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Kidney Week

Abstract: TH-PO846

High Salt Intake but Not High Protein Intake Leads to Increased Disease Progression in ADPKD

Session Information

Category: Genetic Diseases of the Kidneys

  • 1001 Genetic Diseases of the Kidneys: Cystic


  • Kramers, Bart J., University Medical Center Groningen, Groningen, Netherlands
  • Koorevaar, Iris Willianne, University Medical Center Groningen, Groningen, Netherlands
  • Gansevoort, Ron T., University Medical Center Groningen, Groningen, Netherlands
  • De Fijter, Johan W., Leiden University Medical Center, Leiden, Netherlands
  • Peters, Dorien J.M., Leiden University Medical Center, Leiden, Netherlands
  • Vart, Priya, Radboud University, Nijmegen, Netherlands
  • Wetzels, Jack F., Radboud University Medical Center, Nijmegen, Netherlands
  • Zietse, Robert, Erasmus Medical Center, Rotterdam, Netherlands
  • Meijer, Esther, University Medical Center Groningen, Groningen, Netherlands

In chronic kidney disease salt restriction is advocated as renoprotective treatment, especially in proteinuric diseases. Whether protein restriction is beneficial remains controversial. It has been suggested that in autosomal dominant polycystic kidney disease (ADPKD), a mostly non-proteinuric disease, moderate salt restriction may also be beneficial. We investigated the association of sodium and protein intake with rate of disease progression in ADPKD, and what mediating factors could be.


We performed a post-hoc analysis of the DIPAK-1 trial, in which 305 ADPKD patients were randomized to 2.5 years treatment with lanreotide or standard care. Blood was collected every 3 months for eGFR assessment and 3 MRI-scans were performed to analyze total kidney volume (TKV). Blood pressure and plasma copeptin (a surrogate for vasopressin) were measured at baseline. Salt and protein intake were estimated from 24h urines, which were collected 6 times and calculated per kg ideal body weight. The effect of salt and protein intake on eGFR decline and TKV growth was analyzed with mixed models. We performed mediation analyses to elucidate potential mechanisms.


Of the participants 53% was female, with an age of 48±7 yr, eGFR 51±11 mL/min/1.73m2, TKV 2.4±1.6 L, salt intake 9.5±3.9 g/day and protein intake of 87±25 g/day. Salt intake was associated with annual eGFR decline during follow-up (-0.18 mL/min/1.73m2 per gram of salt, p=0.02), whereas protein intake was not (p=0.3). Results were similar per kg ideal body weight (p=0.02 and p=0.3, respectively). The association between salt intake and annual change in TKV did not reach statistical significance (0.30% per gram of salt, p=0.07). There was also no association between total protein intake and TKV growth (p=0.1). The effect of salt intake on eGFR slope was not mediated by systolic blood pressure (3.5% mediation, p=0.3), but was significantly mediated by plasma copeptin (53% mediation, p<0.001).


Higher salt intake, but not higher protein intake may be detrimental in ADPKD. A five grams lower salt intake was associated with a 0.9 ml/min/1.73m2 lower rate of annual eGFR decline. The substantial mediation by plasma copeptin suggests that this effect is primarily a consequence of a sodium-induced rise in vasopressin.