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      Oxalate nephropathy: a review

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          Abstract

          This review describes the clinical and pathological features of oxalate nephropathy (ON), defined as a syndrome of decreased renal function associated with deposition of calcium oxalate crystals in kidney tubules. We review the different causes of hyperoxaluria, including primary hyperoxaluria, enteric hyperoxaluria and ingestion-related hyperoxaluria. Recent case series of biopsy-proven ON are reviewed in detail, as well as the implications of these series. The possibility of antibiotic use predisposing to ON is discussed. Therapies for hyperoxaluria and ON are reviewed with an emphasis on newer treatments available and in development. Promising research avenues to explore in this area are discussed.

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          Lumasiran, an RNAi Therapeutic for Primary Hyperoxaluria Type 1

          Sander F. Garrelfs, Yaacov Frishberg, Sally Hulton … (2021)
          Primary hyperoxaluria type 1 (PH1) is a rare genetic disease caused by hepatic overproduction of oxalate that leads to kidney stones, nephrocalcinosis, kidney failure, and systemic oxalosis. Lumasiran, an investigational RNA interference (RNAi) therapeutic agent, reduces hepatic oxalate production by targeting glycolate oxidase.
          Article 0 comments Cited 136 times – based on 0 reviews     Review now
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            Primary hyperoxaluria.

            Pierre Cochat, Gill Rumsby (2013)
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              Gastrointestinal complications of diabetes mellitus.

              Babu Krishnan, Shithu Babu, Jessica Walker … (2013)
              Diabetes mellitus affects virtually every organ system in the body and the degree of organ involvement depends on the duration and severity of the disease, and other co-morbidities. Gastrointestinal (GI) involvement can present with esophageal dysmotility, gastro-esophageal reflux disease (GERD), gastroparesis, enteropathy, non alcoholic fatty liver disease (NAFLD) and glycogenic hepatopathy. Severity of GERD is inversely related to glycemic control and management is with prokinetics and proton pump inhibitors. Diabetic gastroparesis manifests as early satiety, bloating, vomiting, abdominal pain and erratic glycemic control. Gastric emptying scintigraphy is considered the gold standard test for diagnosis. Management includes dietary modifications, maintaining euglycemia, prokinetics, endoscopic and surgical treatments. Diabetic enteropathy is also common and management involves glycemic control and symptomatic measures. NAFLD is considered a hepatic manifestation of metabolic syndrome and treatment is mainly lifestyle measures, with diabetes and dyslipidemia management when coexistent. Glycogenic hepatopathy is a manifestation of poorly controlled type 1 diabetes and is managed by prompt insulin treatment. Though GI complications of diabetes are relatively common, awareness about its manifestations and treatment options are low among physicians. Optimal management of GI complications is important for appropriate metabolic control of diabetes and improvement in quality of life of the patient. This review is an update on the GI complications of diabetes, their pathophysiology, diagnostic evaluation and management.
              Article 0 comments Cited 57 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Kidney J
                Journal ID (iso-abbrev): Clin Kidney J
                Journal ID (publisher-id): ckj
                Title: Clinical Kidney Journal
                Publisher: Oxford University Press
                ISSN (Print): 2048-8505
                ISSN (Electronic): 2048-8513
                Publication date Collection: February 2022
                Publication date (Electronic): 12 August 2021
                Publication date PMC-release: 12 August 2021
                Volume: 15
                Issue: 2
                Pages: 194-204
                Affiliations
                [1 ] Division of Nephrology, Lenox Hill Hospital, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell , New York, NY, USA
                [2 ] Department of Pathology, North Shore University Hospital and Long Island Jewish Medical Center, Donald and Barbara Zucker School of Medicine at Hostra/Northwell , New York, USA
                [3 ] Division of Kidney Diseases and Hypertension, North Shore University Hospital and Long Island Jewish Medical Center, Donald and Barbara Zucker School of Medicine at Hostra/Northwell , New York, NY, USA
                Author notes
                Correspondence to: Jordan L. Rosenstock; E-mail: jrosenstock@ 123456northwell.edu
                Article
                Publisher ID: sfab145
                DOI: 10.1093/ckj/sfab145
                PMC ID: 8825217
                PubMed ID: 35145635
                SO-VID: 2e265aef-6d4c-4d9b-966c-eeefa338f7a1
                Copyright © © The Author(s) 2021. Published by Oxford University Press on behalf of the ERA.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Date received : 02 February 2021
                Date accepted : 21 July 2021
                Date: 15 December 2021
                Page count
                Pages: 11
                Categories
                Subject: CKJ Review
                Subject: AcademicSubjects/MED00340

                ScienceOpen disciplines: Nephrology
                Keywords: acute kidney injury,oxalate nephropathy,pathology,primary hyperoxaluria,secondary hyperoxaluria
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: acute kidney injury, oxalate nephropathy, pathology, primary hyperoxaluria, secondary hyperoxaluria

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