Maternal GFR increases by approximately 40–50% during pregnancy. The primary mechanism is:

• A Progesterone-mediated dilatation of efferent arterioles reducing filtration fraction
• B Increased cardiac output alone raising renal perfusion pressure
• C hCG-stimulated proximal tubular glucose reabsorption reducing tubuloglomerular feedback
• D Relaxin-mediated reduction in renal afferent arteriolar resistance, increasing renal plasma flow and GFR ✓

Explanation

Relaxin, secreted by the corpus luteum and placenta, is the primary mediator of gestational hyperfiltration. It acts on renal vasculature to reduce myogenic tone of afferent arterioles via NO-dependent mechanisms, increasing renal plasma flow by ~70% and GFR by ~40–50%. This explains why normal serum creatinine is lower in pregnancy (0.4–0.7 mg/dL); values of 0.9 mg/dL, normal in non-pregnant women, indicate significant renal impairment in pregnancy. Increased cardiac output contributes but alone does not account for the magnitude; efferent arteriolar changes are minor.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.