.

Unless excessive, dietary calcium should not be restricted 200 mg/24 h in pregnant women. Values >300 mg/24 h are because this will increase oxalate absorption. Oxalate excre- considered abnormal. Prepartum proteinuria may also worsen tion can be decreased by limiting foods high in oxalate such during pregnancy, making pregnancy-related changes difficult as nuts, cocoa, spinach, rhubarb, and beets. Potassium citrate to distinguish from a flare of an underlying kidney disease or or potassium bicarbonate will increase urinary citrate excre- development of preeclampsia. tion, which helps prevent crystallization. An additional Because of increased renal vascular and interstitial vol- benefit of potassium citrate is a decrease in renal calcium ume, kidney size may increase by 1 to 1.5 cm. Physiologic excretion, possibly related to preventing calcium release hydronephrosis and hydroureter, due in part to external com- from bone. pression of the ureters, are common in pregnancy, increase as In patients with uric acid stones, management consists of pregnancy advances, and may take weeks to resolve postpar- increasing the solubility of uric acid by alkalinizing the urine tum. The dilated collecting system can lead to urinary stasis, with potassium citrate or bicarbonate; allopurinol can be ben- which increases the risk for pyelonephritis. Therefore, screen- eficial if uric acid excretion is elevated. ing for asymptomatic bacteriuria at least once in early preg- In patients with cystine stones, urine output should be nancy is recommended, and treatment is indicated. See maintained at >3000 mL/d to decrease solubility of urinary MKSAP 19 Infectious Disease for more information. cystine. Urinary cystine excretion can be further reduced by Chronic respiratory alkalosis due to progesterone-induced limiting sodium intake and by alkalizing the urine to a pH 57.0. hyperventilation commonly decreases Pco, to 27 to 32 mm Hg Struvite stones typically require urologic intervention. (3.6-4.3 kPa). Renal compensation results in decreased serum Before any surgical procedure, it is important that active infec- bicarbonate levels between 18 to 20 mEq/L (18-20 mmol/L), tion be treated with antibiotics to avert sepsis. To prevent with a serum pH of approximately 7.45. recurrent stone formation, all stone fragments must be Changes in antidiuretic hormone response to osmolality removed from the kidney. In patients unable to undergo sur- (reset osmostat) cause mild hyponatremia (decrease in serum gery, the urease inhibitor acetohydroxamic acid may reduce sodium of 4 to 5 mEq/L [4-5 mmol/L]) with a decrease in urine alkalinity and decrease stone growth; however, this is serum osmolality by 8 to 10 mOsm/kg H,O. No treatment is best used as an adjunct to urologic intervention. indicated. Rarely, transient gestational diabetes insipidus can develop due to excessive metabolism of antidiuretic hormone by placental vasopressinase. e Acute management of symptomatic nephrolithiasis includes pain management and facilitation of stone passage. e Pregnancy is associated with increased glomerular e Urologic intervention is required in all patients with filtration rate with decreased serum creatinine and evidence of infection, acute kidney injury, intractable increased proteinuria. pain, and stones that fail to pass. e Screening for asymptomatic bacteriuria at least once in e Increased fluid intake to >2500 mL/d is the most impor- early pregnancy is recommended, and treatment is tant intervention to prevent recurrent kidney stones, indicated. regardless of stone composition. e Mild hyponatremia from a reset in antidiuretic hormone response to hypo-osmolality occurs normally during pregnancy and requires no management.

