1. A group of eight patients with advanced renal failure, and a creatinine clearance of 3·8–24 ml/min, were subjected to sodium loading and sodium depletion.

2. With sodium loading there was a consistent increase in blood pressure (0·01 < P <0·02), an increase in creatinine clearance that was significantly related to changes in mean arterial pressure (r = +0·3, 001 < P < 0·02); an increase in urinary sodium excretion that was closely correlated with changes in creatinine clearance (r = +0·82, P < 0·001); a decrease in fractional reabsorption of filtered sodium that was inversely proportional to creatinine clearance (r = −0·63, 0·05< P < 0·1).

3. Fractional reabsorption of filtered sodium was proportional to creatinine clearance both in the sodium-loaded (r = +0·86, 0·001 < P < 0·01) and sodium-depleted states (r = +0·92, 0·001 < P < 0·01).

4. Urinary aldosterone excretion and plasma renin activity consistently increased with sodium depletion, the percentage increases of the two being significantly related (r = +0·95, P < 0·001).

5. The results suggest that excretion of a sodium load in uraemia may be effected in part as the result of a raised blood pressure that elevates the glomerular filtration rate; by increasing the peritubular capillary pressure this may be responsible for the observed decrease in reabsorption of filtered sodium. The responsiveness of glomerular filtration rate to blood pressure changes suggests a decrease in afferent arteriolar tone that may account for the increased sodium excretion per nephron which occurs even in uraemic patients without hypertension.

6. It is suggested that aldosterone may continue to play an important regulatory role in sodium homeostasis in uraemia and that renin concentrations are the major determinants of aldosterone production in uraemia.

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