Chronic hypophosphatemia in the renal homograft recipient.

Tubular dysfunctions of renal homograft cases have been reported from several aspects (I). However, chronic hypophosphatemia of the kidney transplant recipient is a relatively new topic (4). It is encountered frequently and is considered to be very important in differential diagnosis of persistent hyperparathyroidism. We studied this chronic hypophosphatemia in our intrafamiliar renal homograft recipients. SUBJECTS AND METHOD 83 Since June, 1972, 109 renal homografts have been transplanted at our two facilities (98 cases from living-related donors and II cases from cadaveric donors). For this series 32 living-related cases were selected who had a minimum follow-up period of longer than one year, stable and· good kidney functions (serum creatinine levels below 2.0 mgt dl) and were on regular diet without taking any phosphate-binding antiacids. The patients were divided into three groups according to their serum phosphate levels (serum and urine phosphate levels were measured by SMA-phosphomolybdate with reduction method). Group I (hypophosphatemic, serum phosphate below 2.5 mgt dl): 9 cases. Group II (intermediate, serum phosphate around 3.0 mgt dl): 18 cases. Group III (normal, serum phosphate between 3.2 mgt dl and 4.4 mgt dl): 10 cases. The following items were compared in the above three groups: serum calcium levels measured by SMA-OCPC method, tubular resorption of phosphate (% T.R.P.) (3), phosphate excretion index (P.E.I.) (6), twenty-four hour urinary excretion of Ihmicroglobulin (5), serum parathyroid hormone (P.T.H.) (7), and serum la'25(OHhD3 (2). RESULTS Although the serum calcium levels were compared in these groups, they all were within the normal ranges (between 8.5 mgt dl and 10.5 mgt dl) and showed no significant differences. The % T.R.P. level displayed remarkable differences in the three groups, and P.E.I. Received for Publication December 15, 1981