pain, and stones that fail to pass. e Screening for asymptomatic bacteriuria at least once in e Increased fluid intake to >2500 mL/d is the most impor- early pregnancy is recommended, and treatment is tant intervention to prevent recurrent kidney stones, indicated. regardless of stone composition. e Mild hyponatremia from a reset in antidiuretic hormone response to hypo-osmolality occurs normally during pregnancy and requires no management. The Kidney in Pregnancy Hypertension in Pregnancy Normal Physiologic Changes Chronic Hypertension in Pregnancy The American College of Obstetricians and Gynecologists Pregnancy is a state of volume expansion and vasodilation. (ACOG) defines chronic hypertension as a systolic blood pres- Sodium and water retention increase plasma volume, aug- sure (BP) >140 mm Hg or diastolic BP >90 mm Hg starting menting renal blood flow and increasing glomerular filtration before pregnancy or before 20 weeks of gestation or persists rate (GFR) by up to 50%. With the GFR increase, serum creati- longer than 12 weeks postpartum. It is associated with worse nine levels decrease. Therefore, high normal serum creatinine maternal and fetal outcomes. Hypertension first recognized levels may indicate significant kidney impairment. Despite the during pregnancy before 20 weeks’ gestation usually indicates volume expansion, blood pressure begins to decrease in the chronic hypertension. The lower BP measurements associated first trimester and reaches the nadir in the second trimester with physiologic changes of pregnancy can mask hypertension due to peripheral vasodilation. during the first trimester. Proteinuria increases, with the upper limit of normal ACOG recommends treating persistent systolic BP increasing from 100 mg/24 h in nonpregnant to approximately 2160 mm Hg or diastolic 2110 mm Hg in pregnant women 72

The Kidney in Pregnancy with chronic hypertension, and maintaining BP at 120-159/ 80-109 mm Hg. These goals remain controversial, with some e First-line therapy of chronic hypertension in pregnancy suggesting lower targets, especially in patients with chronic includes methyldopa and labetalol. kidney disease or other comorbidity. Antihypertensive treat- e Gestational hypertension first manifests after 20 weeks ment reduces the risk for progression to severe hypertension of pregnancy without proteinuria or other end-organ by 50% but has not been shown to prevent preeclampsia, damage and resolves within 12 weeks of delivery. preterm birth, being small for gestational age, or infant mor- tality. Any evidence of end-organ damage requires treatment, regardless of severity of hypertension. Importantly, all antihy- Acute-Onset Severe Hypertension pertensive medications cross the placenta. The 2019 ACOG recommendations on emergent therapy for Renin-angiotensin system agents (ACE inhibitors, angio- acute-onset severe hypertension during pregnancy and the tensin receptor blockers, and direct renin inhibitors) are all postpartum period define acute-onset severe hypertension as contraindicated because of teratogenicity, even early in preg- systolic BP >160 mm Hg and/or diastolic BP 2110 mm Hg. Such nancy, and should be stopped before conception (in those severe BP may occur in the setting of previously controlled planning pregnancy). If conception has already occurred, they chronic hypertension, as a component of preeclampsia, in the should be stopped immediately and the mother counseled HELLP (hemolysis, elevated liver enzymes, low platelets) syn- regarding possible fetal effects. drome, or de novo in women without these complications. First-line therapy includes methyldopa and _labetalol, Women with acute-onset severe hypertension persisting which have been used safely and extensively in pregnancy. >15 minutes require emergent therapy, most typically with Methyldopa monotherapy may be insufficient, in which case it intravenous labetalol or hydralazine, or with immediate- can be replaced with labetalol. Calcium channel blockers can release oral nifedipine. be added; nifedipine has been used most extensively. The The target goal of treatment is not normalization of BP but B-blockers metoprolol and pindolol have also been used in rather BP of 140-150/90-100 mm Hg. Maternal and fetal moni- pregnancy, but atenolol and propranolol may have adverse toring is advised. Maternal BP should be controlled before fetal effects. Diuretics must be used with caution because they delivery. Magnesium sulfate is also advised as emergent ther- may induce oligohydramnios if started during pregnancy. apy for seizure prophylaxis and should be given to women ACOG also recommends low-dose aspirin (81 mg/d) for with acute-onset severe hypertension regardless of other signs all pregnant women with chronic hypertension to be taken of preeclampsia or eclampsia. from weeks 12 to 28 of gestation.

