Renal disease and pregnancy

Renal Disease and Pregnancy

By-:

Omnia Abd Elazim

Supervised by-:

prof:-Ahmed Fathy Elkoraie

Agenda:

The normal kidney in Pregnancy. pregnancy-induced hypertension. Acute kidney injury in pregnancy. Chronic kidney disease and pregnancy. End-stage renal disease and pregnancy. Transplantation and pregnancy.

The normal kidney in Pregnancy

Renal Function During Pregnancy

Renal plasma flow increases by 50-70% in pregnancy, and this change occur mainly in the first two trimesters. This is the factor that lead to an increased glomerular filtration rate (GFR). The GFR peaks around the 13th week of pregnancy and can reach levels up to 150% of normal. So, both BUN and creatinine levels, the plasma markers of GFR, are decreased. This decrease has clinical significance in that a normal BUN or creatinine level in a pregnant female may actually indicate

underlying renal disease.

Similarly, in the initial part of pregnancy, increased levels of progesterone enhance relaxation of the arterial smooth muscles and thus decrease peripheral vascular resistance.So, a blood pressure fall of approximately 10 mm Hg occurs in the first 24 weeks of pregnancy. The blood pressure gradually returns to a prepregnancy level by term; thus, a consistent normal or prepregnancy blood pressure may suggest the presence of a condition that

predisposes patients to hypertension.

The drop in blood pressure in normal pregnancy occurs despite increased levels of renin, angiotensin, and aldosterone. There is resistance to the hypertensive effects of both endogenously and exogenously administered angiotensin. The resistance has been attributed to production of prostacyclin by placental endothelial cells as well as other vasodilators.

Renal vasodilatation in pregnancy

EDRF; Endothelial Derived Relaxing Factor, (NO)

Vasodilatory PG’s

Relaxin

ET;Endothelin

All lead to increase RPF& GFR.

Electrolytes & Acid Base Changes

Elevated progesterone levels stimulate hyperventilation and result in a state of mild respiratory alkalosis and a blood gas of

PH: 7.44

PCO2: 30

HCO3: 22

A reset in the osmostat occurs, resulting in increased thirst and decreased serum sodium levels (by approximately 5 mEq/L) compared with nonpregnant females and

also decreased osmolality.

Hyponatremia during pregnancy parallels the increased release of human chorionic gonadotropin (HCG), which appears to mediate these changes via the release of relaxin. Serum potassium levels are normal despite increased serum aldosterone, perhaps due to the potassium-sparing effects of elevated progesterone levels in pregnancy.

Total serum calcium levels fall in pregnancy but ionized calcium remains normal. Accelerated renal and placental production of calcitriol leads to increased gastrointestinal absorption of calcium and absorptive hypercalciuria with urine calcium as high as 300 mg/day.

Serum parathyroid hormone (PTH) concentrations

are lower than normal, partly in response to higher serum levels of calcitriol.

Increased urinary excretion of protein,amino acids,uric acid,glucose and calcium occurs as result of the elevated GFR. Hence,proteinuria in pregnancy is considered abnormal when it exceeds 300mg/day compared with an upper limit of normal of 150mg/day in the nonpregnant population.

Pre-pregnancypregnancy

S.Uric acid43.2

Na140135

KSlight increase

BUN12.79.3

Creatinine0.80.5

Glucoseglucosuria

Osmolality285275

Cadecrease

Hct%4133

The anatomic changes in pregnancy

The anatomic changes are primarily in the collecting system. A dilatation of the ureters and pelvis occurs and it is secondary to the smooth muscle–relaxing effect of progesterone. This dilatation is often more on the right side secondary to dextrorotation of the uterus and dilatation of the right ovarian venous plexus. This can lead to urinary stasis and, an increased risk of developing urinary tract infections

(UTIs).

There is also an increase in overall kidney size by about 1-1.5 cm .

these changes may persist for up to 12 weeks postpartum and should not be over-

interpreted as obstructive uropathy.

