In women with chronic kidney disease who also have renal insuiciency, adverse outcomes are generally directly related to the degree of renal impairment. Outcomes of women with moderate versus severe renal insuiciency are usually not separated (Table 53-5). hat said, Piccoli and associates (2010a) described 91 pregnancies complicated by stage 1 chronic kidney disease. Primarily because of hypertension, 33 percent were delivered preterm, and 13 percent had fetal-growth restriction. Alsuwaida and colleagues (2011) reported similar observations. Other investigators have described pregnancies complicated by moderate or severe renal insuiciency (Cunningham, 1990; Imbasciati, 2007; Zhang, 2015). Despite a high incidence of chronic hypertension, anemia, preeclampsia, preterm delivery, (red points). (Data from Cunningham, 1990; Stettler, 1992. Growth curves are those reported by Alexander, 1996.) and fetal-growth restriction, perinatal outcomes were generally acceptable. As shown in Figure 53-5, fetal growth is frequently impaired and related to renal dysfunction severity.
Prenatal care is tailored for women with chronic renal disease. Frequent monitoring of blood pressure is paramount, and serum creatinine levels, protein/creatinine ratio, and 24-hour protein excretion are quantiied as indicated. Bacteriuria is treated to decrease the risk of pyelonephritis and urther nephron loss. Protein-rich diets are recommended Gim, 2016; Lindheimer, 2000). In some women with anemia from chronic renal insuiciency, a response is seen with recombinant erythropoietin, however, hypertension is a common side efect. Serial sonography is performed to follow fetal growth. he diferentiation between worsening hypertension and superimposed preeclampsia is problematic. Preliminary data indicate that the angiogenic biomarkers placental growth factor (PIGF) and its soluble antiangiogenic receptor (sFlt-l) may be useful to separate chronic from gestational hypertension. This is described in Chapter 40 (p. 716).
In some women, pregnancy may accelerate chronic renal disease progression by increasing hyperfiltration and glomerular pressure to worsen nephrosclerosis (Baylis, 2003; Helal, 2012). his is more likely in women with severe chronic renal insuficiency (Abe, 1991 ; Jones, 1996). For example, Jungers and associates (1995) reported few long-term pregnancy-related adverse efects in 360 women with chronic glomerulonephritis and antecedent normal renal function. However, at 1 year after pregnancy, Jones and Hayslett (1996) reported that 10 percent of such women with moderate or severe renal insuiciency had developed end-stage renal failure-stage 5 chronic kidney disease. In a study from Parkland Hospital, we found that 20 percent of pregnant women with similar insuiciency had developed end-stage renal failure by a mean of 4 years (Cunningham, 1990). Similar indings in women with a median follow-up of 3 years were described by Imbasciati and coworkers (2007). By this time, end-stage disease was apparent in 30 percent of women whose serum creatinine was ::l.4 mg/dL and who had proteinuriaa> 1 g/d. Chronic proteinuria is also a marker for subsequent development of renal failure. In another report from Parkland Hospital, 20 percent of women with chronic proteinuria discovered during pregnancy progressed to end-stage renal failure within several years (Stettler, 1992).