Plasma Vitamin D Level and Change in Albuminuria and eGFR According to Sodium Intake

Abstract

Background and objectives Low circulating 25-hydroxyvitamin D [25(OH)D] and high sodium intake are both associated with progressive albuminuria and renal function loss in CKD. Both vitamin D and sodium intake interact with the renin-angiotensin-aldosterone system. We investigated whether plasma 25(OH)D or 1,25-dihydroxyvitamin D [1,25(OH) 2 D] is associated with developing increased albuminuria or reduced renal function and whether these associations depend on sodium intake.Design, setting, participants, & measurements Baseline plasma 25(OH)D and 1,25(OH) 2 D were measured by liquid chromatography tandem mass spectrometry, and sodium intake was assessed by 24-hour urine collections in the general population-based Prevention of Renal and Vascular End-Stage Disease cohort (n=5051). Two primary outcomes were development of urinary albumin excretion .30 mg/24 h and eGFR (creatinine/cystatin C-based CKD Epidemiology Collaboration) ,60 ml/min per 1.73 m 2 . Participants with CKD at baseline were excluded. In Cox regression analyses, we assessed associations of vitamin D with developing increased albuminuria or reduced eGFR and potential interaction with sodium intake.Results During a median follow-up of 10.4 (6.2-11.4) years, 641 (13%) participants developed increased albuminuria, and 268 (5%) participants developed reduced eGFR. Plasma 25(OH)D was inversely associated with increased albuminuria (fully adjusted hazard ratio [HR] per SD higher, 0.86; 95% confidence interval [95% CI], 0.78 to 0.95; P=0.003) but not reduced eGFR (HR, 0.99; 95% CI, 0.87 to 1.12; P=0.85). There was interaction between 25(OH)D and sodium intake for risk of developing increased albuminuria (P interaction =0.03). In participants with high sodium intake, risk of developing increased albuminuria was inversely associated with 25(OH)D (lowest versus highest quartile: adjusted HR, 1.81; 95% CI, 1.20 to 2.73, P,0.01), whereas this association was nonsignificant in participants with low sodium intake (HR, 1.29; 95% CI, 0.94 to 1.77; P=0.12). Plasma 1,25(OH) 2 D was not significantly associated with increased albuminuria or reduced eGFR.Conclusions Low plasma 25(OH)D is associated with higher risk of developing increased albuminuria, particularly in individuals with high sodium intake, but not of developing reduced eGFR. Plasma 1,25(OH)2D is not associated with risk of developing increased albuminuria or reduced eGFR.

Effects of Vitamin D Receptor Activation and Dietary Sodium Restriction on Residual Albuminuria in CKD: The ViRTUE-CKD Trial

“…In line with this assumption, we recently found that dietary sodium restriction potentiates the antiproteinuric and renoprotective efficacy of VDRA treatment in a rat model of proteinuric nephropathy 19 and that sodium intake modulates the inverse association between plasma vitamin D levels and the risk of developing increased albuminuria in the general population. 20 At variance, however, a post hoc analysis of the VITamin D receptor activator for Albuminuria Lowering (VITAL) trial 16 as well as an observational study in nondiabetic CKD 21 suggested that patients with albuminuria and higher baseline dietary sodium intake had a stronger antiproteinuric response to VDRA treatment than those with lower baseline sodium intake.…”

Determining the Levels of Vitamin D and Parathyroid Hormone in Patients on Hemodialysis

“…The increased synthesis and secretion of PTH stimulates hypocalcemia, hyperphosphatemia and vitamin D defi ciency [16,17]. It is diffi cult to explain if hypocalcemia is not associated with the deposition of calcium in vessels and tissues in our patients, which is mentioned by other authors [3,4,9,[18][19][20][21].…”

Stirring the Pot: Can Dietary Modification Alleviate the Burden of CKD?

“…Coronary artery calcification has been reported in patients with CKD [82], and calcium phosphate levels have been shown to correlate with increased mortality risk in HD patients [83]. Low plasma 25(OH)D is also associated with a higher risk of developing increased albuminuria, particularly in individuals with high sodium intake [84]. Thus it is thought that correcting vitamin D levels may reduce PTH levels, correct alterations in bone turnover and calcium metabolism, and subsequently reduce mortality in the CKD population.…”