Renal Changes in Normal Pregnancy

Anatomic 1 cm incerased in length. Dilatation of the collecting system.

Physiologic 50% increased in GFR: normal BUN 9 mg/dL, creatinine 0.5mg/dL Respiratory alkalosis: normal PCO2 27 – 32 mm Hg, HCO- 3 18 – 22 mEq/L Decreased serum osmolality: normal 276 – 278 mOsm/L Doubling of uric acid clearance: normal 3 – 4 mg/dL Decreased Tubular reabsorption of glucose 40% increased in renal blood flow Decreased afferent and efferent arteriolar resistance Decreased BP: normal < 125/75 mm Hg 2nd trimester, < 125/85 mm Hg 3rd trimester Increased Prostacyclin and thromboxane Increased Renin (8x), angiotensin (4x), aldosterone (10 – 20x)

pregnancy-induced hypertension

Hypertension, the most common medical complication of pregnancy, occurs in up to 10% of pregnancies; it is associated with a significant increase in maternal and fetal morbidity and mortality and is the leading

cause of premature birth.

hypertension in pregnancy is defined as a systolic blood pressure of over 140 mm Hg and a diastolic blood pressure greater than 90 mm Hg.

Types of pregnancy-induced hypertension

1 (Gestational hypertension

de-novo hypertension occurring alone after 20/40 which

resolves post-partum. Risk factor for essential hypertension in later life.

2 (Chronic hypertension

3 (Pre-eclampsia

4 (Chronic hypertension with superimposed pre-eclampsia

Hypertension and adverse outcomes inpregnancy

•Progressive increase in perinatal mortality with each 5mmHg increased in MAP.

•MAP > 90mmHg during 2nd trimester correlates with increased incidence of IUGR, pre-eclampsia.

•1/3 pregnant women with MAP> 90mmHg in 2nd trimester progress to pre-eclampsia .

1 )Gestational hypertension

Gestational hypertension is defined as hypertension that appears after midterm, is not associated with proteinuria, and resolves after delivery. Women at risk for this condition are those with a positive family history of hypertension and patients with obesity and multiparity. Women with gestational hypertension are at risk for chronic hypertension.

2 )Chronic hypertension

Chronic hypertension is defined as a prepregnancy blood pressure of greater than 140/90 or as hypertension occurring before 20 week's gestation. The definition may also include some hypertensive women with minimal proteinuria diagnosed during pregnancy that does not resolve with delivery. Fisher et al showed by renal biopsy that these women may have nephrosclerosis rather than preeclampsia.

Chronic hypertension increases the risk of pre-eclampsia, perinatal mortality, small for gestational age (SGA) babies, premature delivery,, gestational diabetes, intrauterine growth retardation, and second-trimester

fetal death.

treatment

During pregnancy-:*Antihypertensive drugs

1 = methyldopa / labetalol2 = CCB / hydralazine.

No ACE inhibitor/ARB after conception/1st trimester.*Early delivery for severe hypertension.

*Bed rest.

treatment

During lactation-:

Labetalol/propranolol/methyldopa.

Sustained release verapamil/nifedipine.

treament of hypertensive urgency-:

Hydralazine: IV 5mg, then 5-10mg q30min or infusion 0.5-10mg/h.

Labetalol: IV 20mg then 20-80mg q20-30min/ max 300mg or infusion 1-2mg/min.

Nifedipine: PO/SL 5-10mg PO, then 10-20mg every 2- 6 hrs.

Nitroprusside: IV 0.5-10mcg/kg/min.

