2020/06/10 by Bart J. Kramers, Iris W. Koorevaar, Joost P.H. Drenth +8 · 72 citations
Biochemistry, Genetics and Molecular Biology · Medicine · #Albuminuria #Autosomal dominant polycystic kidney disease #Confidence interval #Copeptin #Endocrinology #Genetic and Kidney Cyst Diseases #Internal medicine #Kidney #Kidney disease #Medicine #Pediatric Urology and Nephrology Studies #Renal Diseases and Glomerulopathies #Renal function #Vasopressin
paper · pdf · doi:10.1016/j.kint.2020.04.053
published in Kidney International 98(4), 989-998 (Elsevier BV)
openalex publication_date 2020/06/10 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/04
In autosomal dominant polycystic kidney disease (ADPKD), there are only scarce data on the effect of salt and protein intake on disease progression. Here we studied association of these dietary factors with the rate of disease progression in ADPKD and what the mediating factors are by analyzing an observational cohort of 589 patients with ADPKD. Salt and protein intake were estimated from 24-hour urine samples and the plasma copeptin concentration measured as a surrogate for vasopressin. The association of dietary intake with annual change in the estimated glomerular filtration rate (eGFR) and height adjusted total kidney volume (htTKV) growth was analyzed with mixed models. In case of significant associations, mediation analyses were performed to elucidate potential mechanisms. These patients (59% female) had a mean baseline age of 47, eGFR 64 mL/min/1.73m 2 and the median htTKV was 880 mL. The mean estimated salt intake was 9.1 g/day and protein intake 84 g/day. During a median follow-up of 4.0 years, eGFR was assessed a median of six times and 24-hour urine was collected a median of five times. Salt intake was significantly associated with annual change in eGFR of −0.11 (95% confidence interval 0.20 – −0.02] mL/min/1.73m 2 ) per gram of salt, whereas protein intake was not (−0.00001 [−0.01 – 0.01] mL/min/1.73m 2 ) per gram of protein). The effect of salt intake on eGFR slope was significantly mediated by plasma copeptin (crude analysis: 77% mediation, and, adjusted analysis: 45% mediation), but not by systolic blood pressure. Thus, higher salt, but not higher protein intake may be detrimental in ADPKD. The substantial mediation by plasma copeptin suggests that this effect is primarily a consequence of a salt-induced rise in vasopressin.