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Year : 2012  |  Volume : 2  |  Issue : 1  |  Page : 15-21

Kidney and pregnancy

Department of Nephrology, Osmania Medical College and Osmania General Hospital, Hyderabad, Andhra Pradesh, India

Date of Web Publication3-Dec-2012

Correspondence Address:
Manisha Sahay
Professor and Head, 6-3-852/A, Ameerpet, Hyderabad- 16, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4855.104010

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Pregnancy is associated with many physiological changes in the renal system. Pregnancy can alter the course of some renal diseases as also pre-existing renal diseases may affect pregnancy outcomes. Pregnancy may be complicated by hypertension which warrants proper management. Acute kidney injury may complicate pregnancy. With chronic kidney diseases on the rise, it is important for the physician to be aware of management of pregnancy in these patients. Kidney transplant recipients have their unique set of problems and management of these patients poses a challenge for the physician. Hence, this review highlights the management of pregnant patients with renal diseases including issues related to dialysis and transplantation.

Keywords: AKI, CKD, pre-eclampsia, pregnancy, pregnancy induced hypertension, renal disease, transplantation

How to cite this article:
Sahay M. Kidney and pregnancy. J Acad Med Sci 2012;2:15-21

How to cite this URL:
Sahay M. Kidney and pregnancy. J Acad Med Sci [serial online] 2012 [cited 2021 Jul 27];2:15-21. Available from:

  Introduction Top

The kidney undergoes significant anatomical and physiological changes in pregnancy. All these changes revert to normal by the end of post partum period.

Certain renal diseases are common in pregnant females. Urinary tract infections in pregnancy warrant proper treatment and follow up to avoid fetal and maternal morbidity. Pregnancy induced hypertension is the most common entity which may result in acute kidney injury in pregnancy. Some other important causes of renal failure are acute fatty liver of pregnancy, hemolytic uremic syndrome and hyperemesis gravidarum and septic abortion. The management of these conditions requires a sound knowledge of the renal physiology in pregnancy. Pregnancy is unusual in females with chronic kidney disease, but when it occurs it poses a challenge both for the nephrologist and gynacecologist. Similarly management of pregnancy in a post renal transplant patient requires a good understanding of immunosuppression. This review article deals with the varied aspects of management renal diseases in pregnancy.

  Physiological Changes in Renal Function in Pregnancy Top

The kidney undergoes monumental physiologic and anatomic changes during a normal pregnancy. Renal plasma flow increases by 50-70%. Plasma volume increases by 50% and there is hemodilutional anemia. Cardiac output increases by 40%. Glomerular Filtration Rate (GFR) can reach levels up to 150% of normal. The intraglomerular pressure remains normal. Serum creatinine falls by an average of 0.4 mg/dl to a pregnancy range of 0.4 to 0.8 mg/dl.1 Hence, a serum creatinine of 1.0 mg/dl, although normal in a non-pregnant individual, reflects renal impairment in a pregnant woman. S creatinine rises near term and value of 1 mg% is considered normal. There is a blood pressure fall of approximately 10 mm Hg in the first 24 weeks. The blood pressure gradually returns to prepregnancy level by term. Glycosuria and aminoaciduria occur. Increased uric acid clearance results in low uric acid level (2.5-5.5 mg%) but increase later and reach pre-pregnancy values at term. A value of >6 mg% reflects PIH. Potassium and 900 meq of sodium are retained. Calcium excretion increases but stone formation is not increased as there is increased excretion of inhibitors of stone formation. A reset in the osmostat occurs, resulting in increased thirst and decreased serum sodium levels (by 5 mEq/L) and low plasma osmolality (10 m0sm/kg less). Clearance of ADH is increased by placental vasopressinase (transient Diabetes insipidus of pregnancy) which may respond to DDAVP. On the other hand, there are reports of transient SIADH in pregnancy. Urine concentration and dilution are adequate. There is mild respiratory alkalosis [Table 1]. [1]
Table 1: Physiological changes in pregnancy

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  Anatomic Changes Top

A dilatation of ureters and pelvis occurs till pelvic brim (iliac sign) with dilatation more pronounced on right secondary to dextrorotation of uterus and dilatation of right ovarian venous plexus. This leads to urinary stasis and a risk of urinary tract infections (UTIs). There is an increase in kidney size by 1-1.5 cm. All the physiologic changes maximize by the end of the 2nd trimester and then start to return to the prepartum level, whereas changes in the anatomy take up to 3 months postpartum to subside. [2],[3]

