The Renin–Angiotensin–Aldosterone System and Autosomal Dominant Polycystic Kidney Disease

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Abstract
A high incidence of hypertension (50 to 75 percent) occurs early in the course of autosomal dominant polycystic kidney disease. Cyst enlargement, causing bilateral renal ischemia and subsequent release of renin, is proposed as the cause of this form of hypertension. To investigate this hypothesis, we measured plasma renin activity and aldosterone concentrations during short-term and long-term converting-enzyme inhibition in 14 patients with hypertension due to polycystic kidney disease, 9 patients with essential hypertension, 11 normotensive patients with polycystic kidney disease, and 13 normal subjects. The groups were comparable with respect to age, sex, body-surface area, degree of hypertension, sodium excretion, and renal function. During the short-term study, the mean (±SE) plasma renin activity was significantly higher in the hypertensive patients with polycystic kidney disease than in the patients with essential hypertension, in the supine (0.36±0.06 vs. 0.22±0.06 ng per liter · second, P = 0.05) and upright positions (1.03±0.14 vs. 0.61±0.08 ng per liter · second, P<0.03) and after converting-enzyme inhibition (1.97±0.28 vs. 0.67±0.17 ng per liter · second, P<0.0006). The mean arterial pressures measured in the supine and upright positions and the plasma aldosterone concentrations measured in the upright position were significantly higher in the normotensive patients with polycystic kidney disease than in the normal subjects. After six weeks of converting-enzyme inhibition, renal plasma flow increased (P<0.005), and both renal vascular resistance (P<0.007) and the filtration fraction (P<0.02) decreased significantly in the hypertensive patients with polycystic kidney disease but not in the patients with essential hypertension. The renin–angiotensin–aldosterone system is stimulated significantly more in hypertensive patients with polycystic kidney disease than in comparable patients with essential hypertension. The increased renin release, perhaps due to renal ischemia caused by cyst expansion, probably contributes to the early development of hypertension in polycystic kidney disease. (N Engl J Med 1990; 323:1091–6.)