Antonio Dal Canton

The Causal Role of Salt Depletion in Acute Renal Failure Due to Captopril in Hypertensive Patients with a Single Functioning Kidney and Renal Artery Stenosis

Captopril (C) causes ARF in hypertensive patients with renal artery stenosis (RAS) with a single functioning kidney (SK). Retrospective studies in two patients showed that episodes of C-induced ARF were preceded by a rise in urinary Na+ excretion and a rapid decrease in body weight. These observations prompted us to investigate whether extracellular fluid volume depletion secondary to C-induced natriuresis can be responsible for ARF. Prospective studies were performed in four patients with RAS-SK treated with C. These studies have shown that: ARF is associated with negative Na+ balance and is corrected by salt replacement, even without interrupting C; ARF is preceded by a rise in urinary prostaglandin (PG) E2 and 6-keto-F1 alpha; ARF is prevented by either saline infusion or aspirin administration; ARF does not occur when the dose of C is not sufficient to raise PGs and urinary N + excretion. We conclude therefore that C-induced ARF in patients with RAS-SK can be secondary to salt depletion dependent on a raised secretion of PGs.

Exaggerated Natriuresis in the Hypertensive Man:Clinical Evidence for Intrarenal Hemodynamic Heterogeneity

7 hypertensive patients (H) and 8 normotensive volunteers (N) were loaded with NaCl (4.5 mEq Na +/kg body weight i.v.) during water diuresis (A) and antidiuresis (B). In 6 antidiuretic subjects (3H and 3N) urine volume (V) was progressively raised up to over 30 ml/min, by intravenous infusion (12 ml/min) of hypertonic (3%) saline (C). It is assumed that in (A) CH2O is an index of Na+ reabsorption in short Henles loops. In (B) and (C) TcH2O is proportional to Na+ reabsorption in long Henles loops. In (A) CcH2O was significantly lower in H. In (B) TcH2O was similar in H and N. In (C), TcH2O reached an earlier plateau in H than in N. These results demonstrate that exaggerated natriuresis depends on defective Na+ reabsorption in Henles loops, suggesting that the defect depends upon the transmission of hypertension to medullary circulation. The increase in hemodynamic pressure in vasa recta opposes Na+ reabsorption both in short and in long Henles loops. However, the effects on TcH2O of the decrease in Na+ reabsorption in long loops is blunted by the greater Na+ delivery, secondary to the increase in GFR, that follows the rise in filtration pressure.

Reversal of proximal tubular dysfunction by indomethacin.

This paper reports a patient with salt-losing nephropathy, phosphaturia, glucosuπa, hypercalcmria and bicarbonaturia, i.e. urinary abnormalities due to proximal tubular defects. Oral indomethacin caused a complete normalization of urinary alterations. These results show that indomethacin is effective in the treatment of proximal tubular defects and suggest that this therapeutic effect is due to an overall increase in proximal tubular reabsorption.