Common medications in hypertension

1 .ACE inhibitors, ARBsNot safe to useFetal oligohydramnios pulmonary hypoplasia,skeletal deformities

2 .DiureticsNot safe to useMaternal volume depletion; fetal

thrombocytopenia, hemolytic anemia, jaundice

3 .b-BlockersNot safe to useFetal bradycardia, hypoglycemia, respiratory distress

4 .LabetalolWidely usedLimited data

5- .MethyldopaSafe to useLimited long-term follow-up shows no

developmental problem in children

6 .ClonidineNot safe to useLimited data

7 .Calcium channel blockers

Safe to usePotentiates the hypotensive effect of

magnesium; limit use to refractory hypertension

8 .HydralazineSafe to useGiven intravenously for acute, severe

hypertension

3 )Pre-eclampsia

Pre-eclampsia is characterized by the triad

of edema, hypertension, and proteinuria, in previously normotensive women that typically occurs after 20 weeks' gestation and resolves with delivery.

Eclampsia :is defined as the occurrence of seizures in women with pre-eclampsia.

Cause-:

–unknown.

–Abnormal placentation.

–Maternal endothelial dysfunction.

–Genetic factors.

–Increased maternal inflammatory response.

–Immunologic factors.

–Infectious diseases.

•Predicting pre-eclampsia – no good markers.

Risk Factors for Preeclampsia

– Primigravida. – Different father in pregnancy for multigravida. – Diabetes. – Preexisting hypertension. – Renal disease. – Twin gestation. – Hydatidiform mole. – Fetal hydrops. – Family history.

Clinically-;

preeclampsia usually begins after 20 weeks of pregnancy.it manifested by-:

De novo hypertension .

New onset proteinuria.

Severe Pre-eclampsia

Preeclampsia with one or more of the following-:

*Systolic BP ≥160 mm Hg or diastolic BP ≥110 mm Hg on two occasions at least 6 hr apart while on bedrest.

*Proteinuria >5 g in a 24-hr urine specimen or dipstick proteinuria ≥3+

on two random urine samples at least 4 hr apart.

*Oliguria (<500 mL urine output over 24 hr).

. disturbances *Severe headache, mental status changes, visual

*Hepatocellular injury (transaminase elevation to at least twofold over normal level) .

*Thrombocytopenia (<100,000) .

growth restriction. Fetal*

*Cerebrovascular accident.

*pulmonary edema or cyanosis.

Pathology

The characteristic pathologic changes in the kidney of women with preeclampsia include swelling of the endothelial cells (glomerular endotheliosis), ballooning of capillary loopsinto the tubule, fibrinogen and lipid in endothelial cells, and occasional foam cells.Rarely, changes similar to focal sclerosis occur, with reversal postpartum. Ischemic changes are less marked than in other organs.The renal pathologic changes resolve 2 – 4 weeks postpartum.

Prevention of Preeclampsia

Two interventions have been extensively investigated to determine whether they prevent preeclampsia: low-dose aspirin and calcium supplementation. Despite initial promise, the effects of these two treatments

have been disappointing in large trials.

Management-:

Delivery if viable / termination if remote from term.

Temporizing measures if stable maternal/fetal unit and benefit of increased fetal maturity outweight risk.

Antihypertensive therapy: PO or IV (not diuretics).

Seizure control – magnesium sulfate.

Indications for delivery

≥ 36 weeks gestation. BP ≥ 160/110 after 24 hours of hospitalization. HELLP syndrome. ≥ 3 g of protein in 24 hours. Rising serum creatinine. Headache, blurred vision, scotomata, right upper

quadrant pain, clonus.

4 )Chronic hypertension with superimposed pre-eclampsia

If the systolic blood pressure exceeds 200 mm Hg, pre-eclampsia superimposed on chronic hypertension is suggested. In this setting, pulmonary capillary permeability may be increased, resulting in pulmonary edema, central nervous system excitability may occur, causing hyper-reflexia and cerebral hemorrhage.

Diagnosis of pre-eclampsia superimposed on chronic hypertension

If proteinuria prior to 20 wk is absent:

*New-onset proteinuria in a woman with chronic hypertension .

If proteinuria prior to 20 wk is present, any of the following raise concern for superimposed preeclampsia:

A sudden increase in proteinuria .

A sudden increase in hypertension.

Thrombocytopenia .

Increased in liver enzymes .

