Disorders of Pregnancy



Three important relations exist between renal disease and the pregnant state: the effect of ex­isting renal disease on the outcome of the preg­nancy; the effect of the normal hemodynamic, en­docrinological, and immunological changes of pregnancy on pre-existing renal disease; and the occurrence of distinct renal syndromes in asso­ciation with pregnancy.

Since uremia causes a disruption in normal hor­monal cycles, fertility in women is greatly dimin­ished when the BUN is greater than 40 to 50 mg/ dl. However, those patients with mild renal in­sufficiency [BUN <25 mg/dl) have about a 75 per cent chance of completing a normal, full-term pregnancy. Fetal loss is significant at higher levels of azotemia and when hypertension is a promi­nent part of the renal disease. The nephrotic syn­drome, without azotemia, does not usually affect the outcome of pregnancy, but the birth weight of the infant is decreased in the face of significant maternal hypoalbuminemia.

In most cases, pregnancy does not appear to ad­versely affect the course of pre-existing renal dis­ease. Of particular note is the case of lupus ne­phritis (see below), in which the renal activity of the disease is generally decreased during preg­nancy. However, some patients with more severe glomerular disease experience an exacerbation of nephritis in the first trimester of pregnancy and a significant number of patients have an increase in nephritic signs with a decrease in GFR after de­livery. Increased doses of steroids may prevent this occurrence. Finally, patients with sclero­derma will often experience a significant decline in GFR and an increase in blood pressure during pregnancy.

Hypertension in pregnancy requires careful consideration. Blood pressure usually falls in the first weeks of a normal pregnancy and returns to progestational values only near term. Normal pregnancy is characterized by ECF volume ex­pansion, an increased cardiac output, a decreased systemic vascular resistance, and resistance to the vasopressor effects of angiotensin II. Therefore, any absolute elevation of blood pressure or a pat­tern of rising blood pressure in early pregnancy is abnormal. At least three categories of preg­nancy-related hypertension exist.

Toxemia is a syndrome of hypertension, pro­teinuria, hyperuricemia, and edema that is seen in the third trimester of pregnancy. It occurs pre­dominantly in young primagravidas or in women over the age of 40. The signs may be deceptive, since mild edema is common in normal pregnan­cies, and the elevated blood pressure and serum uric acid concentrations must be interpreted in light of the values for a normal pregnancy. A blood pressure of 130/80 may be abnormal at 30 weeks gestation. Likewise, the serum uric acid concen­tration is often reduced to less than 3 mg/dl in a normal pregnancy, so that a value of 5 to 6 mg/dl is distinctly abnormal.

The renal lesion in toxemia is known as en-dotheliosis and is totally reversible. The histo-pathology consists of endothelial cell swelling in an ischemic glomerulus with fibrin deposited be­tween the endothelial cell and the basement mem­brane. Treatment of toxemia consists of vigorous control of blood pressure and delivery of the fetus as soon as it is judged to be viable. Modest azo­temia may be seen, but renal failure is rare. Com­plete normalization of blood pressure and cessa­tion of proteinuria occur following delivery. There is no increased risk of developing sustained hypertension after the single occurrence of tox­emia in a young woman.

Essential hypertension may be present before pregnancy and may have little effect on the out­come of the pregnancy. Hypertensive patients are more prone to develop toxemia. Only when dias­tolic blood pressures remain above 100 mm Hg is there significant fetal loss.

A final group of patients consists of those in whom hypertension develops in late (third trimester) pregnancy in successive gestations. These patients seem to have an increased likeli­hood of developing sustained hypertension later in life.
Besides toxemia, two other distinct renal syn­dromes may be seen in association with preg­nancy. Bilateral renal cortical necrosis is a rare syndrome that almost always follows a dire ob­stetric complication; abruptio placentae, retained fetal fragments, or septic abortion. The presenta­tion is usually that of a scant output of bloody urine, followed by sudden, virtually complete an­uria. Renal failure is always present, and evidence of disseminated intravascular coagulation is com­mon. The renal histopathology is that of frank necrosis throughout the cortex. The degree of necrosis ranges from patchy areas to confluent cortical necrosis. Oligoanuria is prolonged in all cases, but a few patients recover sufficient renal function to stop dialysis after weeks to months of treatment.

Postpartum renal failure, or the adult hemo­lytic-uremic syndrome, is a rare disorder that has its onset from two to three days up to eight to nine weeks postpartum. The preceding pregnancy and delivery are usually normal. A microangiopathic hemolytic anemia with prominent fragmentation of red blood cells is evident. The kidneys show marked deposition of fibrin in arterioles and glo­meruli and intimal proliferation in blood vessels. The vascular proliferative lesion is the same as that seen in accelerated hypertension, although patients with postpartum renal failure are typi­cally normotensive. About 75 per cent of patients have permanent renal failure and require dialysis or transplantation.