with chronic hypertension, and maintaining BP at 120-159/ 80-109 mm Hg. These goals remain controversial, with some e First-line therapy of chronic hypertension in pregnancy suggesting lower targets, especially in patients with chronic includes methyldopa and labetalol. kidney disease or other comorbidity. Antihypertensive treat- e Gestational hypertension first manifests after 20 weeks ment reduces the risk for progression to severe hypertension of pregnancy without proteinuria or other end-organ by 50% but has not been shown to prevent preeclampsia, damage and resolves within 12 weeks of delivery. preterm birth, being small for gestational age, or infant mor- tality. Any evidence of end-organ damage requires treatment, regardless of severity of hypertension. Importantly, all antihy- Acute-Onset Severe Hypertension pertensive medications cross the placenta. The 2019 ACOG recommendations on emergent therapy for Renin-angiotensin system agents (ACE inhibitors, angio- acute-onset severe hypertension during pregnancy and the tensin receptor blockers, and direct renin inhibitors) are all postpartum period define acute-onset severe hypertension as contraindicated because of teratogenicity, even early in preg- systolic BP >160 mm Hg and/or diastolic BP 2110 mm Hg. Such nancy, and should be stopped before conception (in those severe BP may occur in the setting of previously controlled planning pregnancy). If conception has already occurred, they chronic hypertension, as a component of preeclampsia, in the should be stopped immediately and the mother counseled HELLP (hemolysis, elevated liver enzymes, low platelets) syn- regarding possible fetal effects. drome, or de novo in women without these complications. First-line therapy includes methyldopa and _labetalol, Women with acute-onset severe hypertension persisting which have been used safely and extensively in pregnancy. >15 minutes require emergent therapy, most typically with Methyldopa monotherapy may be insufficient, in which case it intravenous labetalol or hydralazine, or with immediate- can be replaced with labetalol. Calcium channel blockers can release oral nifedipine. be added; nifedipine has been used most extensively. The The target goal of treatment is not normalization of BP but B-blockers metoprolol and pindolol have also been used in rather BP of 140-150/90-100 mm Hg. Maternal and fetal moni- pregnancy, but atenolol and propranolol may have adverse toring is advised. Maternal BP should be controlled before fetal effects. Diuretics must be used with caution because they delivery. Magnesium sulfate is also advised as emergent ther- may induce oligohydramnios if started during pregnancy. apy for seizure prophylaxis and should be given to women ACOG also recommends low-dose aspirin (81 mg/d) for with acute-onset severe hypertension regardless of other signs all pregnant women with chronic hypertension to be taken of preeclampsia or eclampsia. from weeks 12 to 28 of gestation. Preeclampsia Gestational Hypertension Preeclampsia is defined by new-onset hypertension and protein- Gestational hypertension first manifests after 20 weeks of uria (urine collection >300 mg/24 h or urine protein-creatinine pregnancy without proteinuria or other end-organ damage ratio >300 mg/g) that occurs after 20 weeks of pregnancy (features of preeclampsia) and resolves within 12 weeks of (Table 31). New-onset hypertension with new-onset end-organ delivery. Preeclampsia occurs in approximately one third of damage (such as liver or kidney injury, pulmonary edema, cases. Hypertension persisting beyond 12 weeks’ postpartum cerebral or visual symptoms, or thrombocytopenia) is also is considered chronic hypertension. Gestational hypertension diagnostic of preeclampsia. Severe preeclampsia is identified by can recur in subsequent pregnancies and is associated with an persistent systolic BP >160 mm Hg or diastolic BP >110 mm Hg approximately fourfold risk for development of chronic and end-organ damage. Eclampsia is the presence of seizures hypertension. in context of preeclampsia without other cause. The HELLP syndrome is a life-threatening state complicating 10% to 20% of e Chronic hypertension precedes pregnancy or is present preeclampsia cases. Risk factors for preeclampsia include prior before 20 weeks’ gestation and persists longer than preeclampsia (with an approximate 20% recurrence rate), 12 weeks’ postpartum. nulliparity, diabetes mellitus, advanced maternal age, multiple

