EFFECTS OF PARATHYROID-HORMONE AND 1,25(OH2)D-3 ON PROTEIN GLYCATION IN MODERATE UREMIA

Glucose intolerance in uraemia may be a consequence of secondary hyper parathyroidism. In this study fructosamine and glycated albumin have b een used as markers of long-term glycaemic control in a group of pre-e nd-stage, non-diabetic uraemic patients with secondary hyperparathyroi dism. The serum fructosamine level (mu mol/100 g total protein) was si gnificantly higher (p = 0.005) in uraemic patients (364 +/- 42) than i n a group of 25 non-uraemic controls (332 +/- 27), but the content of glycated albumin did not differ (p > 0.05; 1.6 +/- 0.5 vs. 1.5 +/- 0.3 %). In the uraemic patients, there was a significant relationship betw een serum 1,25-dihydroxycholecalciferol [1,25(OH2)D] (median 4.2, rang e 1.0-38 ng/l) and fructosamine (r = -0.66, p < 0.01; fructosamine = - 2.76 1,25(OH2)D + 389), but not glycated albumin (r = -0.22, p > 0.1). No relationship existed between serum parathyroid hormone (median 15. 4, range 7.0-55 pmol/l) and either glycated albumin or fructosamine (p > 0.1). In patients treated with oral calcitriol (0.25 mu g/day), sig nificant reductions in serum parathyroid hormone after both 4 (p = 0.0 3) and 8 weeks (p = 0.02) and concomitant increases in serum 1,25(OH2) D (p < 0.02) after 8 weeks of treatment were not accompanied by any ch ange in fructosamine, glycated albumin, total calcium, or ionized calc ium (p > 0.05). Elevation of serum fructosamine in these patients is c onsistent with the impaired glucose tolerance of uraemia. The evidence presented supports a relationship between long-term glycaemic control and 1,25(OH2)D-3, but not parathyroid hormone, in moderately uraemic patients with secondary hyperparathyroidism; however, serum fructosami ne was not altered by treatment with calcitriol over an 8-week period.