  Hormones Top

There is increase in aldosterone, desoxycorticosterone, progesterone, relaxin, oxytocin, and vasodilating prostaglandins and a decrease in vasopressin (due to vasopressinase) and also resistance to action of aldosterone and renin. [4]

  Renal Function Tests Top

  • Microscopic hematuria may be seen in 20%, disappears after delivery
  • GFR
    • MDRD formula-The modification of diet in renal disease (MDRD) formula underestimates GFR by 40 ml/min while Cockroft-Gault formula overestimates GFR by 40 ml/min. Creatinine clearance by 24-h urine collection is the gold standard in pregnancy
  • Estimating of proteinuria during pregnancy

    Urine protein excretion increases and up to 300 mg/d is normal. Albumin excretion is also increased. These values return to normal by 6 th month post-partum. Twenty-four hour urine collection, although a gold standard for proteinuria quantification, is cumbersome and inaccurate. The use of the P:C ratio to estimate 24-h protein excretion is controversial in pregnancy. Most misclassifications occur in women with borderline proteinuria (250 to 400 mg/d). Hence, it is reasonable to use the urine P:C ratio for diagnosis, with 24-h collection undertaken when result is equivocal.
  • Renal biopsy in pregnancy-Indications include severe symptomatic nephrotic syndrome, rapidly progressive renal failure. A biopsy can be done in 2nd trimester with patient in the lateral position.

  Renal Diseases Occurring in Pregnancy Top

Certain renal diseases are common in pregnancy. [5],[6]

Urinary Tract Infections

Urinary tract infections (UTIs) are the most common renal disease occurring during pregnancy and range from asymptomatic bacteriuria to pyelonephritis. UTIs have been associated with small for gestational age (SGA) babies, premature labor, intrauterine fetal death (IUD), anemia, and hypertension in mother. Pregnant females are at risk for development of UTIs (2-10%), because of anatomic and physiologic changes that occur in normal pregnancy.

  • Asymptomatic bacteriuria-A clean-voided specimen containing more than 100,000 organisms per milliliter suggests infection. 30% of patients develop pyelonephritis if asymptomatic bacteriuria is left untreated. Universal screening is therefore recommended in all pregnant females. Dipstick has a sensitivity of <50% and routine microscopy and culture are needed. Treatment with a 10-day course of oral antibiotics (nitrofurantoin, ampicillin, amoxicillin, sulfonamides, cephalexin, or co-amoxiclav) reduces incidence of pyelonephritis to 3%. Urinalysis with culture should be performed on a monthly basis after resolution. Recurrence occurs in 35%. If bacteriuria is persistent, suppressive therapy (Nitrofurantoin 100 mg at night, cephalexin or amoxicillin) is indicated.
  • Cystitis (3%) is associated with dysuria, urgency, and frequency, without systemic signs. Occurs in 2nd trimester. Common even in patients with negative urine cultures. Cystitis recurs in 17% and does not progress to acute pyelonephritis. It should be aggressively treated with oral antibiotic regimens. The symptoms of cystitis and pyuria accompanied by a "sterile" urine culture finding may be due to Chlamydia trachomatis urethritis. Mucopurulent cervicitis coexists, and erythromycin therapy is effective.
  • Pyelonephritis (3%)-70% patients with PN have asymptomatic bacteriuria. 50% occur in 2nd trimester. Onset is abrupt with fever, chills, flank pain, anorexia, nausea, vomiting, and costovertebral tenderness. The etiologic organisms include Escherichia coli, Klebsiella, Enterobacter, and Proteus. 10% are due to Gram+ organisms. 15% patients have concurrent bacteremia. Other complications include hemolysis, sepsis, adult respiratory distress syndrome, hepatic dysfunction, and death. Pyelonephritis requires hospitalization and intravenous antibiotics and fluids till fever resolves. Effective regimens include ampicillin plus gentamicin or a third-generation cephalosporin followed by oral administration of antibiotics (14 days). This leads to complete resolution of infection in 70%. In infections recurring in 2 weeks, 2-3 weeks of treatment and suppressive therapy throughout the pregnancy should be given. Post-coital cephalexin 250 mg or NFT 50 mg may be preventive. Perinephric or cortical abscesses may be seen.