Preeclampsia Gestational Hypertension Preeclampsia is defined by new-onset hypertension and protein- Gestational hypertension first manifests after 20 weeks of uria (urine collection >300 mg/24 h or urine protein-creatinine pregnancy without proteinuria or other end-organ damage ratio >300 mg/g) that occurs after 20 weeks of pregnancy (features of preeclampsia) and resolves within 12 weeks of (Table 31). New-onset hypertension with new-onset end-organ delivery. Preeclampsia occurs in approximately one third of damage (such as liver or kidney injury, pulmonary edema, cases. Hypertension persisting beyond 12 weeks’ postpartum cerebral or visual symptoms, or thrombocytopenia) is also is considered chronic hypertension. Gestational hypertension diagnostic of preeclampsia. Severe preeclampsia is identified by can recur in subsequent pregnancies and is associated with an persistent systolic BP >160 mm Hg or diastolic BP >110 mm Hg approximately fourfold risk for development of chronic and end-organ damage. Eclampsia is the presence of seizures hypertension. in context of preeclampsia without other cause. The HELLP syndrome is a life-threatening state complicating 10% to 20% of e Chronic hypertension precedes pregnancy or is present preeclampsia cases. Risk factors for preeclampsia include prior before 20 weeks’ gestation and persists longer than preeclampsia (with an approximate 20% recurrence rate), 12 weeks’ postpartum. nulliparity, diabetes mellitus, advanced maternal age, multiple ¢ The American College of Obstetricians and Gynecologists gestation, and family history. The pathophysiology of preec- lampsia is poorly understood. Abnormal placental vascular recommends treating persistent systolic blood pressure development and generalized endothelial dysfunction occur. (BP) >160 mm Hg or diastolic >110 mm Hg in pregnant women with chronic hypertension, and maintaining BP Symptoms of preeclampsia include rapid weight gain due

¢ The American College of Obstetricians and Gynecologists gestation, and family history. The pathophysiology of preec- lampsia is poorly understood. Abnormal placental vascular recommends treating persistent systolic blood pressure development and generalized endothelial dysfunction occur. (BP) >160 mm Hg or diastolic >110 mm Hg in pregnant women with chronic hypertension, and maintaining BP Symptoms of preeclampsia include rapid weight gain due at 120-159/80-109 mm Hg. to edema, nausea, vomiting, abdominal pain (particularly concerning if in the right upper quadrant, signifying possible e Renin-angiotensin system agents (ACE inhibitors, angio- HELLP syndrome), headaches, altered mental status, and tensin receptor blockers, and direct renin inhibitors) are blurred vision. If untreated, preeclampsia ultimately leads to contraindicated in pregnancy because of teratogenicity. maternal end-organ damage and fetal growth retardation, and (Continued) it may cause maternal and/or fetal death. 73

The Kidney in Pregnancy TABLE 31. Diagnostic Criteria for Preeclampsia Blood pressure 2140 mm Hg systolic or 290 mm Hg diastolic on two occasions at least 4 hours apart after 20 weeks of gestation in a woman with a previously normal blood pressure 2160 mm Hg systolic or 2110 mm Hg diastolic; hypertension can be confirmed within a short interval (minutes) to facilitate timely antihypertensive therapy | and | Proteinuria 2300 mg/24 h urine collection (or this amount extrapolated from a timed collection) or Urine protein-creatinine ratio [300 mg/g Dipstick reading of 2+ (used only if other quantitative methods are not available) Sa | Or, in the absence of proteinuria, new-onset hypertension with the new onset of any of the following: (= | Thrombocytopenia Platelet count <100,000/uL (100 x 10°/L) Kidney dysfunction Serum creatinine concentrations >1.1 mg/dL (97.2 mol/L) or a doubling of the serum creatinine concentration in the absence of other kidney disease Impairedliver function Elevated blood concentrations of liver aminotransaminases to twice the normal concentration Pulmonary edema - Cerebral or visual symptoms - With permission from American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins. Gestational hypertension and preeclampsia: ACOG practice bulletin, number 222. Obstet Gynecol. 2020;135:e237-e60. [PMID: 32443079] doi:10.1097/AOG.0000000000003891

