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Biomedical subjects

C Chaimowitz

Publications and source records attributed to C Chaimowitz.

12 recordsLinked to original sources
PubMed1977

Renal tubular acidosis due to the milk-alkali syndrome.

A 60-year-old man with a history of excessive ingestion of calcium carbonate presented with azotemia, hypercalcemia and hyperphosphatemia. His acid-base status was initially normal. Following the cessation of calcium carbonate treatment, the hypercalcemia and azotemia disappeared, and the patient was found to be in metabolic acidosis with blunted acid excretion and a urine pH of 6.1. Kidney biopsy showed focal tubular calcification; the tubular damage was apparently caused by hypercalcemia and had resulted in renal tubular acidosis. During the three months of observation since that time there has been a tendecy for spontaneous remission of the renal tubular acidosis. Impaired renal hydrogen ion excretion prevented the development of metabolic alkalosis despite ingestion of alkali initially, and was later responsible for the metabolic acidosis. Renal tubular acidosis occurring as a sequel to the milk-alkali syndrome may aggravate the danger of nephrocalcinosis in this syndrome.

Acidosis, Renal Tubular↗
PubMed1976

Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.

We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. Hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. Hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.

Acidosis↗
PubMed1975

Hypertensive crisis, erythrocytosis, and uraemia due to renal-artery stenosis of kidney transplants.

Two patients with kidney transplants had hypertensive encephalopathy and rapidly progressive kidney failure 10 weeks and 18 months postoperatively. In one patient renal failure was associated with erythrocytosis. Absence of proteinuria, despite progressive renal insufficiency in both patients, suggested that these abnormalities were not due to rejection episodes. Subsequently, angiography proved that each of these patients had renal-artery stenosis. Surgical repair of this lesion increased creatinine clearance at least threefold, and the hypertension and erythrocytosis disappeared. Apparent "rejection" episodes in which there is no proteinuria should alert clinicians to the possiblity of renal-artery stenosis of the graft. Restoration of kidney function and amelioration of hypertension may follow revascularisation, even after many months of renal ischaemia producing severe uraemia.

Adult↗