Metabolic disorders in acute myeloid leukaemia.
Metabolic balance studies were carried out in 17 unselected patients with acute myeloid leukaemia. Widespread metabolic disturbances were observed. Serum Na fell below 135 mmol/1 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 proteinuria before and eight others developed it during antileukemic therapy. Nine patients (53%) developed proximal renal tubular dysfunction with aminoaciduria, hyperphosphaturia and incomplete reabsorption of urate. No significant relation was found between this widespread glomerulo-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. Hypocalcemia in seven patients (41%) had a multifactorial basis: hyperphosphaturia, septicaemia, malnutrition and cytotoxic drugs were among the probable causes.
D005438:Fludrocortisone / Q000009:adverse effects; D006030:Glycosuria, Renal / Q000209:etiology; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000150:complications / Q000378:metabolism*; D008274:Magnesium / Q000097:blood; D008659:Metabolic Diseases / Q000209:etiology*; D009994:Osmolar Concentration; D011507:Proteinuria / Q000209:etiology; D000608:Renal Aminoacidurias / Q000209:etiology; D014883:Water-Electrolyte Imbalance / Q000209:etiology
D008274:Magnesium; D005438:Fludrocortisone