To035calcium Oxalate Crystals Promote Cytogenesis and Aggravate Polycystic Kidney Disease

Rezaei, Mina; Torres, Jacob A.; Lin, Louis M.; Broderick, Caroline; Cowley, Benjamin D.; Torres, Vicente E.; Khan, Saeed R.; Weimbs, Thomas

doi:10.1093/ndt/gfx133.to035

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“…In pcy/pcy PKD mice, a low phosphate diet resulted in slower polycystic kidney size, cystic index, and kidney fibrosis [137]. In experimental rat PKD, high phosphate diets caused calcium phosphate crystal deposition in collecting ducts, accelerating disease progression [138]. This is interesting in view of the reported higher phosphate urine clearance in early ADPKD [107]; the issue might not be as much from a systemic positive phosphate balance but from excess urinary phosphate.…”

Section: What Did We Learn From Recent Preclinical Studies?mentioning

confidence: 99%

“…ADPKD patients are at increased risk of kidney stone formation and there is recent interest of how urinary crystal formation may promote CKD progression [141,142]. In PKD rats, increased urinary calcium oxalate crystals promoted cystogenesis and PKD progression in male but not female animals [138] This finding may also have dietary implications. Thus, current dietary trends such as “juicing” which the general population may consider a healthy lifestyle to increase vegetable intake, has already been associated to kidney damage by oxalate crystals [143,144,145].…”

Section: What Did We Learn From Recent Preclinical Studies?mentioning

confidence: 99%

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Dietary Care for ADPKD Patients: Current Status and Future Directions

et al. 2019

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Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic nephropathy, and tolvaptan is the only therapy available. However, tolvaptan slows but does not stop disease progression, is marred by polyuria, and most patients worldwide lack access. This and recent preclinical research findings on the glucose-dependency of cyst-lining cells have renewed interest in the dietary management of ADPKD. We now review the current dietary recommendations for ADPKD patients according to clinical guidelines, the evidence base for those, and the potential impact of preclinical studies addressing the impact of diet on ADPKD progression. The clinical efficacy of tolvaptan has put the focus on water intake and solute ingestion as modifiable factors that may impact tolvaptan tolerance and ADPKD progression. By contrast, dietary modifications suggested to ADPKD patients, such as avoiding caffeine, are not well supported and their impact is unknown. Recent studies have identified a chronic shift in energy production from mitochondrial oxidative phosphorylation to aerobic glycolysis (Warburg effect) as a contributor to cyst growth, rendering cyst cells exquisitely sensitive to glucose availability. Therefore, low calorie or ketogenic diets have delayed preclinical ADPKD progression. Additional preclinical data warn of potential negative impact of excess dietary phosphate or oxalate in ADPKD progression.

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Section: What Did We Learn From Recent Preclinical Studies?mentioning

confidence: 99%