Relationships among egfr, vitamin d metabolites and pth 1-84 in ckd.

Abstract

Vitamin D undergoes 25-hydroxylation in the liver (25D) and 1-alpha hydroxylation in the kidney (1,25D). Both [25D] and [1,25D] fell with GFR in surveys of patients with CKD. Because 1,25D suppresses transcription of the PTH gene, low [1,25D] is thought to be a cause of high [PTH] in CKD. To examine relationships among eGFR, [PTH] 1–84 (Scantibodies), [25D], and [1,25D], we studied 8 normal subjects with eGFR 73–103 and 29 patients with eGFR 14–49 ml/min/1.73 m2. Most patients had been taking supplemental vitamin D. Means (SEM) were compared by two-tailed t-test, and regressions were examined as indicated below. Results are summarized in the tables. Variable CKD (n=29) Nl (n=8) p eGFR (ml/min/1.73 m2) 30.0 (1.7) 88.6 (4.0) < 0.001 [PTH] pg/ml 80.6 (8.6) 30.1 (3.7) 0.005 [25D] ng/ml 35.2 (2.5) 39.7 (3.4) 0.4 [1,25D] pg/ml 42.5 (3.6) 55.1 (4.8) 0.1 CKD (n=29) Nl (n=8) Regression R2 p R2 p [PTH] on eGFR 0.36 < 0.001 0.13 0.4 [25D] on eGFR 0.001 0.9 0.01 0.8 [1,25D] on eGFR 0.20 0.014 0.12 0.4 [1,25D] on [25D] 0.37 < 0.001 0.18 0.3 [PTH] on [25D] 0.02 0.5 0.03 0.7 [PTH] on [1,25D] 0.03 0.4 0.003 0.9In comparison to normal subjects, patients with CKD had lower eGFR, higher [PTH], and similar [25D] and [1,25D]. In the patients with CKD, [1,25D] varied directly and [PTH] inversely with eGFR. Unlike [1,25D], [25D] was not associated with eGFR, but [1,25D] nevertheless correlated strongly with [25D]. [PTH] was not related to [25D] or [1,25D]. In our patients with CKD, many of whom were vitamin D-replete, [25OHD] was the principal determinant of [1,25D]. Increased [PTH] could not be attributed to decreased [1,25D].