| Summary: | 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].
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