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.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220346 | PMC |
http://dx.doi.org/10.5527/wjn.v3.i4.122 | DOI Listing |
Introduction: Free radical-mediated oxidative renal tubular injury secondary to hyperoxaluria is a proposed mechanism in the formation of calcium oxalate stones. Vitamin E, an important physiologic antioxidant, has been shown in rat models to prevent calcium oxalate crystal deposition. Our objective was to determine if low dietary vitamin E intake was associated with a higher incidence of stones.
View Article and Find Full Text PDFUrolithiasis
December 2024
The Stone Centre at Vancouver General Hospital, Department of Urologic Sciences, University of British Columbia, Jack Bell Research Centre, 2660 Oak Street, Vancouver, BC, V6H 3Z6, Canada.
Currently available animal models for calcium oxalate kidney stones are limited in their translational potential. Particularly with increasing interest in gut microbiota involvement in kidney stone disease, there are limited animal models which can be used. As such, we have developed a novel diet-induced hyperoxaluria murine model which addresses some of the shortcomings of other currently available models.
View Article and Find Full Text PDFPediatr Nephrol
December 2024
Department of Pediatrics, Aster MIMS (Malabar Institute of Medical Sciences), Calicut, Kerala, India, 673016.
A 3-month-old girl presented with symptoms indicative of dysuria, gross hematuria, chronic diarrhea, and nephrocalcinosis. She was born to fourth-degree consanguineous parents. The infant exhibited hypercalciuria and hyperoxaluria, and her stool tested positive for reducing sugars.
View Article and Find Full Text PDFKidney Int Rep
November 2024
Division of Pediatric Nephrology and Hypertension, Mayo Clinic Children's Center, Rochester, Minnesota, USA.
Hyperoxaluria is a condition in which there is a pathologic abundance of oxalate in the urine through either hepatic overproduction (primary hyperoxaluria [PH]) or excessive enteric absorption of dietary oxalate (enteric hyperoxaluria [EH]). Severity can vary with the most severe forms causing kidney failure and extrarenal manifestations. To address the current challenges and innovations in hyperoxaluria, the 14th International Hyperoxaluria Workshop convened in Perugia, Italy, bringing together international experts for focused presentation and discussion.
View Article and Find Full Text PDFClin Nephrol Case Stud
October 2024
Department of Medicine, Division of Nephrology and Hypertension Care, and.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!