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A prospective study of severe hyponatraemia in adult hospital inpatients showed that 44 patients had plasma sodium concentrations below 125 mmol(mEq)/1. Eighteen cases (41%) were iatrogenic, caused by diuretic treatment or postoperative administration of intravenous 5% dextrose, or both. Chest infection, a seldom-recognised and ill-understood cause of hyponatraemia, proved more common than carcinoma of the bronchus. Thirty-one patients had symptoms attributable to the hyponatraemia, but these were severe in only five cases. Analysis of blood and urine was of no value in distinguishing the different diagnostic groups in an emergency.

The effect of a six-week course of spironolactone 300 mg/day was examined in 25 unselected patients with essential hypertension. In the blood spironolactone produced a significant rise in urea and potassium concentrations and a fall in sodium and bicarbonate concentrations. In six patients blood pressure was normal at the end of the course, while in five patients there was almost no change. Studies of the effects of spironolactone on various indices usually affected by mineralocorticoids-namely, blood electrolytes, total body potassium, and rectal electrical properties-showed no differences between responding and non-responding patients. Mineralocorticoid excess therefore seems to be rarely responsible for essential hypertension and the influence of spironolactone cannot at present be fully explained.

Three patients were seen who had sarcoidosis associated with glomerulonephritis. Subsequent review of published reports of cases in which the two conditions occurred simultaneously showed a pattern of histological type of glomerulonephritis different from that seen in patients without associated disease. In sarcoidosis with glomerulonephritis there appeared to be a dearth of minimal-change disease and an excess of membranous glomerulonephritis compared with the prevalence that would be expected if the renal disease was merely a chance occurrence. These findings may provide evidence for an important relation between sarcoidosis and glomerulonephritis.

Biopsy of renal tissue from four patients with idiopathic focal nephritis and three patients with Henoch-Schönlein syndrome showed that C3 and properdin were deposited with IgA in the glomerular mesangium, C1q could not be detected. These observations suggest that glomerular injury in disorders characterized by mesangial deposits of IgA and C3 is mediated via the properdin system.