Terminology of hypertensive disorders varies according to source, but the system recommended by the National High Blood Pressure Education Program describes the following five entities (NHBPEP, 2000): [7]

  • Gestational hypertension/transient hypertension is defined as blood pressure of 140/90 mm Hg or greater with no hypertension before pregnancy. Pre-eclampsia does not develop, with blood pressure returning to normal levels within 12 weeks postpartum. Patients are usually asymptomatic or have symptoms or signs like pre-eclampsia. It usually affects nulliparous females mostly in 3rd trimester. It is a retrospective diagnosis and is confused with pre-eclampsia at the time of onset and with essential hypertension postpartum until the blood pressure returns to normal. Proteinuria does not occur, serum uric acid is normal. It may predict the development of hypertension later in life. It is prudent to manage it as pre-eclampsia when first diagnosed.
  • Chronic hypertension is associated with underlying or pre-existing hypertension. The diagnosis is established by a blood pressure of 140/90 mm Hg or greater before pregnancy or before 20 weeks' gestation, or by persistent hypertension long after delivery. This diagnosis can be difficult to make, especially if no prior blood pressure readings are available or if the patient is not seen until late in pregnancy. Complications of chronic hypertension include superimposed pre-eclampsia, abruptio placentae, growth restriction and fetal death.
  • Pre-eclampsia is associated with intrauterine growth retardation and SGA babies. Occurs in 7% of all pregnancies mostly in primigravidas. It is a triad of hypertension, proteinura, and edema occurring after the 20 th week of gestation with few cases developing postpartum within hours. Hypertension is defined as rise in systolic BP >30 mm Hg and diastolic BP >15 mm Hg. Proteinuria is defined as >300 mg protein in urine per day. The risk factors associated with the development of pre-eclampsia include age older than 35 years or younger than 16 years, multiple pregnancies, chronic hypertension, obesity and African American race. HELLP syndrome (Hemolysis, Elevated liver enzymes, and low platelets) is observed when severe pre-eclampsia or eclampsia is accompanied by significant liver involvement. Acute renal failure (ARF) may develop. [8]
  • Eclampsia is the occurrence of seizure activity with no other explainable cause in setting of pre-eclampsia.
  • Pre-eclampsia superimposed on chronic hypertension defined as new-onset proteinuria (i.e., >300 mg/d) after 20 weeks' gestation in a hypertensive patient or as a sudden increase in proteinuria or blood pressure in a patient with hypertension and proteinuria before 20 weeks' gestation [Figure 1].
    Figure 1: Classification of hypertension in pregnancy

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Utero-placental ischemia: A combination of genetic and environmental factors results in inadequate invasion of uterine spiral arteries by placental trophoblasts resulting in inability of uterine vessels to transform from low-caliber resistive channels to a high-caliber capacitance system. This results in utero-placental ischemia. In normal pregnancy, vascular endothelial growth factor (VEGF) and placental-induced growth factor (PIGF) are made by placenta and circulate in high concentrations in pregnancy. VEGF and PIGF induce synthesis of nitric oxide and vasodilating prostacylin in endothelial cells decreasing vascular tone and blood pressure. In PIH, the utero-placental ischemia results in oxidative stress and release of a soluble cytokine, the sFlt-1 (soluble fms-like tyrosine kinase-1). sFlt-1 is a potent antagonist of VEGF and PIGF. In PET, concentrations of sFlt-1 rise in the 2 nd trimester with a decrease in VEGF and PIGF. Overproduction of sFlt-1 explains increased susceptibility to PET in multiple gestation, hydantidiform mole, trisomy 13, and first pregnancy. In addition, increased concentration of circulating pre-ecclamptic factors-angiotensin 1/Bradykinin B2 receptor heterodimers, agonistic antibodies to angiotensin I receptor, and soluble endoglin are seen in PET [Figure 2]. [9],[10],[11],[12]
Figure 2: Pathogenesis of pre-eclampsia

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Screening tests-Laboratory data reveals proteinuria, high uric acid, thrombocytopenia. Schistocytes and anemia may be present in more severe disease, thus indicating microangiopathic hemolytic anemia. Recently, urinary PlGF values and sFlt-1 values have shown great promise as a means of identifying preclinical pre-eclampsia.