HELLP Syndrome

HELLP, a syndrome characterized by

hhemolysis, emolysis, eelevated levated lliver enzyme iver enzyme levels and a levels and a llow ow pplatelet countlatelet count, is an obstetric complication that is frequently misdiagnosed at initial presentation. Many investigators consider the syndrome to be a variant of pre-eclampsia.

Clinical Presentation

90%of patients present with generalized malaise,

65 % with epigastric pain, 30 % with nausea and vomiting, 31 percent with headache.

90

65

30 31

0

10

20

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symptoms

general malase

epigastric pain

vomiting

haedache

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30 31

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90

symptoms

general malase

epigastric pain

vomiting

haedache

The physical examination may be normal in patients with HELLP syndrome.

1 -right upper quadrant tenderness 90.%

2 -Edema is not a useful marker .

3 -Hypertension and proteinuria may be absent or mild .

90

30 30

0

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signs

Rt.hypochond.pain

edema

hypertention + proteinuria

Diagnosis

Haemolysis Abnormal peripheral smear : spherocytes, schistocytes,

triangular cells and burr cells Total Bilirubin level > 1.2 mg/dL Lactate dehydrogenase level > 600U/L

Elevated liver function test result Serum aspartate amino transferase level > 70U/L Lactate dehydrogenase level >600 U/L

Low platelet count Platelet count < 150 000/mm3

Complications

The mortality rate for women with HELLP syndrome is approximately 1.1 %

From 1 to 25 % of affected women develop serious complications such as DIC, placental abruption, adult respiratory distress syndrome, hepatorenal failure, pulmonary edema, subcapsular hematoma and hepatic rupture.

A significant percentage of patients receive blood products.

Infant morbidity and mortality rates range from 10 to 60 %, depending on the severity of maternal disease.

Infants affected by HELLP syndrome are more likely to experience intrauterine growth retardation and respiratory distress syndrome.

1.10%

25%

60%

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

matern.mort. maternalcomplication

fetalcomplication

Management

Delivery.

Corticosteroids.

Magnesium sulphate.

Hypotensive drugs.

Blood products.

1-Corticosteroids-:

The antenatal administration of dexamethasone in a high dosage of 10 mg intravenously every 12 hours has been shown to markedly improve the laboratory abnormalities associated with HELLP syndrome.

Steroids given antenatally do not prevent the typical worsening of laboratory abnormalities after delivery. However, laboratory abnormalities resolve more quickly in patients who continue to receive steroids postpartum.

2-Magnesium sulphate-:

Patients with HELLP syndrome should be treated

prophylactically with magnesium sulfate to

prevent seizures, whether hypertension is present or

not.

3-Antihypertensive therapy

should be initiated if blood pressure is consistently greater than 160/110 mm hg despite the use of magnesium sulfate. The goal is to maintain diastolic blood pressure between 90 and 100 mm hg.

4-Blood products-:

Patients who undergo cesarean section Patients who undergo cesarean section should be transfused if their platelet count is should be transfused if their platelet count is less than 50,000 per mm3.less than 50,000 per mm3.

Prophylactic transfusion of platelets at Prophylactic transfusion of platelets at delivery does not reduce the incidence of delivery does not reduce the incidence of postpartum hemorrhage or hasten postpartum hemorrhage or hasten normalization of the platelet count. normalization of the platelet count.

Patients with DIC should be given fresh Patients with DIC should be given fresh frozen plasma and packed red blood cells.frozen plasma and packed red blood cells.

Acute kidney injury in pregnancy

Classification

Renal failure in early pregnancy. Renal failure in late pregnancy. Postpartum renal failure .

Renal failure in early pregnancy


1-prerenal azotemia-:Causes

--Hyperemesis gravidarum associated with metabolic alkalosis; diagnosis is made by history. Treatment requires the

administration of intravenous fluids. -Hemorrhage associated with spontaneous

abortion.


2-Acute tubular necrosis-:Causes

Severe volume depletion associated with hyperemesis gravidarum, hemorrhage from spontaneous abortion, or shock secondary to septic abortion.

