Relationships among eGFR, vitamin D metabolites, and PTH 1-84 in chronic kidney disease

摘要

Vitamin D undergoes 25-hydroxylation in the liver (25D) and 1-alpha hydroxy-lation in the kidney (1,25D). Both [25D] and [L25D] 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, [25D], and [1,25D], we studied 14 normal subjects with eGFR 73-103 and 30 patients with eGFR 14-49 ml/min/1.73m2. Most patients had been taking supplemental vitamin D. Means were compared by two-tailed t-test. The following linear regressions were examined: [PTH], [25D], and [1,25D] on eGFR; [1,25D] and [PTH] on [25D]; and [PTH] on [1,25D].In comparison to normal subjects, patients with CKD had lower eGFR, higher [PTH], and similar [25D] and [L25D]. 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, [25D] was the principal determinant of [1,25D]. Increased [PTH] could not be attributed to decreased [1,25D].