Salt, but not protein intake, is associated with accelerated disease progression in autosomal dominant polycystic kidney disease

The wind of change in the management of autosomal dominant polycystic kidney disease in childhood

“…Higher salt intake is prospectively associated with worse kidney outcomes in the general population [122], as well as with higher kidney volume and growth in ADPKD [123,124]. A recent study could also demonstrate a negative effect of salt intake on prospective GFR decline in adults with ADPKD with a wide range of eGFR [125], while in patients with advanced ADPKD it has been shown to increase the risk for a composite renal endpoint including death [124]. While in the general CKD population the negative effects of sodium intake are probably mediated via increased blood pressure and activation of the renin-angiotensin system, in ADPKD sodiuminduced increase of vasopressin is a likely additional mechanism leading to cyst growth [125].…”

“…A recent study could also demonstrate a negative effect of salt intake on prospective GFR decline in adults with ADPKD with a wide range of eGFR [125], while in patients with advanced ADPKD it has been shown to increase the risk for a composite renal endpoint including death [124]. While in the general CKD population the negative effects of sodium intake are probably mediated via increased blood pressure and activation of the renin-angiotensin system, in ADPKD sodiuminduced increase of vasopressin is a likely additional mechanism leading to cyst growth [125]. Unfortunately, there is a lack of prospective interventional trials [126], but counselling patients with ADPKD to adhere to recommendations on salt intake appears wise, as especially younger patients often have much higher salt intake than recommended for the general population [125].…”

“…While in the general CKD population the negative effects of sodium intake are probably mediated via increased blood pressure and activation of the renin-angiotensin system, in ADPKD sodiuminduced increase of vasopressin is a likely additional mechanism leading to cyst growth [125]. Unfortunately, there is a lack of prospective interventional trials [126], but counselling patients with ADPKD to adhere to recommendations on salt intake appears wise, as especially younger patients often have much higher salt intake than recommended for the general population [125].…”

“…However, a small interventional trial suggests the opposite clinical effect [127], so results of an ongoing larger randomized trial are eagerly awaited [128]. Others have shown that a low osmolar diet (low sodium, low protein and adjusted water intake) can decrease copeptin in adults with ADPKD [129], but protein intake itself did not correlate with GFR decline in ADPKD [125]. Also, protein restriction has potential side effects in growing children and could not be shown to slow GFR decline in a pediatric group of mixed-cause CKD [130]; therefore, low osmolar diet and protein restriction should not be recommended for children with ADPKD.…”

Urinary Potassium and Kidney Function Decline in the Population—Observational Study

“…As recently reviewed by Wey et al [ 12 ], high potassium intake stimulates natriuresis reducing the activity of the thiazide-sensitive sodium-chloride cotransporter in the kidney distal convoluted tubule. Given that high sodium intake related to greater kidney function decline in clinical studies and in population-based studies [ 28 , 46 ], the natriuretic effects of high potassium intake could be an indirect pathway linking potassium intake to kidney function decline. Other possibilities cannot be excluded.…”