Treatment of primary hyperoxaluria.

progress are discussed in relation to the known natural history of the disease. 6 of them probably have the usual form of primary hyperoxaluria associated with increased glycollic acid excretion, while 3 who are sibs have the recently described variant associated with L-glyceric aciduria and normal glycollic acid excretion. All 9 patients have been on regimens designed to increase the urinary solubility of calcium oxalate, with or without the simultaneous lowering of urinary calcium and raising of urinary phosphate excretions. 8 patients have been treated for 1 -7j years (average duration 4 years) with oral magnesium hydroxide, and 2 patients have been treated with sodium phosphate. One of the latter was changed after 31 years to magnesium hydroxide and the other has been on sodium phosphate combined with a low calcium diet and cellulose phosphate continuously for 5j years. 2, not at first diagnosed as hyperoxalurics, were first given sodium bicarbonate for their presumably secondary renal tubular acidosis. The over-all progress of the whole group is felt to have been better than could be expected from the known natural history of primary hyperoxaluria. They average 41 years on treatment during 5 years of our observation and all remain clinically well after an average of 9i years since the onset of their first symptoms. Results warrant the recommendation that, until reliable means are available to decrease oxalate overproduction, affected patients should be treated continuously with magnesium hydroxide. A more final opinion must await many more years of follow-up. The failure of several attempts to lower urinary oxalate excretion in these patients is also reported.