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Abstract
BackgroundVitamin D receptor activators reduce albuminuria, and may improve survival in chronic kidney disease (CKD). Animal studies suggest that these pleiotropic effects of vitamin D may be mediated by suppression of renin. However, randomized trials in humans have yet to establish this relationship.MethodsIn a randomized, placebo-controlled, double-blinded crossover study, the effect of oral paricalcitol (2 μg/day) was investigated in 26 patients with non-diabetic, albuminuric stage III-IV CKD. After treatment, plasma concentrations of renin (PRC), angiotensin II (AngII) and aldosterone (Aldo) were measured. GFR was determined by 51Cr-EDTA clearance. Assessment of renal NO dependency was performed by infusion of NG-monomethyl-L-arginine (L-NMMA). Albumin excretion rate (AER) was analyzed in 24-h urine and during 51Cr-EDTA clearance.ResultsParicalcitol did not alter plasma levels of renin, AngII, Aldo, or urinary excretion of sodium and potassium. A modest reduction of borderline significance was observed in AER, and paricalcitol abrogated the albuminuric response to L-NMMA.ConclusionsIn this randomized, placebo-controlled trial paricalcitol only marginally decreased AER and did not alter circulating levels of renin, AngII or Aldo. The abrogation of the rise in albumin excretion by paricalcitol during NOS blockade may indicate that favourable modulation of renal NO dependency could be involved in mediating reno-protection and survival benefits in CKD.Trial registrationClinicalTrials.gov identifier: NCT01136564
Highlights
Vitamin D receptor activators reduce albuminuria, and may improve survival in chronic kidney disease (CKD)
Hemodynamic and non-hemodynamic effects of paricalcitol were assessed by measurement of 24-hour ambulatory BP (24-h BP), arterial stiffness, GFR, albumin excretion rate, renal sodium and potassium excretion, and plasma concentrations of angiotensin II (AngII), aldosterone (Aldo), vasopressin (AVP), brain natriuretic peptide (BNP) and fibroblast growth factor 23 (FGF23)
These subjects did not differ from the overall study population regarding age, Estimate GFR (eGFR) and baseline albuminuria
Summary
Vitamin D receptor activators reduce albuminuria, and may improve survival in chronic kidney disease (CKD). Animal studies suggest that these pleiotropic effects of vitamin D may be mediated by suppression of renin. Vitamin D receptor activators (VDRAs) have been used in the management of secondary hyperparathyroidism in chronic kidney disease (CKD) for several decades [1]. Conclusions from animal studies strongly suggest that vitamin D’s proposed reno-protective properties may be mediated by Despite pharmacological advances in the treatment of renal disease, the progressive nature of CKD still warrants new strategies to preserve kidney function. Placebo-controlled, double-blind crossover trial, we wanted to test the hypothesis that paricalcitol decreases albuminuria in CKD by suppressing plasma renin. We hypothesized that paricalcitol modulates renal NO bioavailability. Hemodynamic and non-hemodynamic effects of paricalcitol were assessed by measurement of 24-hour ambulatory BP (24-h BP), arterial stiffness, GFR, albumin excretion rate, renal sodium and potassium excretion, and plasma concentrations of angiotensin II (AngII), aldosterone (Aldo), vasopressin (AVP), brain natriuretic peptide (BNP) and fibroblast growth factor 23 (FGF23)
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