Pulmonary edema - Cerebral or visual symptoms - With permission from American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins. Gestational hypertension and preeclampsia: ACOG practice bulletin, number 222. Obstet Gynecol. 2020;135:e237-e60. [PMID: 32443079] doi:10.1097/AOG.0000000000003891 Low-dose (81 mg/d) aspirin started after 12 weeks of Chronic Kidney Disease pregnancy reduces the rate of preeclampsia in women at high risk. Antihypertensive medications do not prevent pre- in Pregnancy eclampsia but reduce complications of stroke, heart failure, Chronic kidney disease and a serum creatinine level >1.4 mg/ and kidney injury. Most experts initiate treatment at BP dL (124 umol/L) increases the risk of kidney and pregnancy- >150-160/100-110 mm Hg, although there is no consensus. associated complications. Proteinuria may also increase risk, Emergent management of acute-onset severe hyperten- but an elevated serum creatinine has greater impact. sion of preeclampsia includes intravenous labetalol or hydrala- Complications include preeclampsia, acute kidney injury, pro- zine, or oral short-acting nifedipine, and is indicated before gression of chronic kidney disease, end-stage kidney disease, delivery. preterm delivery, gestational hypertension, intrauterine Definitive treatment of preeclampsia is delivery. Maternal growth retardation, and fetal loss. Preconception counseling risk for complications diminishes in the hours after delivery, regarding these risks is essential. although proteinuria may take months to resolve. Maternal Pregnancy is uncommon in women receiving dialysis,

Definitive treatment of preeclampsia is delivery. Maternal growth retardation, and fetal loss. Preconception counseling risk for complications diminishes in the hours after delivery, regarding these risks is essential. although proteinuria may take months to resolve. Maternal Pregnancy is uncommon in women receiving dialysis, benefits must be weighed against neonatal risks for a preterm which is associated with infertility. Levels of B-human chori- delivery, but severe preeclampsia is an indication for immedi- onic gonadotropin may increase in nonpregnant dialysis ate delivery regardless of gestational age. Mild preeclampsia patients; therefore, ultrasonography is usually necessary to may be managed conservatively, with maternal and fetal mon- confirm pregnancy. Pregnancy in the context of dialysis is itoring and treatment of hypertension. In all cases, close atten- associated with very high risk of preeclampsia and fetal loss, tion to hypertension is recommended in the postpartum although live birth rates have improved to 60% to 80%. To

may be managed conservatively, with maternal and fetal mon- confirm pregnancy. Pregnancy in the context of dialysis is itoring and treatment of hypertension. In all cases, close atten- associated with very high risk of preeclampsia and fetal loss, tion to hypertension is recommended in the postpartum although live birth rates have improved to 60% to 80%. To period. optimize fetal outcomes, hemodialysis frequency and dose are increased to improve BP and volume status. Pregnancy in women with kidney transplants is more ¢ Preeclampsia is defined by new-onset hypertension and common than in those receiving dialysis. Outcomes are proteinuria that occurs after 20 weeks of pregnancy. improved with better allograft function (serum creatinine ¢ Low-dose (81 mg/d) aspirin started after 12 weeks of <1.5 mg/dL [132.6 umol/L]) and stable immunosuppression; pregnancy reduces rates of preeclampsia in women at transplant patients should await 1 to 2 years with a stable allo- high risk. graft before attempting conception. No immunosuppressive medication has been extensively studied in pregnancy, and all e Emergent management of acute-onset severe hyperten- have some associated risk. Although calcineurin inhibitors sion of preeclampsia includes intravenous labetalol or hydralazine, or oral short-acting nifedipine. (tacrolimus and cyclosporine) have been used safely, mycophe- nolate mofetil is teratogenic and needs to be replaced 3 to ¢ Definitive treatment of preeclampsia is delivery. 6 months before conception with azathioprine, which has an

