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

Keyzer, Charlotte A.; Breda, G.; Vervloet, Marc G.; Jong, Maarten A. de; Laverman, Gozewijn D.; Hemmelder, Marc H; Janssen, Wmt; Heerspink, Hiddo J L; Kwakernaak, Arjan J.; Bakker, Stephan J. L.; Navis, Gerjan; Borst, Martin H. de

doi:10.1681/asn.2016040407

Cited by 36 publications

(27 citation statements)

References 50 publications

(69 reference statements)

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“…51 There was no significant association between sodium and any renal outcome (primary outcome OR, 0.99; 95% CI, 0.89-1.09 for highest [median 6.2 g/d] vs. lowest third [median 3.3 g/d]). 51 On the other hand, in a cross-over trial of 45 patients with nondiabetic CKD (stages 1-3) and 24-hour albuminuria in excess of 300 mg, Keyzer et al 52 found that moderate dietary sodium restriction substantially reduced the residual albuminuria during fixed-dose angiotensin-converting enzyme inhibition. The wide gap between available evidence and the guidelines to prevent CKD and its progression by reducing sodium intake also mirrors the controversy about the hypothesized but unproven benefit that a population-wide reduction of sodium intake would reduce blood pressure and thereby decrease cardiovascular mortality and morbidity rates.…”

Section: Discussionmentioning

confidence: 99%

Renal function in relation to sodium intake: a quantitative review of the literature

Nomura

Asayama

Jacobs

et al. 2017

Kidney International

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We undertook a quantitative literature review to search for evidence underpinning current guidelines proposing a reduction of sodium intake to less than 2.4 g/d for the management of chronic kidney disease. We searched PubMed for peer-reviewed articles published from January 1980 through May 2016. Two investigators screened 5072 publications and extracted data from 36, including 11 cross-sectional and 5 longitudinal observational studies and 20 intervention trials. Within-study effect sizes were pooled and standardized to a sodium gradient of 100 mmol/d by using inverse-variance weighted random effects models. Among cross-sectional studies, the pooled odds ratio for albuminuria was 1.23 (95% confidence interval [CI], 0.92-1.64, P = 0.16), and the pooled mean difference in glomerular filtration rate amounted to 8.5 ml/min (CI, -2.3 to 19.2 ml/min; P = 0.12). In the cohort studies, the pooled relative risk of a renal endpoint was 1.08 (CI, 0.92-1.29; P = 0.35). In the intervention trials (median duration, 14 days [range, 4-186 days]), the mean differences in estimated glomerular filtration rate and albuminuria (high vs. low sodium intake) averaged 4.6 ml/min (CI, 3.4-5.8 ml/min; P < 0.0001) and 53% (CI, 21-84; P = 0.001), respectively. Cochran's Q statistic indicated significant heterogeneity among cross-sectional studies for both estimated glomerular filtration rate and albuminuria (P < 0.0001) and among intervention trials for albuminuria (P = 0.04). In conclusion, there is no robust evidence suggesting that long-term reduction of salt intake would prevent chronic kidney disease or delay its progression. However, our current findings, which were mainly obtained in people with slight renal impairment, cannot be extrapolated to patients with moderate or severe chronic kidney disease.

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Section: Discussionmentioning

confidence: 99%

Renal function in relation to sodium intake: a quantitative review of the literature

Nomura

Asayama

Jacobs

et al. 2017

Kidney International

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“…Interventional studies have demonstrated that estimated glomerular filtration rate (eGFR) and albuminuria (proteinuria) increased with higher salt intake, and a recent study showed that reduction of sodium intake reduced albuminuria. 57 In the United Kingdom, voluntary food-manufacturing targets achieved a lower sodium intake of 15% between 2001 and 2011, which was associated with a decrease in mean BP (3 mm Hg) and 40% reduction in deaths owing to stroke and ischemic heart disease. 50,58 However, the respective role of sodium reduction versus other treatments for hypertension, dyslipidemia, and CVD are not clearly delineated.…”

Section: Prioritization Of Ckd and Detection And Investigation Of Ckdmentioning

confidence: 99%

Reducing major risk factors for chronic kidney disease

Luyckx

Tuttle

Garcia-Garcia

et al. 2017

Kidney International Supplements

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“…Several clinical studies in CKD demonstrated that sodium restriction is an effective non‐pharmacological intervention to increase RAAS blockade efficacy . In line with these observations, a recent prospective study in nondiabetic patients with CKD showed that sodium restriction significantly reduced albuminuria during RAAS blockade, while paricalcitol provided only a mild further reduction of residual albuminuria . However, the effect of paricalcitol added to sodium restriction remained significant in a per‐protocol analysis restricted to patients with more than 95% compliance with study medication .…”

Section: Discussionmentioning

confidence: 76%

Paricalcitol versus placebo for reduction of proteinuria in kidney transplant recipients: a double-blind, randomized controlled trial

et al. 2018

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Proteinuria after kidney transplantation is accompanied by an increased risk of graft failure. In this single-center, placebo-controlled, double-blind trial we studied whether vitamin D receptor activator paricalcitol might reduce proteinuria. Patients with urinary protein-to-creatinine ratio (UPCR) ≥20 mg/mmol despite optimization of the renin angiotensin aldosterone system (RAAS) blockade were randomly assigned to receive 24 weeks' treatment with 2 μg/day paricalcitol or placebo. Primary endpoint was change in UPCR, and main secondary endpoints were change in urinary albumin-to-creatinine ratio (UACR) and 24-h proteinuria. Analysis was by intention to treat. One hundred and sixty-eight patients undergo randomization, and 83 were allocated to paricalcitol, and 85 to placebo. Compared with baseline, UPCR declined in the paricalcitol group (-39%, 95% CI -45 to -31) but not in the placebo group (21%, 95% CI 9 to 35), with a between group difference of -49% (95% CI -57 to -41; P < 0.001). UACR and 24-h proteinuria decreased only on paricalcitol therapy and significantly differed between groups at end-of-treatment (P < 0.001). Paricalcitol was well tolerated but incidence of mild hypercalcemia was higher than in placebo. In conclusion, addition of 2 μg/day paricalcitol lowers residual proteinuria in kidney transplant recipients. Long-term studies are needed to determine if the reduction in proteinuria improves transplant outcomes (ClinicalTrials.gov, number NCT01436747).

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

Cited by 36 publications

References 50 publications

Renal function in relation to sodium intake: a quantitative review of the literature

Renal function in relation to sodium intake: a quantitative review of the literature

Reducing major risk factors for chronic kidney disease

Paricalcitol versus placebo for reduction of proteinuria in kidney transplant recipients: a double-blind, randomized controlled trial

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