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

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 14–49ml/min/1.73m2. 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.VariableCKD (n=29)Nl (n=8)peGFR (ml/min/1.73m2)30.0 (1.7)88.6 (4.0)< 0.001[PTH]pg/ml80.6 (8.6)30.1 (3.7)0.005[25D]ng/ml35.2 (2.5)39.7 (3.4)0.4[1,25D]pg/ml42.5 (3.6)55.1 (4.8)0.1CKD (n=29)Nl (n=8)RegressionR2pR2p[PTH] on eGFR0.36< 0.0010.130.4[25D] on eGFR0.0010.90.010.8[1,25D] on eGFR0.200.0140.120.4[1,25D] on [25D]0.37< 0.0010.180.3[PTH] on [25D]0.020.50.030.7[PTH] on [1,25D]0.030.40.0030.9In 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]