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Biomedical subjects

P D Mitnick

Publications and source records attributed to P D Mitnick.

9 recordsLinked to original sources
PubMed1990

Rhabdomyolysis associated with severe hyponatremia after prostatic surgery.

Transurethral resection of the prostate gland (TURP) has long been associated with disturbances of plasma sodium concentration. Relatively recent substitution of isotonic irrigation solutions has transformed the predominant laboratory abnormality reported from one of hypotonic hyponatremia to one of nearly isotonic hyponatremia with infrequent clinically significant manifestations. We report the unique association of acute and very severe isotonic hyponatremia with rhabdomyolysis and acute renal failure in the post-TURP setting. The mechanism for rhabdomyolysis is postulated to be an impairment of normal maintenance of cellular integrity by virtue of the acuteness and severity of hyponatremia, in the absence of a disturbance of tonicity. Survival after hyponatremia of this severity has not, to our knowledge, been previously reported.

Acute Disease↗
PubMed1986

Hypercalcemia and reversible renal failure in heavy-chain disease.

We have reported a case of gamma heavy-chain disease associated with hypercalcemia and reversible renal failure. After combined chemotherapy the patient remains well after 21 months of follow-up, and serum calcium levels remain in the normal range. This case supports the notion of Kyle et al that heavy-chain disease may present a diverse picture, and documents the first use of aggressive combination chemotherapy in the management of associated moderately severe hypercalcemia and hypercalcemic renal failure.

Acute Kidney Injury↗
PubMed1984

Piroxicam-induced renal disease.

Two cases of nephrotoxicity associated with piroxicam therapy are reported. In the first case, severe reversible azotemia with hyperkalemia resolved after discontinuation of the medication. In the second case, biopsy-proved acute interstitial nephritis with immune complex glomerulonephritis and hepatitis improved after steroid therapy. The mechanism for such toxicity may be altered hemodynamics, cellular immunity, or humoral immunity related to prostaglandin inhibition.

Acute Kidney Injury↗
PubMed1980

Effects of two nonsteroidal anti-inflammatory drugs, indomethacin and oxaprozin, on the kidney.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been found to cause sodium retention and to decrease glomerular filtration rate (GFR). We studied the effects of two such drugs, indomethacin and oxaprozin, a new propionic acid derivative, on renal function of awake, normal human subjects during sustained water diuresis. Although neither drug had a long-term effect on GFR or sodium clearance (CNa), indomethacin (six subjects) but not oxaprozin (seven subjects) transiently reduced GFR and CNa. Given over the short term, oxaprozin caused a reduction in GFR from 113.7 +/- 5.7 to 99.8 +/- 4.7 ml/min (p < 0.01) and CNa from 0.84 +/- 0.07 to 0.61 +/- 0.08 ml/min (p < 0.005). The results were much the same when an additional dose of indomethacin was given to subjects who had been receiving the drug for a week. Inference from clearance data at a time when urinary osmolality (Uosm) remained constant but urine flow per GFR (V/GFR) fell suggests that both drugs stimulated proximal tubular sodium and fluid resorption. Both suppressed renin and aldosterone levels comparably and reduced potassium excretion transiently, but only indomethacin caused a sustained change in serum potassium concentration; serum potassium rose from 4.32 +/- 0.10 to 4.56 +/- 0.11 mEq/l (p < 0.05) after 1 wk. These disparate findings suggest that prostaglandin synthesis inhibition may not be the sole mechanism of action of NSAIDs.

Aldosterone↗
PubMed1980

Calcium and phosphate metabolism in tumoral calcinosis.

We have recently seen a patient with tumoral calcinosis, a syndrome comprising hyperphosphatemia, normocalcemia, normal glomerular filtration rate (GFR), and extensive periarticular calcific masses. Parathyroid hormone (PTH) deficiency or target organ resistance was ruled out by demonstration of normal serum PTH and urinary 3'5'cyclic AMP excretion and normal response to exogenous PTH and to endogenous stimulation by ethylenediaminetetraacetate. An intrinsic proximal tubular defect allowing enhanced renal PO4 reabsorption was probably present because there was no phosphaturic response to acetazolamine and renal PO4 threshold remained abnormally elevated even after PTH infusion. We then studied the mechanism by which serum calcium level is maintained in the normal range despite hyperphosphatemia and absence of secondary hyperparathyroidism. Normal 1,25-(OH)2 vitamin D was found, suggesting normal gastrointestinal calcium absorption. This, combined with markedly reduced urinary calcium excretion, perhaps a direct effect of hyperphosphatemia, may maintain calcium balance and prevent secondary hyperparathyroidism. A rise in urinary cyclic AMP excretion after furosemide-induced calciuria supports this hypothesis.

Adult↗