demeclocycline and Uremia

Seventeen patients with cancer or aplastic anemia received demeclocycline as treatment for hyponatremia. Prior to demeclocycline therapy no patients showed clinical signs of fluid overload or saline depletion. In all patients inappropriately concentrated urine (mean urine osmolality = 548 mOSM/kg H2O) or increased urine content of sodium (mean urine sodium = 91 mEq/L) were documented prior to demeclocycline therapy. No patient had developed hyponatremia in association with antineoplastic drug therapy. The average serum sodium (NaS) at the time of initiation of therapy was 121 mEq/L. NaS increased in all patients despite the simultaneous administration of generous volumes of fluid. NaS exceeded 130 mEq/L and average of 3.5 days following institution of demeclocycline. Patients lost an average of 2.3 kg during demeclocycline. The toxicity noted following demeclocycline was azotemia and increased serum creatinine. Eight patients developed serum urea nitrogen (SUN) in excess of 25 mg/dl; average maximum creatinine in these eight patients was 1.9 mg/dl. Average peak creatinine in eight patients who did not develop azotemia was 0.87 mg/dl. Azotemia seemed to be correlated with simultaneous administration of other nephrotoxic agents and with administration of higher doses (1200 mg/day) of demeclocycline.

Topics: Creatinine; Demeclocycline; Humans; Hyponatremia; Neoplasms; Osmolar Concentration; Uremia; Water Intoxication

Fourteen patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been treated with demethylchlortetracycline (demeclocycline) 1200 mg daily. In 12 patients the underlying lesion was malignant. The serum sodium returned to normal (greater than 135 mmol/l) in all patients after a mean of 8.6 days (SD +/- 5.3 days). Blood urea rose significantly from the pretreatment level of 4.2 +/- 2.3 mmol/l to 10.1 +/- 5.1 mmol/l at ten days (P less than 0.001). The average maximum blood urea was 13.4 +/- 6.8 mmol/l. In four patients the urea rose above 20 mmol/l, and in two of these demecyocycline was discontinued because of thie rise. The azotaemia could be attributed to a combination of increased urea producation and a mild specific drug-induced nephrotoxicity. Discontinuation of demeclocycline in six patients led to a fall in serum sodium, in one case precipitously, and return of the urea towards normal levels. Demeclocycline appears therefore to be an effective maintenance treatment of SIADH, and the azotaemia that occurs is reversible and probably dose dependent.

Topics: Adult; Aged; Creatinine; Demeclocycline; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Sodium; Urea; Uremia