Septic abortion, most commonly due to Escherichia coli; in some cases, however, Clostridium, which can cause myonecrosis of the uterus and myoglobinuria, is responsible.

The diagnosis of acute tubular necrosis can be established via the clinical setting, urinalysis, and urinary indices.

Treatment includes fluids, antibiotics and, if necessary, dialysis.


3-Renal cortical necrosis-:Cause;

The disorder is most likely initiated by primary disseminated intravascular coagulation in the setting of severe renal ischemia.

This is a rare cause of severe acute renal failure; it is more commonly associated

with pregnancy.

Renal cortical necrosis presents with gross hematuria, flank pain, and severe oliguria/anuria following an obstetric

catastrophe:

)septic abortion, retained fetus, amniotic fluid embolism.(

Laboratory Studies

*check for hyperkalemia, hypocalcemia, metabolic acidosis, and elevated creatinine levels.

*A CBC count may reveal hemolytic anemia and thrombocytopenia.

*Coagulation studies detect low fibrinogen levels and increased fibrin-degradation products.

*Urinalysis detects hematuria, proteinuria, RBC casts, and granular casts.

Imaging Studies

*Ultrasonography

The sonogram initially shows enlarged kidneys with reduced blood flow.

Cortical tissue becomes shrunken later in disease progression.

Imaging Studies

Contrast-enhanced CT scanning* CT scanning with contrast are the most sensitive

imaging modality. Diagnostic features include absent opacification of the renal cortex and enhancement of subcapsular and juxtamedullary areas and of the

medulla without excretion of contrast medium. Initiating hemodialysis immediately after the procedure may be necessary to minimize further contrast-mediated renal damage.

Histologic Findings

Renal cortical necrosis is classified into 5 pathologic forms, depending on severity, as shown below. Renal cortical necrosis classifications are as

follows: Focal pathologic form: Kidneys show focally necrotic glomeruli

without thrombosis and patchy necrosis of tubules. Minor pathologic form: Larger foci of necrosis are evident with

vascular and glomerular thrombi. Patchy pathologic form: Patches of necrosis may occupy two thirds

of the cortex. Gross pathologic form: Almost all cortex is involved. Thrombosis of the arteries is more widespread.

Confluent pathologic form: Kidneys show widespread glomerular and tubular necrosis with no arterial involvement.

Recovery typically requires months, and renal functional recovery is usually incomplete.


4-pyelonephritis-:-Acute pyelonephritis is associated with a GFR

reduction that can be reversed with treatment of the underlying infection.


:-5-TTP&HUS

represent a spectrum that includes microangiopathic hemolytic anemia, thrombocytopenia, and renal failure, TTP is more likely to occur in the first trimester and generally

does not cause severe renal failure.

Patients may have a severe deficiency of ADAMTS-13.

Plasma exchange is the primary treatment.

Renal failure in late pregnancy

Renal failure in late pregnancy

1 -Pre-eclampsia &eclampsia.

2-HELLP syndrome.

3-Acute tubular necrosis.

4-Acute fatty liver of pregnancy.

Acute fatty liver of pregnancy

Acute fatty liver of pregnancy (or hepatic lipidosis of pregnancy) usually manifests in the third trimester of pregnancy, but may occur any time in the second half of pregnancy or in the the period immediately

after delivery.

Causes-:

It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the mother, caused by deficiency in the LCHAD((long-chain 3-hydroxyacyl-coenzyme

A dehydrogenase) enzyme .

Clinical manifestations

.The usual symptoms in the mother are non-specific including nausea ,vomiting , anorexia and abdominal pain.

Jaundice and fever may occur in 70% of patients.

In patients with more severe disease pre-eclampsia may occur.

This may progress to involvement of additional systems, including acute renal failure,hepatic encephalopathy and pancreatitis.

There have also been reports of diabetes insipidus complicating this condition.

Diagnosis

*Elevation of liver enzymes.* Bilirubin is elevated

*Alkaline phosphatase is often elevated in pregnancy due to production from the placenta.

