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Disorders of the kidneys and urinary tract are commonly encountered in pregnancy. Some precede pregnancy—one example is nephrolithiasis. Pregnancy-induced changes may predispose to the development or worsening of urinary tract disorders—an example is the markedly increased risk for pyelonephritis. Last, renal pathology unique to pregnancy, such as preeclampsia, can develop. In one Australian study, kidney disorders had an incidence of 0.3 percent in 407,580 births (Fitzpatrick, 2019).


During normal pregnancy, significant changes in both structure and function take place in the urinary tract (Chap. 4, p. 67). The kidneys become larger, and dilation of the renal calyces and ureters can be striking. Some dilation develops before 14 weeks and likely is due to progesterone-induced relaxation of the muscularis. More marked dilation is apparent beginning in midpregnancy and stems from ureteral compression, especially on the right side. Vesicoureteral reflux also occurs during pregnancy. Important consequences of these physiological changes are an increased risk of upper urinary infection and erroneous interpretation of studies.

Evidence of functional renal hypertrophy becomes apparent very soon after conception. Glomeruli are larger, although cell numbers are not greater (Strevens, 2003). Intrarenal vasodilation lowers resistance of both afferent and efferent arterioles, and leads to higher effective renal plasma flow and glomerular filtration (Helal, 2012; Hussein, 2014). By 12 weeks’ gestation, the glomerular filtration rate (GFR) is already 20 percent above nonpregnant values (Hladunewich, 2004). Ultimately, renal plasma flow rises by 40 percent and GFR by 65 percent. Consequently, serum concentrations of creatinine and urea decline substantively across pregnancy. Thus, values within a nonpregnant normal range may be abnormal for pregnancy (Appendix, p. 1232). Other alterations include those related to acid–base homeostasis and osmoregulation.

Assessment of Renal Function During Pregnancy

Urinalysis results are essentially unchanged during normal pregnancy, except for occasional glucosuria. In nondiabetic gravidas, glucosuria is thought to stem from a pregnancy-related reduced rate of renal tubular glucose reabsorption (Welsh, 1960). This normal physiological change may add confusion and concerns for a gestational diabetes mellitus (GDM) diagnosis. Indeed, 1+ or greater urine dipstick readings have been associated with subsequent GDM diagnosis later in pregnancy. Despite this association, urine dipstick testing alone shows poor sensitivity to diagnose GDM (Buhlin, 2004; Olagbuji, 2015). For women with glucosuria, no guidelines in the United States direct practice, but in the United Kingdom, early oral glucose testing is considered for those with an isolated 2+ or repetitive 1+ urine dipstick readings (National Institute for Health And Clinical Excellence, 2015). This seems to be a reasonable approach.

Protein excretion is slightly elevated, but it seldom reaches levels that are detected by usual screening methods. Higby and colleagues (1994) reported 24-hour protein excretion in normal pregnancy to be 115 mg, with a 95-percent confidence level of 260 mg/d ...

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