Management of hypertension-Patient should be advised bed rest. Weight loss and salt restriction are not recommended. ACE inhibitors are contraindicated. Teratogenic effects of angiotensin-converting enzyme inhibitors (ACEi/ARBs) include fetal hypotension, anuria-oligohydramnios, growth restriction, pulmonary hypoplasia, renal tubular dysplasia, neonatal renal failure, limb contractures, hypocalvaria, congenital abnormalities of cardiovascular, central nervous system. Diuretics lead to intravascular volume depletion, organ and placental hypoperfusion. They are used with caution if significant edema. If pre-eclampsia develops, diuretics must be discontinued. Beta-blockers have no major contraindications, although neonatal bradycardia, hypoglycemia, and respiratory depression are reported. Labetalol is not associated with neonatal bradycardia. Alpha-methyldopa is the drug of choice for essential hypertension. Clonidine is also used. Calcium channel blockers may cause tocolysis in 3 rd trimester hence are limited to hypertension unresponsive to other medications. Hydralazine is a first-line agent for hypertensive emergencies. Experience with minoxidil and prazosin is limited.

Management of pre-eclampsia-Basic management includes early prenatal detection by serial blood pressure measurements, weight determination and duration of gestation, hospitalization if worsening hypertension or proteinuria. In mild pre-eclampsia, physical activity should be reduced. If symptoms worsen (e.g., headache, visual disturbances, epigastric pain, oliguria), it can be assumed that eclampsia is imminent, and pregnancy must be terminated. Controversial prevention strategies include calcium supplementation, fish oils, sodium restriction, low-dose aspirin, and antioxidants.

  Renal Failure Top

Incidence of ARF in pregnancy is 1:20,000. Causes of renal failure in pregnancy can be divided into (i) Early pregnancy-Hyperemesis gravidarum, septic abortion. (ii) Late pregnancy-PIH and its complications, HELLP, post-partum HUS, acute fatty liver of pregnancy, volume loss-APH, PPH, sepsis.

Septic abortion-Commonest causative organism is Clostrium. It manifests few hours to 1-2 days after abortion with fever, vomiting, and pain abdomen. Progression to shock and death is rapid. Jaundice may occur. Anemia, leucocytosis, and thrombocytopenia with DIC may be seen. Management consists of antibiotics, volume resuscitation, hysterectomy, hyperbaric oxygen, antitoxin, and exchange transfusion.

Pregnancy-induced Hypertension

PIH alone is an uncommon cause of AKI.

PIH may be associated with hemolytic anemia, low platelets and elevated liver enzymes (HELLP) and is commonly associated with AKI, jaundice, and bleeding. Usually occurs antepartum but can occur peri-partum or post-partum. DIC can complicate HELLP. HELLP is the most common cause of renal failure in pregnancy, [13],[14] Outcome is good, maternal mortality is 1%. Rarely placental abruption, subcapsular liver hematoma, retinal detachment, ARDS, ascites, pleural effusion may occur.

Ecclampsia may be associated with bleeding, jaundice, and oliguric renal failure. Renal failure is unusual even with severe cases, unless there is significant bleeding or hemodynamic instability or marked DIC. Severe pre-eclampsia may be associated with a true DIC state with prolongation of the prothrombin, partial thromboplastin times, low levels of clotting factors, elevated FDP, and positive D-dimer test. There is activation of the coagulation cascade. Fibrin forms crosslinked networks in the small blood vessels (MAHA). The abnormalities typically resolve spontaneously within the first 2 weeks postpartum. In some cases, however, pre-eclampsia begins in postpartum period without prior proteinuria and may be difficult to initially differentiate from postpartum HUS. Only the subsequent spontaneous recovery will point toward pre-eclampsia. Treatment consists of delivery of the baby. Mag sulfate decreases risk of seizures; anti-hypertensive drugs are used as described for PIH. For DIC, fresh frozen plasma, blood transfusion, anti-thrombin 3 concentrate are indicated. Incidence 0.2-0.6% of all pregnancies occurs in 10-20% of women with pre-eclampsia.