* Elevated white blood cell count. *disseminated intravascular coagulation.

*Hypoglycemia.

Diagnosis

Abdominal ultrasound may show fat deposition in the liver but, as the hallmark of this condition is microvesicular steatosis this may not be seen on ultrasound Rarely, the condition can be complicated by rupture or necrosis of the liver, which may be identified

by ultrasound

Treatment

Initial treatment involves supportive management with intravenous fluids, intravenous glucose and blood products, including fresh frozen plasma and cryoprecipitate to correct DIC.

The fetous should be monitored with cardiotocography. After the mother is stabilized, arrangements are usually made for delivery. This may occur vaginally, but, in cases of severe bleeding or compromise of the mother's status, a caesarian section may be

needed .

Liver transplantation is rarely required for treatment of the condition, but may be needed for mothers with severe DIC, those with rupture of the liver, or those with severe encephalopathy.

Postpartum renal failure

Postpartum renal failure

Postpartum acute renal failure usually presents days to weeks following a normal delivery and may be related to retained placental

fragments.

DIFFERENTIAL DIAGNOSIS OF MICROANGIOPATHICSYNDROMES DURING PREGNANCY-:

HELLPAFLPTTPHUS

Hypertension80%25-50%occasionalpresent

Renal insufficiency

Mild to moderate

ModerateMild to moderate

Severe

Fever, neurologic

symptoms00++0

onest3rd trimester3rd trimesterAny timePostpartum

Plt count Low to very lowLow to very lowLow to very lowLow to very low

PTTNormal to highHighNormalNormalLiver function testHigh to very highHigh to extremelyUsually normalUsually normal

Antithrombin IIILowLowNormalNormal

Chronic kidney disease and pregnancy

Relationship between pregnancy and kidney disease.

Effects of pregnancy on kidney disease

Worsening proteinuria Loss of kidney function Hypertension and

preeclampsia

Effects of kidneydisease on pregnancy

Infertility Preterm delivery IUGR Decreased fetal

survival Preeclampsia

1*preserved/mildly reduced renal function, Cr < 1.4 –good outcome for pregnancy and renal disease

2 *Moderately impaired renal function, Cr 1.4 – 2.8 –risk progression of renal failure, increased fetal risk

3 *Severe renal insufficiency, Cr > 2.8 –high fetal/maternal morbidity/mortality, low likelihood

of successful outcome, pregnancy discouraged.

4*High grade proteinuria and severe hypertension

–also important risk factors for progression of renal disease in pregnancy, worse outcomes.

CKD and pregnancy – diabetic nephropathy

6% of pregnant women with type I DM have overt diabetic nephropathy (<20/40: U prot>300mg/d, macroalbuminuria >300mg/d, alb/creat. ratio >0.3mg/mg)

•Microalbuminuria also associated with an increased risk of adverse fetal-maternal outcomes

•Effect of nephropathy on pregnancy: prematurity(22%), IUGR(15%), pre-eclampsia.

•Effect of pregnancy on nephropathy: exacerbation of proteinuria and hypertension.

Return to baseline post-partum with well preserved renal function.

*Pre-eclampsia is the most frequent complication of pregnancy in women with diabetic nephropathy.

CKD and pregnancy - ADPKD

Exacerbation of HTN, increased risk of pre-eclampsia.

Prenatal genetic testing for PKD1 disease (C16) – available.

No increased incidence of simple UTI during pregnancy.

CKD and pregnancy - Lupus

Rate of relapse not different between pregnant women and concurrent controls (9-60%).

Major factor determining a pregnancy related exacerbation is the stability of the disease before conception

If in remission for >6mths pre-conception, low incidence of clinical flare during pregnancy.

Women with intracranial aneurysms may be at increased risk of subarachnoid hemorrhage

during labor .

the frequency of exacerbations during pregnancy was higher for women with membranous nephropathy than for those with diffuse proliferative glomerulonephritis.

