MINERAL HOMEOSTASIS IN ACUTE-RENAL-FAILURE COMPLICATING SEVERE FALCIPARUM-MALARIA

Disturbances in calcium metabolism in acute renal failure (ARF) remain incompletely understood. Most data are from patients with rhabdomyoly sis. As renal impairment commonly accompanies severe malaria in the ab sence of rhabdomyolysis, falciparum malaria provides an alternative mo del of mineral homoeostasis in ARF. We studied 25 Vietnamese subjects, aged 18-63 yr, with severe malaria and 10 controls. Fourteen patients had a serum creatinine level of 250 mu mol/L or less during treatment (group 1), five developed ARF but were not dialyzed (group 2a), and s ix required dialysis (group 2b). Group 1 patients presented with mild hypocalcemia (mean +/- SD serum ionized calcium, 1.18 +/- 0.05 vs. 1.2 3 +/- 0.02 mmol/L in controls; P = 0.01) that persisted until discharg e in the presence of normal serum phosphate, PTH, and vitamin D metabo lite levels. Group 2 patients were more hypocalcemic on admission (1.1 0 +/- 0.08 mmol/L; P < 0.0001 vs. controls), especially those in group 2b whose serum ionized calcium fell to 0.88 +/- 0.13 mmol/L when rena l dysfunction was maximal. In group 2 patients, the admission serum PT H level was raised (5.4 +/- 3.8 vs. 2.7 +/- 0.9 pmol/L in controls; P < 0.02) and changed reciprocally with calcemia. Significant rises in s erum phosphate occurred only in group 2b patients who had depressed se rum free 1,25-dihydroxyvitamin D levels throughout. Hypercalcemia did not accompany the diuretic phase of ARF. These data suggest that parat hyroid gland dysfunction is a cause of hypocalcemia in severe malaria without ARF, as seen in group 1 patients; in patients with ARF, the ef fect of the combination of phosphate retention and altered vitamin D m etabolism on skeletal PTH sensitivity is of prime significance.