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      Idiopathic Oxalate Nephropathy Leading to End-Stage Kidney Disease: A Case Report

      case-report
      Author(s): 1 , 2 , 3 , , 4 , 5 , 6 , 1
      Editor(s): ,
      Publication date (Electronic, pub):
      Publication date (Electronic, collection):
      Journal: Cureus
      Publisher: Cureus
      Keywords: end stage kidney disease (eskd), idiopathic hyperoxaluria, primary hyperoxaluria, oxalate nephropathy, aki

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          Abstract

          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. This case report details the clinical course of a patient who initially presented with progressively worsening renal function and ultimately developed end-stage kidney disease (ESKD) as a consequence of idiopathic hyperoxaluria.

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          Molecular mechanisms of crystal-related kidney inflammation and injury. Implications for cholesterol embolism, crystalline nephropathies and kidney stone disease.

          Shrikant Mulay, Andrew P Evan, Hans-Joachim Anders (2014)
          Crystals are particles of endogenous inorganic or organic composition that can trigger kidney injury when deposited or formed inside the kidney. While decades of research have focused on the molecular mechanisms of solute supersaturation and crystal formation, the pathomechanisms of crystal-induced renal inflammation remain largely unknown. The recent discovery of the intracellular NLRP3 inflammasome as a pattern recognition platform that translates crystal uptake into innate immune activation via secretion of IL-1β and IL-18 revised the pathogenesis of gout, silicosis, asbestosis, atherosclerosis and other crystal-related disorders. As a proof of concept, the NLRP3 inflammasome was now shown to trigger inflammation and acute kidney injury (AKI) in oxalate nephropathy. It seems likely that this and potentially other innate immunity mechanisms drive crystalline nephropathies (CNs) that are associated with crystals of calcium phosphate, uric acid, cysteine, adenine, certain drugs or contrast media, and potentially of myoglobin during rhabdomyolysis and of light chains in myeloma. Here, we discuss the proven and potential mechanisms of renal inflammation and kidney injury in crystal-related kidney disorders. In addition, we list topics for further research in that field. This perspective may also provide novel therapeutic options that can help to avoid progressive tissue remodeling and chronic kidney disease in patients with kidney stone disease or other CNs.
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            Crystal nephropathies: mechanisms of crystal-induced kidney injury

            Shrikant Mulay, Hans-Joachim Anders (2017)
            Crystals can trigger different types of renal injury according to their speed at which they form and their localization. Here, the authors discuss shared and specific mechanisms underlying crystal formation and renal injury, such as regulated cell death and inflammasome activation.
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              The management of patients with enteric hyperoxaluria.

              John Asplin (2016)
              Enteric hyperoxaluria is a common occurrence in the setting of fat malabsorption, usually due to intestinal resection or intestinal bypass surgery. Enhanced intestinal absorption of dietary oxalate leads to elevated renal oxalate excretion, frequently in excess of 100 mg/d (1.14 mmol/d). Patients are at increased risk of urolithiasis and loss of kidney function from oxalate nephropathy. Fat malabsorption causes increased binding of diet calcium by free fatty acids, reducing the calcium available to precipitate diet oxalate. Delivery of unabsorbed bile salts and fatty acids to the colon increases colonic permeability, the site of oxalate hyper-absorption in enteric hyperoxaluria. The combination of soluble oxalate in the intestinal lumen and increased permeability of the colonic mucosa leads to hyperoxaluria. Dietary therapy consists of limiting oxalate and fat intake. The primary medical intervention is the use of oral oxalate binding agents such as calcium salts to reduce free intestinal oxalate levels. Bile acid sequestrants can be useful in patients with ileal resection and bile acid malabsorption. Oxalate degrading bacteria provided as probiotics are being investigated but as of yet, no definite benefit has been shown with currently available preparations. The current state of medical therapy and potential future directions will be summarized in this article.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cureus
                Journal ID (iso-abbrev): Cureus
                Journal ID (issn): 2168-8184
                Title: Cureus
                Publisher: Cureus (Palo Alto (CA) )
                ISSN (Electronic): 2168-8184
                Publication date (Electronic, pub): 24 July 2023
                Publication date (Electronic, collection): July 2023
                Volume: 15
                Issue: 7
                Electronic Location Identifier: e42402
                Affiliations
                [1 ] Nephrology, Ohio Valley Nephrology Associates, Owensboro, USA
                [2 ] Nephrology, Washington University School of Medicine, St. Louis, USA
                [3 ] Internal Medicine, Waterbury Hospital, Waterbury, USA
                [4 ] Internal Medicine, Faisalabad Medical University, Faisalabad, PAK
                [5 ] Nephrology, Washington University School of Medicine, Saint Louis, USA
                [6 ] Internal Medicine, Saint Francis Medical Center, Trenton, USA
                Author notes
                Article
                DOI: 10.7759/cureus.42402
                PMC ID: 10446903
                SO-VID: 42df311d-423e-4683-880d-f62b0a12305d
                Copyright © Copyright © 2023, Saleem et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date accepted : 23 July 2023
                Categories
                Subject: Internal Medicine
                Subject: Pathology
                Subject: Nephrology

                Keywords: end stage kidney disease (eskd),idiopathic hyperoxaluria,primary hyperoxaluria,oxalate nephropathy,aki
                Data availability:
                Keywords: end stage kidney disease (eskd), idiopathic hyperoxaluria, primary hyperoxaluria, oxalate nephropathy, aki

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