Hemolytic uremic syndrome (HUS)/Idiopathic post partum failure occurs in primipara and is characterized by renal failure, anemia and HT. Onset is within hours to days. Symptoms can begin before delivery, but the onset in most cases is delayed for 48 h or more after delivery (mean 4 weeks). HUS may follow a normal pregnancy or be preceded by findings indistinguishable from pre-eclampsia. The cause is obscure and viral illness, retained placental fragments, drugs e.g., oxytocics, ergot, and oral contraceptives have been implicated. Labs reveal microangiopathic hemolytic anemia (MAHA), thrombocytopenia, LDH (>600 U/L). A biopsy shows mesangiolysis, glomerular simplification. There may be hypocomplementemia, deficiency in PG or anti-thrombin levels. Outcome is poor, high maternal mortality 18-44% and fetal loss 80%. 45% have residual neurologic or chronic renal failure. Recurrences occur in 50%. Recurrence in subsequent pregnancies is low. History (e.g., preceding proteinuria and hypertension favor pre-eclampsia), the absence of DIC, onset more than 2 days after delivery, and/or persistent disease for more than 1 week are the main findings that differentiate the HUS from pre-eclampsia. Treatment includes plasmapheresis, plasma infusion, steroids, anti-platelet therapy, immunoabsorption, splenectomy, IV gamma globulin, hemodialysis, and antihypertensives. Platelet transfusions should be avoided. Heparin and fibrinolytic agents, anti-thrombin III concentrates may be used. Dilatation and curettage should be considered when occurs very close to delivery.

Thrombotic Thrombocytopenic Purpura

TTP is characterized by the pentad of microangiopathic hemolytic anemia, thrombocytopenia, renal insufficiency, fever, and neurologic abnormalities. The degree of renal impairment is often mild. Thrombotic thrombocytopenic purpura almost always occurs antepartum, many cases begin before 24 weeks but the disease also occurs in the 3 rd trimester. [15]

Cortical necrosis-50% of all cortical necrosis is pregnancy related. Causes include Abruptio, septic abortion, placenta previa, prolonged IUD, or amniotic fluid embolism. It is most common in post-partum than antepartum AKI. Renal cortical necrosis may be patchy or total. Patients develop abrupt onset of oligoanuria, gross hematuria, flank pain, and hypotension. The diagnosis can be established by ultrasonography. Renal calcifications on plain film of the abdomen suggest cortical necrosis (6 weeks). CT scanning demonstrates hypoechoic or hypodense areas in renal cortex or may demonstrate cortical tram track calcification. Angio- abrupt cut-off of vascularity. No specific therapy is effective. Many patients develop chronic kidney disease.

Acute Pyelonephritis

Although renal function is well maintained during acute pyelonephritis, some pregnant women develop acute renal failure. Renal biopsy may reveal focal microabscesses and recovery after antimicrobial therapy may be incomplete due to irreversible injury.

Acute Fatty Liver of Pregnancy

It is a rare complication of pregnancy that is associated with AKI in 60%. It is due to mutation in enzyme for long-chain 3 hydroxy acyl CoA dehydrogenase. It is characterized by jaundice, mild renal failure in last trimester, DIC, PIH, hypoglycemia, pancreatitis, and encephalopathy. The diagnosis should be suspected in a woman with pre-eclampsia who has hypoglycemia, hypofibrinogenemia, and a prolonged PTT in the absence of abruptio placentae, high bilirubin, normal/ high transaminases, microvesicular steatosis, and rarely liver necrosis. Renal biopsy shows acute tubular necrosis (ATN), treatment-IV fluids, cryoprecipitate, fresh frozen plasma, glucose. It reverses with delivery. C section is preferred. Liver transplant is the treatment of choice in patients with liver necrosis. Outcome 20-25% maternal and fetal mortality, 25% recur.

Urinary Tract Obstruction

Functional hydronephrosis rarely cause renal failure. The diagnosis can be established in some cases by the normalization of renal function in the lateral recumbent position and its recurrence when supine. In some cases, either insertion of a ureteral catheter or delivery of the fetus is required. Rarely, acute urinary tract obstruction in pregnancy is induced by a kidney stone.

