HIGH-DOSE PHOSPHATE TREATMENT LEADS TO HYPOKALEMIA IN HYPOPHOSPHATEMIC OSTEOMALACIA

The mechanism of the decrease in plasma potassium induced by phosphate treatment was investigated in a 24-year-old hypertensive patient with hypophosphatemic osteomalacia, who was the youngest of four patients, belonging to a 23 number kindred of five generations. Parameters of p otassium, sodium, calcium, and phosphate metabolism as well as specifi c renal functions have been studied in the basal state and during admi nistration of graded doses of phosphate (500-6000 mg). Progressive hyp okalemia developed during phosphate treatment. An inverse correlation was found between plasma potassium and doses of phosphate (plasma pota ssium = -0.2 g phosphate + 3.9 r = -0.49; p < 0.05; N = 21). A renal r oute of potassium loss was suspected, but could not be confirmed as po tassium excretion did not increase although sodium excretion was augme nted [basal sodium output: 56.7 mmol/24 h; phosphate treatment: 153 mm ol/24 h (p < 0.05)]. Transtubular potassium gradient (TTKG) also decre ased and an inverse correlation was found between TTKG and doses of ph osphate (r = -0.37; p < 0.02; N = 38). Decrease of TTKG was possibly t he result of suppressed K+ secretion. It was concluded that potassium loss occurred by a non-renal (intestinal) route in phosphate-induced h ypokalemia. Although major hazards of treatment of hypophosphatemic os teomalacia with phosphate and calcitriol an secondary hyperparathyroid ism and vitamin D intoxication, potassium loss also should be kept in mind.