Summary Seven patients with acute illnesses developed hypophosphataemia whilst receiving intravenous nutrition which included a fat emulsion, Intralipid, a possible source of phosphorus. The authors' observations cast doubt on the bio-availability of the phosphorus contained in the phospholipid content of the fat emulsion. The currently recommended allowance of phosphorus for this type of patient appears to be too low and it is suggested that 0-5-0-75 mmol/kg body weight be provided, preferably as a neutral phosphate solution. Sine hypophosphataemia can occur at various time intervals after starting intravenous nutrition and precede clinical sequelae it is recommended that routine serum phosphate measurements are made in all patients receiving this treatment.

We here report a case of Bartter's syndrome occurring in association with diabetes mellitus. The patient, an insulin-dependent diabetic, presented with hypokalaemia, inappropriate kaliuresis and metabolic alkalosis. He had high plasma renin activity, relatively low plasma aldosterone, and resistance to infused angiotensin II. A high potassium diet raised total body potassium and serum potassium, did not affect plasma renin activity, but raised plasma aldosterone significantly and did not alter the resistance to angiotensin II. Indomethacin administered acutely reduced urinary potassium and kallikrein excretion and, on chronic administration, lowered plasma renin activity, urinary chloride excretion, and raised serum potassium. Salt restriction resulted in a prompt and significant reduction in urinary sodium and chloride excretion. Urinary kallikrein excretion was very high throughout, increased with sodium restriction, and decreased with sodium loading. Oral potassium supplementation partially corrected the hypokalaemia, but did not affect blood sugar control. In this patient the primary defect appears to have been primary urinary potassium wasting, rather than sodium or chloride wasting. The striking effects of indomethacin suggest that prostaglandins may play a fundamental role in the genesis of the syndrome.

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