Although renal biopsy is relatively safely performed during pregnancy, it usually is postponed unless results may change therapy. From a review of 243 biopsies in pregnant women, the incidence of complications was 7 percent-this compares with 1 percent in postpartum women (Piccoli, 2013). Some consider biopsy for rapid deterioration of renal function with no obvious cause or for symptomatic nephrotic syndrome (Lindheimer, 2007 a). We and others have found biopsy helpful in selected cases to direct management (Chen, 2001; Piccoli, 2013). In one series, renal biopsy in 12 normal pregnant volunteers showed that five had slight to moderate glomerular endotheliosis (Strevens, 2003). Recall this is the histopathological lesion that is putatively typical of preeclampsia and is characterized by ibrin deposition within the glomerular endothelium leading to capillary occlusion. In contrast, all 27 women with protein uric hypertension had endotheliosis, and in all but one, it was moderate to severe.
In these cases, if the remaining kidney is normal, renal function becomes augmented. However, women who have donated a kidney have a higher frequency of gestational hypertension or preeclampsia in subsequent pregnancy-IaI versus 5 percent compared with non-donors (Garg, 2015). Otherwise, women with one normal kidney most often have no diiculty in pregnancy. Moreover, kidney donation does not lead to long-term adverse consequences. That said, thorough functional evaluation of the remaining kidney is essential (Ibrahim, 2009).
These infections are the most frequent bacterial infections complicating pregnancy. Although asymptomatic bacteriuria is the most common, symptomatic infection includes cystitis, or it may involve the renal calyces, pelvis, and parenchyma to cause pyelonephritis. Organisms that cause urinary infections are those from the normal perineal lora. Approximately 90 percent of Escherichia coli strains that cause nonobstructive pyelonephritis have adhesins such as P-and S-imbriae. These are cell-surface protein structures that enhance bacterial adherence and, thereby, virulence (Foxman, 2010; Hooton, 2012).
Data suggest that pregnant women have more severe sequelae from urosepsis. One possible underlying factor is the T -helper cell-Th1/h2 ratio-reversal of normal pregnancy, which is discussed in Chapter 4 (p. 59). Other perturbations of cytokine or of adhesin expression may be contributory (Chaemsaithong, 2013; Sledzinska, 2011). But even if pregnancy itself does not enhance these virulence factors, urinary stasis, vesicoureteral relux, and diabetes predispose to symptomatic upper urinary infections (Czaja, 2009).
In the puerperium, several risk factors predispose to urinary infections. Bladder sensitivity to intravesical fluid tension is often diminished due to labor trauma or epidural analgesia.
Bladder sensations can also be obscured by discomfort from vaginal or perineal injury. Normal postpartum diuresis may worsen bladder overdistention, and catheterization to relieve retention often leads to urinary infection. Postpartum pyelonephritis is treated in the same manner as antepartum renal infections (McDonnold, 2012).