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 rhabdomyolysis. As renal impairment commonly accompanies severe malaria in the absence of rhabdomyolysis, falciparum malaria provides an alternative model 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 six required dialysis (group 2b). Group 1 patients presented with mild hypocalcemia (mean +/- SD serum ionized calcium, 1.18 +/- 0.05 vs. 1.23 +/- 0.02 mmol/L in controls; P = 0.01) that persisted until discharge in the presence of normal serum phosphate, PTH, and vitamin D metabolite levels. Group 2 patients were more hypocalcemic on admission (1.10 +/- 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 renal dysfunction was maximal. In group 2 patients, the admission serum PTH 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 serum phosphate occurred only in group 2b patients who had depressed serum free 1,25-dihydroxyvitamin D levels throughout. Hypercalcemia did not accompany the diuretic phase of ARF. These data suggest that parathyroid gland dysfunction is a cause of hypocalcemia in severe malaria without ARF, as seen in group 1 patients; in patients with ARF, the effect of the combination of phosphate retention and altered vitamin D metabolism on skeletal PTH sensitivity is of prime significance.