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Intestinal adaptations in chronic kidney disease and the influence of gastric bypass surgery
Author(s) -
Hatch Marguerite
Publication year - 2014
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2014.078782
Subject(s) - oxalate , kidney stones , kidney , medicine , endocrinology , kidney disease , excretion , context (archaeology) , calcium oxalate , urinary system , chemistry , biology , paleontology , organic chemistry
New FindingsWhat is the topic of this review? This review primarily focuses on the compensatory adaptations in gastrointestinal oxalate transport that can impact urinary oxalate excretion in the context of hyperoxaluria, a major risk factor in kidney stone disease. What advances does it highlight? The intestine, which is generally considered an absorptive organ, contributes to oxalate homeostasis by playing a role in enteric elimination/excretion of oxalate that has beneficial effects, especially when renal function is compromised. Conversely, when enteric elimination of oxalate is promoted, urinary oxalate can be reduced even in hyperoxaluric conditions. This report highlights the physiological signalling between the kidney and the gut and vice versa.Studies have shown that compensatory adaptations in gastrointestinal oxalate transport can impact the amount of oxalate excreted by the kidney. Hyperoxaluria is a major risk factor in the formation of kidney stones, and oxalate is derived from both the diet and the liver metabolism of glyoxylate. Although the intestine generally absorbs oxalate from dietary sources and can contribute as much as 50% of urinary oxalate, enteric oxalate elimination plays a significant role when renal function is compromised. While the mechanistic basis for these changes in the direction of intestinal oxalate movements in chronic renal failure involves an upregulation of angiotensin II receptors in the large intestine, enteric secretion/excretion of oxalate can also occur by mechanisms that are independent of angiotensin II. Most notably, the commensal bacterium Oxalobacter sp. interacts with the host enterocyte and promotes the movement of oxalate from the blood into the lumen, resulting in the beneficial effect of significantly lowering urinary oxalate excretion. Changes in the passive permeability of the intestine, such as in steatorrhoea and following gastric bypass, also promote oxalate absorption and hyperoxaluria. In summary, this report highlights the two‐way physiological signalling between the gut and the kidney, which may help to alleviate the consequences of certain kidney diseases.