Mild natriuretic effect: It competes with aldosterone at mineralocorticoid receptors in the renal tubule, reducing sodium reabsorption. This stimulates compensatory activation of the renin-angiotensin-aldosterone system, so pregnancy still results in net sodium and water retention. Katzung's Basic and Clinical Pharmacology, 16th ed., “Effects of Progesterone”

Potassium conservation: Despite high aldosterone concentrations, progesterone reduces renal potassium loss, helping prevent hypokalemia. Creasy & Resnik’s Maternal-Fetal Medicine, “Potassium”

Ureteral smooth-muscle relaxation: Progesterone lowers ureteric tone, peristalsis, and contraction pressure. Together with compression by the enlarging uterus, this causes dilatation of the ureters and renal pelvis, termed physiologic hydroureter/hydronephrosis of pregnancy. Urinary stasis also contributes to greater susceptibility to urinary tract infection. The NCBI pregnancy physiology review describes this reduction in ureteral tone.

Renal vasodilation and higher filtration: Progesterone may contribute to increased renal plasma flow and GFR, but does not fully explain these changes. Relaxin, nitric oxide, reduced vascular resistance, and altered sensitivity to angiotensin II are important contributors. Overall, GFR rises roughly 40% to 50%, making serum creatinine, urea, and uric acid lower than before pregnancy. Creasy & Resnik’s Maternal-Fetal Medicine, “Renal Function” The renal physiology review makes the same distinction between progesterone’s role and the broader pregnancy hemodynamic response.