period. optimize fetal outcomes, hemodialysis frequency and dose are increased to improve BP and volume status. Pregnancy in women with kidney transplants is more ¢ Preeclampsia is defined by new-onset hypertension and common than in those receiving dialysis. Outcomes are proteinuria that occurs after 20 weeks of pregnancy. improved with better allograft function (serum creatinine ¢ Low-dose (81 mg/d) aspirin started after 12 weeks of <1.5 mg/dL [132.6 umol/L]) and stable immunosuppression; pregnancy reduces rates of preeclampsia in women at transplant patients should await 1 to 2 years with a stable allo- high risk. graft before attempting conception. No immunosuppressive medication has been extensively studied in pregnancy, and all e Emergent management of acute-onset severe hyperten- have some associated risk. Although calcineurin inhibitors sion of preeclampsia includes intravenous labetalol or hydralazine, or oral short-acting nifedipine. (tacrolimus and cyclosporine) have been used safely, mycophe- nolate mofetil is teratogenic and needs to be replaced 3 to ¢ Definitive treatment of preeclampsia is delivery. 6 months before conception with azathioprine, which has an 74

Chronic Kidney Disease extensive history of use in pregnancy. Sirolimus is contraindi- have a reduction in eGFR and therefore is defined by the cated because of fetal toxicity. Glucocorticoids increase the presence of anatomical defects or markers of kidney dam- risk for pregnancy-induced hypertension and diabetes. age such as albuminuria, hematuria, or electrolyte abnor- malities. Because albuminuria is associated with increased renal and cardiovascular morbidity and mortality, the e¢ Women with chronic kidney disease (CKD) have a Kidney Disease: Improving Global Outcomes (KDIGO) greater risk for preeclampsia, acute kidney injury, pro- group further subdivides the eGFR-based kidney stages by gression of CKD, end-stage kidney disease, preterm degree of albuminuria (Figure 21). This dual eGFR and delivery, gestational hypertension, intrauterine growth albuminuria staging algorithm provides a means for pre- retardation, and fetal loss. dicting which patients are at highest risk for progression e Kidney transplant recipients should wait at least 1 to 2 years of CKD to end-stage kidney disease (ESKD), defined as after transplantation with a stable allograft and stable CKD stage GS treated with chronic dialysis or kidney immunosuppression before attempting conception. transplantation.

extensive history of use in pregnancy. Sirolimus is contraindi- have a reduction in eGFR and therefore is defined by the cated because of fetal toxicity. Glucocorticoids increase the presence of anatomical defects or markers of kidney dam- risk for pregnancy-induced hypertension and diabetes. age such as albuminuria, hematuria, or electrolyte abnor- malities. Because albuminuria is associated with increased renal and cardiovascular morbidity and mortality, the e¢ Women with chronic kidney disease (CKD) have a Kidney Disease: Improving Global Outcomes (KDIGO) greater risk for preeclampsia, acute kidney injury, pro- group further subdivides the eGFR-based kidney stages by gression of CKD, end-stage kidney disease, preterm degree of albuminuria (Figure 21). This dual eGFR and delivery, gestational hypertension, intrauterine growth albuminuria staging algorithm provides a means for pre- retardation, and fetal loss. dicting which patients are at highest risk for progression e Kidney transplant recipients should wait at least 1 to 2 years of CKD to end-stage kidney disease (ESKD), defined as after transplantation with a stable allograft and stable CKD stage GS treated with chronic dialysis or kidney immunosuppression before attempting conception. transplantation. e Mycophenolate mofetil and sirolimus used in kidney transplant recipients are teratogenic and must be dis- continued before attempting conception. Epidemiology and Pathophysiology CKD affects approximately 15% of the U.S. adult population. About 50% of patients with prevalent CKD have stage G3 dis- ease or worse. The prevalence of CKD has remained stable in Chronic Kidney Disease the United States, with the highest prevalence seen in patients aged 260 years. Patients with lower eGFR are more likely to Definition and Staging have higher degrees of albuminuria. Advanced CKD, defined Chronic kidney disease (CKD) is defined as abnormal by stages G4 or G5, is present in <1% of the population. kidney structure or function present for >3 months. CKD Compared with men, women have a higher prevalence of both is stratified into stages 1 to 5 based on the level of esti- eGFR <60 mL/min/1.73 m2 (7.6% versus 6.1%) and albuminu- mated glomerular filtration rate (eGFR). Stage G1 does not ria (11.2% versus 8.9%).

