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J B Wish

Publications and source records attributed to J B Wish.

25 records · Page 2Linked to original sources

Hospital-acquired renal insufficiency: a prospective study.

Twenty-two hundred sixty-two consecutive medical and surgical admissions were evaluated prospectively to determine the contribution of iatrogenic factors to the development of renal insufficiency in hospital. Of 2,216 patients at risk, some degree of renal insufficiency developed in 4.9 percent. Decreased renal perfusion, postoperative renal insufficiency, radiographic contrast media, and aminoglycosides accounted for 79 percent of the episodes. Iatrogenic factors, broadly defined, accounted for 55 percent of all episodes. Poor prognostic indicators included oliguria, urine sediment abnormalities and, most importantly, severity of renal insufficiency; with an increase in serum creatinine of 3 mg/dl or greater, the mortality rate was 64 percent. Age, admission serum creatinine levels, and the number of episodes of renal insufficiency did not significantly affect outcome. We conclude that there is a substantial risk of the development of renal failure in hospital and that the mortality rate due to hospital-acquired renal insufficiency remains high.

Acute Kidney Injury↗

Failure of increased sodium avidity to facilitate renal acid excretion in dogs fed sulfuric acid.

Previous studies have suggested that the increment in renal acid excretion caused by sulfuric acid feeding is mediated solely by an interplay between the sulfate-induced increase in distal sodium delivery and the gradual augmentation of distal sodium reabsorption that occurs as sodium losses accumulate. This hypothesis predicts that if distal sodium reabsorption were stimulated sufficiently prior to the administration of sulfuric acid, excretion of the hydrogen ion load would occur promptly, thus obviating the fall in plasma bicarbonate or loss of cation that normally occurs. To test this prediction, we fed sulfuric acid (7 mEq of H+/kg/day) to dogs in which distal sodium avidity had been enhanced prior to acid feeding either by diuretic-induced sodium depletion (N = 6) or by deoxycorticosterone acetate 7.5 mg, twice a day and a low-sodium diet (N = 8). Contrary to expectation, over the first 3 days of acid feeding there was a significant fall in plasma bicarbonate (7.1 and 7.5 mEq/liter) and an increase in urinary sodium excretion (48 mEq in both groups). Moreover, changes in both plasma bicarbonate and urinary sodium excretion were similar to those observed previously (5.9 mEq/liter and 46 mEq, respectively) in normal dogs fed the same dose of sulfuric acid.

Acid-Base Imbalance↗

Medspeak.

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