Aman Pal, Emmanuel Aydin-Ghormoz, Andrea Lightle, Geovani Faddoul
{"title":"饮食诱发的高草酸尿症:基于病例的微型综述。","authors":"Aman Pal, Emmanuel Aydin-Ghormoz, Andrea Lightle, Geovani Faddoul","doi":"10.5414/CNCS111505","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Oxalate nephropathy (ON) is a rare condition involving the precipitation of calcium oxalate crystals within the nephrons. Primary hyperoxaluria involves enzymatic defects in the metabolism of glyoxylate, while secondary hyperoxaluria includes dietary and malabsorption-related etiologies.</p><p><strong>Case presentation: </strong>We discuss the case of a White male in his 80s who presented to the hospital with acute kidney injury on chronic kidney disease stage 4 in the setting of a new antibiotic prescription. Creatinine had increased to 4.2 mg/dL from a baseline of 2.2 mg/dL, with no etiology identified on urinalysis or renal ultrasound. Renal biopsy then revealed an acute tubular injury with intraluminal calcium oxalate crystals deposits, confirming a diagnosis of ON.</p><p><strong>Discussion: </strong>A detailed history revealed an excessive dietary intake of oxalate-rich foods, including nuts, and daily ingestion of 2 g of vitamin C. The patient was counselled on adjusting his diet and stopping vitamin C supplementation, which led his creatinine to return close to baseline 2 months post-discharge.</p><p><strong>Conclusion: </strong>Thorough history-taking enables early recognition and timely interventions to possibly avoid hyperoxaluria from progressing to end-stage kidney disease (ESRD).</p>","PeriodicalId":510898,"journal":{"name":"Clinical nephrology. Case studies","volume":"12 ","pages":"52-57"},"PeriodicalIF":0.0000,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465136/pdf/","citationCount":"0","resultStr":"{\"title\":\"Diet-induced hyperoxaluria: A case based mini-review.\",\"authors\":\"Aman Pal, Emmanuel Aydin-Ghormoz, Andrea Lightle, Geovani Faddoul\",\"doi\":\"10.5414/CNCS111505\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Oxalate nephropathy (ON) is a rare condition involving the precipitation of calcium oxalate crystals within the nephrons. Primary hyperoxaluria involves enzymatic defects in the metabolism of glyoxylate, while secondary hyperoxaluria includes dietary and malabsorption-related etiologies.</p><p><strong>Case presentation: </strong>We discuss the case of a White male in his 80s who presented to the hospital with acute kidney injury on chronic kidney disease stage 4 in the setting of a new antibiotic prescription. Creatinine had increased to 4.2 mg/dL from a baseline of 2.2 mg/dL, with no etiology identified on urinalysis or renal ultrasound. Renal biopsy then revealed an acute tubular injury with intraluminal calcium oxalate crystals deposits, confirming a diagnosis of ON.</p><p><strong>Discussion: </strong>A detailed history revealed an excessive dietary intake of oxalate-rich foods, including nuts, and daily ingestion of 2 g of vitamin C. The patient was counselled on adjusting his diet and stopping vitamin C supplementation, which led his creatinine to return close to baseline 2 months post-discharge.</p><p><strong>Conclusion: </strong>Thorough history-taking enables early recognition and timely interventions to possibly avoid hyperoxaluria from progressing to end-stage kidney disease (ESRD).</p>\",\"PeriodicalId\":510898,\"journal\":{\"name\":\"Clinical nephrology. Case studies\",\"volume\":\"12 \",\"pages\":\"52-57\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-10-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465136/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical nephrology. Case studies\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5414/CNCS111505\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical nephrology. Case studies","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5414/CNCS111505","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
Diet-induced hyperoxaluria: A case based mini-review.
Introduction: Oxalate nephropathy (ON) is a rare condition involving the precipitation of calcium oxalate crystals within the nephrons. Primary hyperoxaluria involves enzymatic defects in the metabolism of glyoxylate, while secondary hyperoxaluria includes dietary and malabsorption-related etiologies.
Case presentation: We discuss the case of a White male in his 80s who presented to the hospital with acute kidney injury on chronic kidney disease stage 4 in the setting of a new antibiotic prescription. Creatinine had increased to 4.2 mg/dL from a baseline of 2.2 mg/dL, with no etiology identified on urinalysis or renal ultrasound. Renal biopsy then revealed an acute tubular injury with intraluminal calcium oxalate crystals deposits, confirming a diagnosis of ON.
Discussion: A detailed history revealed an excessive dietary intake of oxalate-rich foods, including nuts, and daily ingestion of 2 g of vitamin C. The patient was counselled on adjusting his diet and stopping vitamin C supplementation, which led his creatinine to return close to baseline 2 months post-discharge.
Conclusion: Thorough history-taking enables early recognition and timely interventions to possibly avoid hyperoxaluria from progressing to end-stage kidney disease (ESRD).