Antiphospholipid antibody syndrome in pregnancy-:

The presence of antiphospholipid antibodies or the lupus anticoagulant is associated with increased fetal loss, particularly in the second trimester;

increased risk of arterial and venous thrombosis;

manifestations of vasculitis such as thrombotic microangiopathy; and an increased risk of

preeclampsia .

Treatment consists of anticoagulation with heparin and aspirin.

LUPUS FLARE-UP VERSUS PREECLAMPSIA

SLEPE

Proteinuria++

Hypertension++

RBCs cast+-

Azotemia++

Low C3, C4+-Abnormal liver function test results

-+/-

Low platelet count++/-Low leukocyte count+-

End-stage renal disease and pregnancy

ESRD requiring dialysis is associated with a marked decrease in fertility. Pregnancy, however, occurs in approximately 1% of patients, usually within the first few years of

starting dialysis.

The fetal outcome is quite poor. Only 23-55% of pregnancies result in surviving infants, and a large number of second-trimester spontaneous abortions occur. In addition, surviving infants have significant morbidities. Approximately 85% of surviving infants are born premature, and 28% are born SGA. Maternal complications occur as well. Several maternal deaths have been reported. Hypertension worsens in more than 80% of pregnant females on

dialysis and is a major concern.

Recommendations-:

Some general recommendations apply to patients who become pregnant while receiving dialysis. Place the patient on a transplant list (if not on already) because outcomes with allograft transplant patients are markedly better. During hemodialysis, uterine and fetal monitoring and make every attempt to avoid dialysis-induced hypotension. Some evidence indicates that the use of erythropoietin may improve fetal survival; however, no findings from randomized studies supports this. Erythropoietin can also increase hypertension and must be used cautiously. Increased frequency of dialysis may improve mortality and morbidity. Aggressive dialysis to keep BUN levels less than 50 mg/dL may be need daily dialysis. Controlling uremia in this fashion may avoid polyhydramnios, control hypertension, and improve the mother's nutritional status.

Medications

Common medications in CKD/ESRD

Safety issuesComments

1 .ErythropoietinSafe to useLimited data.

2 .IronSafe to useLow dose intravenous iron recommended

3 .Vitamin DWidely usedLimited data.

4 .HeparinSafe to useMinimize dose of heparin

Transplantation and pregnancy

Guidelines for pregnancy in kidney transplant recipient-:

Two years post-transplant, with good general

health and serum creatinine less than 2.0 mg/dL )preferably <1.5 mg/dL).

No recent or ongoing rejection . Normotension, or minimal antihypertensives Absent or minimal proteinuria No evidence of pelvicalyceal dilation on renal

ultrasonogram

Immunosuppression-:

Prednisone - Less than 15 mg per day Azathioprine - Less than or equal to 2 mg/kg/d Calcineurin inhibitor–based therapy -

Therapeutic levels Mycophenolate mofetil and sirolimus -

Discontinue 6 weeks prior to conception Methylprednisolone - The preferred agent for

treatment of rejection during pregnancy

Common medications in kidney transplantation

1 .PrednisoneSafe to useFetal adrenal insuffi ciency

2 .CyclosporineSafe to useIUGR

3 .TacrolimusNot safe to useSevere IUGR, renal failure, hyperkalemia

4.Mycophenolate mofetil

Not safe to useTeratogenic in animals

5 .AzathioprineWidely usedFetal neutropenia, teratogenic in high doses

6 .Polyclonal antibodies

Not safe to useVery limited data

Complication Risks-:

Immunosuppressive agents increase the risk of hypertension during pregnancy.

Preeclampsia occurs in approximately one-third of transplant recipients.

Almost 50% of pregnancies in these women end in preterm delivery due to hypertension.

Blood levels of calcineurin inhibitors need to be frequently monitored due to changes in volumes of distribution of extracellular volume.

There is an increased risk of infection included cytomegalovirus, toxoplasmosis, and herpes infections, and bacterial infection which arouse concern for the fetus.

Renal disease and pregnancy

Education

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