Metabolic Disorders in Acute Myeloid Leukaemia

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Abstract
SUMMARY Metabolic balance studies were carried out in 17 utiselected patients with acute myeloid leukaemia. Widespread metabolic disturbances were observed. Serum Na fell below 135 mmol/l in 14 patients (82%) and 11 patients (64%) developed hypokalaemia. An increased osmolal clearance caused by a release of electrolyte and blast cell waste (i.e. urea, urate, etc.) during chemotherapy appeared to be the principle cause of natriuresis and hyperkaluria. Seven patients had pro‐teinuria before and eight others developed it during antileukaemic therapy. Nine patients (53%) developed proximal renal tubular dysfunction with aniinoaciduria, hyperphosphaturia and incomplete reabsorption of urate. No significant relation was found between this widespread glotnerulo‐tubular dysfunction and lysozymuria. We suggest that antileukaemic drugs release unidentified substances from blast cells which are toxic to the kidney. Metabolic alkalosis in six patients (35%) was probably related to volume depletion and hypokalaemia, while two patients developed acidaemia with the onset of renal failure. Hypocalcaemia in seven patients (41%) had a multifactorial basis: hyperphosphaturia, septicaemia, malnutrition and cytotoxic drugs were among the probable causes.