During pregnancy, the maternal glomerular filtration rate (GFR) increases by 40–50%. The primary mechanism responsible for this gestational hyperfiltration is:

• A Increased mean arterial pressure due to expanded blood volume
• B Progesterone-induced afferent arteriolar dilation via nitric oxide
• C Increased plasma oncotic pressure due to dilutional effects reducing oncotic resistance to filtration
• D Relaxin-mediated renal vasodilation (particularly of the afferent arteriole), reducing renal vascular resistance and increasing renal plasma flow ✓

Explanation

Relaxin, produced by the corpus luteum and placenta from early pregnancy, is the primary mediator of gestational hyperfiltration. Relaxin acts on endothelial cells to upregulate endothelin B receptors and stimulate constitutive nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF), causing profound renal vasodilation—particularly of the afferent arteriole. This reduces renal vascular resistance, increases effective renal plasma flow by 50–80%, and secondarily increases GFR. The GFR rise lowers serum creatinine and urea (normal values are thus lower in pregnancy). Reduced plasma oncotic pressure (due to dilutional hypoalbuminemia) does contribute to increased filtration fraction, but relaxin-mediated vasodilation is the primary mechanism.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.