  Pregnancy in the Setting of CKD /Dialysis/ Transplant Top

Effects of the Renal Insufficiency on Pregnancy

Renal insufficiency-Current consensus suggests degree of renal insufficiency, rather than underlying renal diagnosis, is the primary determinant of outcome. Women with only mild renal impairment (S cr <1.4mg%)), normal BP, and little or no proteinuria have good maternal and fetal outcomes, (95% live births, 75% AGA) with 16% showing a mild decline in renal function, only 6% having increased risk for accelerated progression toward ESRD or preterm delivery. There is increased PIH and nephrotic syndrome. Moderate CKD (S Cr 1.5-2.5mg%) live births 90% but fetal growth retardation or preterm exceed 50%. 40% have decline in renal function and 50% of these recover postpartum. More than 70% of women who become pregnant with a serum creatinine 2.5 mg/dl (Severe CKD) experience preterm delivery and 40% develop pre-eclampsia. 70% have an accelerated decline in renal function and 1/3 rd progress to ESRD. The normal increase in GFR during pregnancy is attenuated in these women and they should be counseled to avoid pregnancy. [16],[17],[18],[19]

Nephrotic proteinuria is associated with thromboembolism, variable IUGR, preterm labor, and poor long-term maternal and renal prognosis. These females need low-molecular-weight heparin prophylaxis till 6 weeks postpartum with double the usual dose as heparin clearance is increased in pregnancy. Mild proteinuria >500 mg/d is associated with 30% increased risk of PET, 45% preterm, 23% IUGR, and also decline in GFR. These females need serial monitoring. [5]

Preconceptional hypertension leads to IUGR, pre-eclampsia, preterm labor, and accelerated decline in renal functions. Perinatal mortality is 23% versus 4% in normotensives with CKD.

Effect of Pregnancy on Renal Disease

Pregnancy may result in deterioration in renal function in some renal diseases-lupus, scleroderma, MPGN, and periarteritis nodosa. The effect of pregnancy on FSGS, IgA, and Reflux nephopathy is controversial. [5]

DN has accelerated progression in 45% of patients. [5],[20]

Lupus nephritis-50% experience a flare during pregnancy although it is less common in patients who have been in remission for > 6 months. Exacerbations (flares) increase risk of renal failure. Fetal loss occurs in 50% of patients. Lupus anticoagulant and anticardiolipin antibody increase risk. Therapeutic abortion is generally recommended if a lupus flare is associated with worsening renal function or worsening hypertension prior to 34 weeks' gestation. Delivery is recommended after 34 weeks' gestation. Infant should be screened for neonatal lupus. Treatment for flares includes prednisone or azathioprine. Cyclophosphamide is avoided because it is teratogenic. Fetal survival rates are good (95%). Complications, including SGA preterm labor and stillbirth, are increased even in mild renal insufficiency. [5],[21],[22]

Pregnancy in patients on dialysis-Pregnancy occurs only in 1% of patients. The cause of infertility is multifactorial. Up to 42% of women receiving dialysis have regular menses, but many are anovulatory. Anemia probably also plays a role. The fetal outcome is quite poor. Only 23-55% of pregnancies result in surviving infants and a large number of 2 nd -trimester spontaneous abortions occur. Approximately 85% of surviving infants are born premature and 28% are SGA. Polyhydramnios is seen in 50%. Premature rupture of membranes may occur. Maternal complications including death may occur. Hypertension worsens in more than 80% of pregnant females on dialysis. The diagnosis of pregnancy is also difficult because levels of beta-human chorionic gonadotropin (beta-hCG) are normally elevated in patients receiving dialysis and ultrasound should be done to aid in diagnosis. The patient should be placed on transplant list because outcomes with allograft transplant patients are markedly better. During hemodialysis, uterine and fetal monitoring is needed, and hypotension should be avoided. Judicious use of erythropoietin and aggressive dialysis to keep BUN levels less than 50 mg may improve mortality and morbidity. PD can also be done but is inferior to HD. [23]

