Renal and Hepatic Pathophysiology of Pregnancy

Pregnancy induces multiple adaptive changes to the kidney and liver. The kidney increases in size up to 30% with the following functional changes: a marked increase in both glomerular filtration rate and renal plasma flow and an increase in creatinine clearance leads to decreased blood urea nitrogen (6–9 mg/dL) and serum creatinine concentration (0.4–0.6 mg/dL). Higher total protein and glucose excretion are expected. The renin-angiotensin-aldosterone system is elevated, and with alterations in the threshold for antidiuretic hormone secretion, plasma osmolality is decreased. A compensatory increase in bicarbonate excretion occurs to counteract respiratory alkalosis. Compared to the kidney, liver size or blood flow does not change during pregnancy. Serum transferase, gamma-glutamyl transpeptidase, and lactic dehydrogenase levels are increased, which does not necessarily reflect hepatic disease. The total protein and albumin to globulin ratio are decreased, which may result in increased serum concentrations of highly protein-bound drugs. Notably, estrogen and progesterone are involved in the pathophysiology of both organs. Dilated renal calyces, pelvises, and ureters in combination with atony and physical compression predispose parturients to hydronephrosis and urinary tract infections. In the liver, it causes hypomotility of the gallbladder, which increases the risk of gallbladder disease.