e Mycophenolate mofetil and sirolimus used in kidney transplant recipients are teratogenic and must be dis- continued before attempting conception. Epidemiology and Pathophysiology CKD affects approximately 15% of the U.S. adult population. About 50% of patients with prevalent CKD have stage G3 dis- ease or worse. The prevalence of CKD has remained stable in Chronic Kidney Disease the United States, with the highest prevalence seen in patients aged 260 years. Patients with lower eGFR are more likely to Definition and Staging have higher degrees of albuminuria. Advanced CKD, defined Chronic kidney disease (CKD) is defined as abnormal by stages G4 or G5, is present in <1% of the population. kidney structure or function present for >3 months. CKD Compared with men, women have a higher prevalence of both is stratified into stages 1 to 5 based on the level of esti- eGFR <60 mL/min/1.73 m2 (7.6% versus 6.1%) and albuminu- mated glomerular filtration rate (eGFR). Stage G1 does not ria (11.2% versus 8.9%). Persistent albuminuria categories Description and range Al A2 A3

e Mycophenolate mofetil and sirolimus used in kidney transplant recipients are teratogenic and must be dis- continued before attempting conception. Epidemiology and Pathophysiology CKD affects approximately 15% of the U.S. adult population. About 50% of patients with prevalent CKD have stage G3 dis- ease or worse. The prevalence of CKD has remained stable in Chronic Kidney Disease the United States, with the highest prevalence seen in patients aged 260 years. Patients with lower eGFR are more likely to Definition and Staging have higher degrees of albuminuria. Advanced CKD, defined Chronic kidney disease (CKD) is defined as abnormal by stages G4 or G5, is present in <1% of the population. kidney structure or function present for >3 months. CKD Compared with men, women have a higher prevalence of both is stratified into stages 1 to 5 based on the level of esti- eGFR <60 mL/min/1.73 m2 (7.6% versus 6.1%) and albuminu- mated glomerular filtration rate (eGFR). Stage G1 does not ria (11.2% versus 8.9%). Persistent albuminuria categories Description and range Al A2 A3 Normal to Moderately Severely mildly increased increased increased

Al A2 A3 Normal to Moderately Severely mildly increased increased increased <30 mg/g 30-300 mg/g >300 mg/g = G1 Normal or high >90 — a) Pe G2 Mildly decreased 60-89 le = £ Es Mildly to = 5 Gea moderately decreased ad Ec ° “= is G3b Moderately to 30-44 o's severely decreased Da 2 2 o eee G4 Severely decreased 15-29 f oO G5 Kidney failure <15 Green: low risk (if no other markers of kidney disease, no CKD); Yellow: moderately increased risk; Orange: high risk; Red: very high risk. FIGURE 21. The Kidney Disease: Improving Global Outcomes (KDIGO) chronic kidney disease staging system. Prognosis of chronic kidney disease by glomerular filtration rate and albuminuria category. CKD = chronic kidney disease; GFR = glomerular filtration rate. Reprinted with permission from KDIGO: Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3:1-150. Copyright 2013. 75