Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020
The gut flora modulates intestinal barrier integrity but not progression of chronic kidney disease in hyperoxaluria-related nephrocalcinosis.
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Konrad Lukas, Andersen Kirstin, Kesper Marie Sophie, Kumar Santhosh V, Mulay Shrikant R, Anders Hans-Joachim
Аннотация
BACKGROUND: Dysbiosis, bacterial translocation and systemic inflammation have been found to be associated with human and experimental forms of chronic kidney disease (CKD), but the functional contribution of the intestinal microbiota to CKD-related intestinal barrier dysfunction and CKD progression is unknown, especially in CKD secondary to hyperoxaluria and nephrocalcinosis.
METHODS: C57BL/6N mice fed an oxalate-rich diet for either 10 or 20 days developed reversible or progressive kidney disease, respectively.
RESULTS: Oxalate-induced CKD manifested as azotaemia, renal anaemia and hyperkalaemia. CKD was associated with persistent dysbiosis and intestinal barrier dysfunction. Local as well as systemic inflammation was evident and partially persisted despite better renal function after returning to an oxalate-free diet, indicating some innate immune memory. Eradication of the microbiota with a combination of antibiotics improved intestinal barrier function but had no effect on renal function, nephrocalcinosis, kidney remodelling and atrophy compared with control mice not receiving antibiotics.
CONCLUSIONS: Together, in chronic oxalate nephropathy, the intestinal microbiota contributes to the CKD-related dysfunction of the intestinal barrier but not to the progression of nephrocalcinosis itself, as well to its related kidney atrophy and excretory dysfunction.
METHODS: C57BL/6N mice fed an oxalate-rich diet for either 10 or 20 days developed reversible or progressive kidney disease, respectively.
RESULTS: Oxalate-induced CKD manifested as azotaemia, renal anaemia and hyperkalaemia. CKD was associated with persistent dysbiosis and intestinal barrier dysfunction. Local as well as systemic inflammation was evident and partially persisted despite better renal function after returning to an oxalate-free diet, indicating some innate immune memory. Eradication of the microbiota with a combination of antibiotics improved intestinal barrier function but had no effect on renal function, nephrocalcinosis, kidney remodelling and atrophy compared with control mice not receiving antibiotics.
CONCLUSIONS: Together, in chronic oxalate nephropathy, the intestinal microbiota contributes to the CKD-related dysfunction of the intestinal barrier but not to the progression of nephrocalcinosis itself, as well to its related kidney atrophy and excretory dysfunction.