[Oak]

Yup your hunch is absolutely correct, the correct answer is C.

Renal artery stenosis can decrease the renal perfusion pressure sufficiently to increase renin secretion significantly, which increases angiotensin II (AII), which, in turn, increases aldosterone. Chronic hypertension due to renal artery stenosis is the result of elevated levels of AII and aldosterone. Aldosterone increases retention of sodium from the collecting duct, and water follows; AII increases reabsorption of sodium from the proximal tubule, and water follows. AII is also a vasoconstrictor, increasing peripheral vascular resistance.

Vasoconstriction of the renal vasculature decreases renal plasma flow, which would be expected to decrease glomerular filtration rate proportionately. AII, however, preferentially vasoconstricts the efferent arteriole in the nephron, maintaining a reasonable glomerular filtration rate even with the reduced renal plasma flow. Captopril (an angiotensin-converting enzyme inhibitor) inhibits the conversion of angiotensin I to AII. The captopril-mediated decrease of AII will actually decrease glomerular filtration in the kidney with renal artery stenosis, because decreasing efferent constriction causes the glomerular capillary pressure to fall.

Atrial natriuretic peptide (choice A) levels would be expected to increase with increased water and sodium retention due to renal artery stenosis.

BUN (choice B) would be expected to increase or stay the same with renal artery stenosis, depending on the extent of AII-mediated efferent arteriole vasoconstriction.

Metabolic alkalosis, due to the increased net acid secretion (compare with choice D) from hyperaldosteronism, is typical in renal artery stenosis.

Potassium secretion would increase, rather than decrease (choice E), due to the effects of excessive aldosterone secondary to renal artery stenosis.