High sodium sensitivity and glomerular hypertension/hyperfiltration in primary aldosteronism.

Abstract

To assess sodium sensitivity and glomerular haemodynamics in patients with primary aldosteronism. Two-week studies were performed in six patients with primary aldosteronism whose diagnosis had been confirmed by histology of the removed adrenal adenoma. Patients were fed normal or sodium-restricted diets for 1 week each and renal clearance measured during the normal sodium diet. Pressure-natriuresis relationships were drawn by plotting the urinary sodium excretion on the y-axis as a function of the systemic mean arterial pressure on the x-axis. The extrapolated x-intercept of the pressure-natriuresis curve was 118 +/- 9 mmHg. The sodium sensitivity, which corresponds to the reciprocal of the slope, was augmented to 0.111 +/- 0.013 mmHg/mmol per day, and the reduction in mean arterial pressure by sodium restriction was 11 +/- 2%. As we had reported previously, the difference between the mean arterial pressure (137 +/- 5 mmHg) with the normal-sodium diet and the x-intercept was assumed to be the effective filtration pressure across the glomerular capillary walls (18.2 +/- 2.0 mmHg). By dividing the glomerular filtration rate (128 +/- 10 ml/min per 1.73 m2) by the effective filtration pressure, the whole kidney ultrafiltration coefficient in these patients was estimated to be 0.127 +/- 0.021 ml/s per mmHg, which was approximately normal. The glomerular capillary pressure was calculated to be 54 +/- 2 mmHg. Compared with non-sodium-sensitive essential hypertension patients (n = 18) whose glomerular filtration rate and capillary hydraulic pressure were 84 +/- 3 ml/min per 1.73 m2 and 47 +/- 1 mmHg, the sodium sensitivity of blood pressure in patients with primary aldosteronism was augmented, and both glomerular hyper-filtration and glomerular capillary hypertension were observed. We confirmed that the glomerular haemodynamic characteristics in primary aldosteronism are typical of those expected for sodium-sensitive hypertension caused by enhanced tubular sodium reabsorption.