Pregnancy in patients after transplantation-Fertility rates increase after 6 months of transplantation and pregnancy occurs in up to 12%. Uncontrolled hypertension, worsening proteinuria, and poor prepregnancy renal function are prognostic indicators for the risk of renal function deterioration. Patients should wait a year after a living related donor transplant and 2 years after a cadaveric transplant before planning pregnancy. The renal function should be stable, (serum creatinine< 2.0 mg/dL). Attempts should be made to decrease prednisone to 15 mg/d or less, azathioprine to 2 mg/kg/d or less, and cyclosporine to 5 mg/kg/d or less. Prednisone crosses the placenta and may cause neonatal adrenal insufficiency and thymic hypoplasia. These are rare if the dose is less than 15 mg/d. If acute rejection of the kidney occurs during pregnancy, high-dose steroids, OKT3, and ATG may be used. Azathioprine is teratogenic in animals, but not in humans. Although azathioprine crosses the placenta, the immature fetal liver cannot convert it to its active form, 6-mercaptopurine. Use of azathioprine is associated with SGA babies and dose-related myelosuppression in the fetus. Cyclosporine has been associated with SGA babies and pre-eclampsia (29%). Tacrolimus crosses the placenta and has been associated with hyperkalemia and renal insufficiency. Mycophenolate mofetil (MMF) has potentially teratogenic effects in pregnancy, e.g., fetal bone marrow suppression and structural malformations including hypoplastic nails, shortened fingers, microtia, and cleft lip/palate. Women should discontinue MMF at least 6 week before conception. Although there are few human data on the safety of sirolimus in pregnancy, animal studies suggest teratogenicity, so it should be avoided. All pregnant post-transplant patients should receive antibiotic prophylaxis before all surgical procedures. Any UTI in pregnancy warrants continuation of long-term prophylaxis. Most evidence suggests that pregnancy after transplantation does not increase risk for rejection, so long as renal function is good. There is no increased risk for birth defects. 20% pregnancies end in spontaneous abortions with 90% successful outcomes in pregnancies crossing 1st trimester. An elevated prepregnancy creatinine level (i.e., >1.4 mg/dL) is not only associated with a higher risk of renal decline but also with a decreased fetal survival rate (74% with creatinine level >1.4 mg/dL, 96% if < 1.4 mg/dL). Obstruction of the transplant ureter by the pregnant uterus is rare but has been reported. The dose of steroids needs to be increased in the peripartum period. Neonatal outcome in pregnancies among renal transplantation patients is good except a higher rate of preterm birth (50 to 54%), SGA (33 to 45%), and neonatal mortality (1 to 3%) as compared with the general population (12.3, 5, and 0.68%, respectively). Long-term outcome of surviving infants is good.

Management of pregnancy in CKD and transplant-Prenatal visits should be frequent every 2 weeks until 28 weeks' gestation and then weekly. Prenatal monitoring should include daily blood pressure measurements. Biweekly visits with laboratory work consist of urine protein by dipstick (24-h protein if dipstick abnormal), CBC counts, electrolytes, BUN, and creatinine levels. Monthly ultrasounds and urine cultures and determination of CMV-IgM, Toxoplasma IgM for seronegative women (every trimester), IgM for HSV (last trimester) should be done. Biweekly fetal surveillance with a biophysical profile is indicated in the 3 rd trimester. If rubella titers are low, administer the vaccine before transplant because this live virus vaccine is contraindicated after transplantation. [24]

Obstetric management-The most common cause of mortality and morbidity in patients with any renal disease is preterm labor. Magnesium can be cautiously used to avoid toxicity and respiratory depression. The literature is divided about elective early delivery (34-36 wk) in patients with chronic renal insufficiency or those receiving dialysis, especially when fetal lung maturity is present. In patients who have had a transplant, however, delaying delivery until the onset of labor is generally thought to be the most prudent step, provided that the mother and fetus show no signs of distress. Vaginal delivery is preferred.

  References Top

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2.Hou S. The kidney in pregnancy. In: Greenberg A, editor. Primer on Kidney Diseases. 2 nd ed. Academic Press; 1998. p. 388-94.  Back to cited text no. 2
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22.Jungers P, Dougodos M, Pelissier C, Kuttenn F, Tron F, Lesavre P, et al. Lupus nephropathy and pregnancy. Report of 104 cases in 36 patients. Arch Intern Med 1982;142:771-6.  Back to cited text no. 22
23.Hou SH. Pregnancy in women on haemodialysis and peritoneal dialysis. [Review]. Baillieres Clin Obstet Gynaecol 1994;8:481-500.  Back to cited text no. 23
24.Davison JM. Pregnancy in renal allograft recipients: Problems, prognosis, and practicalities. Baillieres Clin Obstet Gynaecol 1994;8:511-35.  Back to cited text no. 24


  [Figure 1], [Figure 2]

  [Table 1]

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1 Urinary tract infection amongst pregnant women in Amassoma, Southern Nigeria
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