High sodium sensitivity and glomerular hypertension/hyperfiltration in primary aldosteronism

Objective To assess sodium sensitivity and glomerular haemodynamics in patients with primary aldosteronism. Design and methods 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. Results 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 m(2)) 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. Conclusion 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 m(2) and 47 +/- 1 mmHg, the sodium sensitivity of blood pressure in patients with primary aldosteronism was augmented, and both glomerular hyperfiltration 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.