Objectives: To examine the effects of dietary manipulation and pyridoxine medical management for idiopathic hyperoxaluria in patients with nephrolithiasis.
Methods: A retrospective longitudinal study of the patients treated in our stone clinics from July 2007 to February 2009 was performed. All patients were evaluated with pre- and postintervention 24-hour urine collection and met a registered dietician. Recommendations to keep urine volume above 2 L per day, sodium restriction, protein moderation, increased calcium intake with meals and low oxalate diet combined with oral pyridoxine were given. Initial dosage ranged from 50 to 100 mg per day depending on the baseline oxalate level, and was titrated to a maximum of 200 mg daily. Subjects with at least two 24-hour urine collections were included in the study.
Results: Of 314 patients with complete metabolic and urinary profile evaluation, 95 subjects were identified with idiopathic hyperoxaluria. Mean follow-up was 18.4 ± 14.8 months and mean age was 50.3 ± 12.8 years. In patients treated with the combination of dietary counseling and pyridoxine, there was a significant change in urinary parameters in 75% of patients with a significant decrease in urinary oxalate excretion (58.26 ± 27.05 to 40.61 ± 15.04, P < .0001). In all, 39% of the patients had a decrease from a high urine oxalate levels (>40 mg/d) to a normal range urine oxalate (55.30 ± 22.04 to 33.45 ± 3.93, P = .0004). No peripheral neuropathy was reported.
Conclusions: Dietary management and medical treatment using pyridoxine may be an effective first-line therapy to decrease hyperoxaluria in patients who form stones.
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http://dx.doi.org/10.1016/j.urology.2010.08.002 | DOI Listing |
Nephrology (Carlton)
December 2024
Department of Clinical Pharmacy, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Magnes Res
July 2024
Department of Clinical Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.
Magnesium is one of the recommended treatments for calcium stone formers (CSFs) with hyperoxaluria. In this study, we compared the effect of magnesium oxide (MgO) or magnesium citrate (MgCit) with placebo on 24-hour urine (24-U) metabolites and the calcium oxalate supersaturation index (CaOx SS). In a randomized, double-blind, placebo-controlled clinical trial, 90 CSFs with idiopathic hyperoxaluria were recruited from a tertiary stone prevention clinic.
View Article and Find Full Text PDFKidney Int Rep
June 2024
Department of Medicine, Division of Nephrology, NYU Langone Medical Center, New York, New York, USA.
Introduction: Hyperoxaluria is a risk factor for kidney stone formation and chronic kidney disease progression. The microbiome is an important protective factor against oxalate accumulation through the activity of its oxalate-degrading enzymes (ODEs). In this cross-sectional study, we leverage multiomics to characterize the microbial community of participants with primary and enteric hyperoxaluria, as well as idiopathic calcium oxalate kidney stone (CKS) formers, focusing on the relationship between oxalate degrading functions of the microbiome.
View Article and Find Full Text PDFMayo Clin Proc
April 2024
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.
Objective: To report the clinicopathologic characteristics, prognostic indicators, prognosis, and transplant outcome of secondary oxalate nephropathy (ON).
Patients And Methods: We performed a retrospective analysis of 113 consecutive patients with secondary ON diagnosed at Mayo Clinic in Rochester, Minnesota, between January 1, 2001, and March 1, 2023.
Results: The incidence of secondary ON among all native biopsies from Mayo Clinic patients over the study period (n=11,617) was 0.
Cureus
July 2023
Nephrology, Washington University School of Medicine, Saint Louis, USA.
Oxalate nephropathy represents a frequently overlooked etiology of renal failure, characterized by the deposition of calcium oxalate crystals within the renal parenchyma. This progressive form of kidney disease is marked by a significant increase in serum creatinine (Cr) level accompanied by evidence of oxalate crystal deposition on renal biopsy causing tubular obstruction and tubular injury leading to fibrosis. In all instances of oxalate nephropathy, examination of stones consistently exhibits multiple birefringent calcium oxalate crystals under polarized light.
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