Published online Nov 6, 2014. doi: 10.5527/wjn.v3.i4.122
Revised: June 12, 2014
Accepted: August 27, 2014
Published online: November 6, 2014
Hyperoxaluria can cause not only nephrolithiasis and nephrocalcinosis, but also renal parenchymal disease histologically characterized by deposition of calcium oxalate crystals throughout the renal parenchyma, profound tubular damage and interstitial inflammation and fibrosis. Hyperoxaluric nephropathy presents clinically as acute or chronic renal failure that may progress to end-stage renal disease (ESRD). This sequence of events, well recognized in the past in primary and enteric hyperoxalurias, has also been documented in a few cases of dietary hyperoxaluria. Estimates of oxalate intake in patients with chronic dietary hyperoxaluria who developed chronic kidney disease or ESRD were comparable to the reported average oxalate content of the diets of certain populations worldwide, thus raising the question whether dietary hyperoxaluria is a primary cause of ESRD in these regions. Studies addressing this question have the potential of improving population health and should be undertaken, alongside ongoing studies which are yielding fresh insights into the mechanisms of intestinal absorption and renal excretion of oxalate, and into the mechanisms of development of oxalate-induced renal parenchymal disease. Novel preventive and therapeutic strategies for treating all types of hyperoxaluria are expected to develop from these studies.
Core tip: Chronic nephropathy secondary to dietary hyperoxaluria has been reported in a limited number of patients. Dietary oxalate intake in these patients was lower than the average intake in certain parts of the world. This raises the question whether dietary hyperoxaluria has been a neglected cause of chronic kidney disease. This question along with recent findings elucidating the pathogenesis of oxalate nephropathy calls for further research in epidemiology, prevention and treatment of hyperoxaluria.