Recurrent hypernatremia; a proposed mechanism in a patient with absence of thirst and abnormal excretion of water.

A 7-year-old girl twice developed severe hypernatremia (serum sodium values up to 194 mEq/l) without obvious cause. The ability of her kidneys to conserve water was normal, and increasing her plasma osmolality stimulated an appropriate ADH response. Unable to excrete a water load, her kidneys continued to conserve water even with a serum sodium concentration of 133 mEq/l. She was never thirsty and did not ingest sufficient fluid by choice. Although there was no demonstrable anatomic lesion, we postulate a localized defect of her thirst center. This may have modified release of ADH and resulted in an inability to dilute the urine by interrupting a pathway that could exist from the thirst center to the supraoptic nuclei. A therapeutic regimen based on these studies has prevented further hypernatremia.

"Pulse" methylprednisolone therapy in the treatment of severe glomerulonephritis.

Eight patients with severe glomerulonephritis and an average inulin clearance of 21.7 ml/min/1.73 m2 body surface were treated with high-dosage intravenous methylprednisolone, 30 mg/kg given over a one-hour period on each of six alternate days. The mean inulin clearance rate doubled after this "pulse" therapy. In the six patients treated early in the course of their disease, GFR increased to a mean of 100.2 ml/min/1.73 m2 during the follow-up period extending for up to three years and was accompanied by clinical improvement. These observations suggest that "pulse" methylprednisolone may be beneficial in treating some patients with potentially life-threatening severe glomerulonephritis.