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Biomedical subjects

S De Castro del Pozo

Publications and source records attributed to S De Castro del Pozo.

At least 19 recordsLinked to original sources

Hyporeninemic hypoaldosteronism in diabetic patients with chronic renal failure.

Plasma renin activity, plasma aldosterone levels and renal tubular capacity to excrete hydrogen ions were studied in 13 patients suffering from diabetes mellitus with a creatinine clearance of less than 40 ml/min. The results were compared with those obtained in a control group, in a group of nondiabetic subjects with chronic renal failure (CRF) and in a group of diabetic patients without CRF. Twelve of the thirteen diabetic patients with CRF had data characteristic of hyporeninemic hypoaldosteronism associated with type IV renal tubular acidosis. On comparing the results with those of the other two groups of patients, it was observed that the manifestations of the latter two groups considered separately were different from those of the problem group, although in the diabetic patients with normal glomerular filtration rate (GFR) hyporeninism but not hypoaldosteronism was present accompanied by a lower net acid excretion (p less than 0.001) due to a lower excretion of NH4 (p less than 0.05) and titratable acid (p less than 0.001) when the patients were challenged with an NH4Cl overload. We believe that a conjunction of diabetes and renal failure is necessary for the diabetic patients with a decrease in GFR to show hyporeninemic hypoaldosteronism and type IV tubular acidosis.

Acidosis, Renal Tubular↗

[Metabolism of phenylbutazone in the liver (author's transl)].

The object of the investigation was to study the capacity of the liver to metabolize drugs under diversified conditions (cirrhosis, hepatitis, cholestasis in alcoholics, in diabetics as well as in eplieptics treated with barbiturates) as well as the possibility of inducing this function. To accomplish this we determined the half-life of Butazolidin. Only in cirrhotics it was shown that the capacity to metabolize Butazolidin was reduced. Induction with barbiturates increased hepatic captation of the drug but did not modify the biotransformation of the same. This is attributed to the development of a "hypoactive hypertrophy" of the reticuloendothelium.

Alcoholism↗