Abstract

Research Article

Unusual presentation of oxalate nephropathy causing acute kidney injury: A case report

Anas Diab*, Michelle M Neuman, Kareem Diab and Daniel Gordon

Published: 04 November, 2020 | Volume 4 - Issue 3 | Pages: 077-079

Oxalate nephropathy due to Hyperoxaluria and elevated serum oxalate level is a well-known cause for interstitial fibrosis, and ESRD. Conditions associated with high serum Oxalate, should be considered as a possible contributing factor for a patient’s tubular injury.

Well known cause for Hyperoxaluria including enteric Hyperoxaluria (due to gastric bypass, chronic pancreatitis, small Bowel resection, or malabsorption, as well as depletion of enteric oxalate-degrading bacteria [e.g., Oxalobacter). Other known causes of oxalate nephropathy include primary Hyperoxaluria, ethylene glycol intoxication, vitamin B6 deficiency, excessive ingestion of vitamin C or dietary substances rich in oxalic acid, aspergillosis, prolonged renal failure and various drugs (e.g., Known medications to cause Oxalate Nephropathy are: Orlistat, Praxilene, COX-2 inhibitors).

Unusual presentation with Acute Kidney Injury with incidental finding of high serum Oxalate in a patient with a known CKD stage III, recently started on Polyethelene Glycol to treat his constipation.

Read Full Article HTML DOI: 10.29328/journal.jcn.1001063 Cite this Article Read Full Article PDF

Keywords:

Polyethylene glycol; Oxalate nephropathy; Acute kidney injury (AKI); Hyperoxaluria; Kidney biopsy; End stage kidney disease

References

  1. Hill P, Karim M, Davies DR, Roberts ISD, et al. Rapidly progressive irreversible renal failure in patients with pancreatic insufficiency. Am J Kidney Dis. 2003; 42: 842-845.
  2. Bleyer AJ, Hart PS, Kmoch S©. Familial Juvenile Gout (Concept Id: C4551496) - MedGen - NCBI.” National Center for Biotechnology Information, U.S. National Library of Medicine. PubMed: www.ncbi.nlm.nih.gov/medgen/1645893
  3. Cartery C, Faguer S, Karras A, Cointault O, et al. Oxalate nephropathy associated with chronic pancreatitis. Clin J Am Soc Nephrol. 2011; 6: 1895-1902. PubMed: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359534/
  4. Cornell LD. Secondary Oxalosis. In: Colvin RB, Chang A, Farris III BA, Kambham N, et al. (eds). Diagnostic Pathology: Kidney Diseases, 2nd edn. Elsevier: Manitoba. 2016; 736-737.
  5. Giannini S, Nobile M, Castrignano R, Pati T, Tasca A, et al. Possible Link between Vitamin D and Hyperoxaluria in Patients with Renal Stone Disease. Clin Sci. 84: 1993, 51–54. PubMed: https://pubmed.ncbi.nlm.nih.gov/8382134
  6. UMOD is a gene that has been associated with autosomal dominant UMOD-related tubulointerstitial kidney disease, previously known as familial juvenile hyperuricemia (gouty) nephropathy type 1, as well as linked to autosomal dominant glomerulocystic kidney disease with hyperuricemia and isosthenuria (2).
  7. Autosomal Dominant Tubulointerstitial Kidney Disease, UMOD-Related Synonyms: ADTKD-UMOD, Familial Juvenile Hyperuricemic Nephropathy 1, Medullary Cystic Kidney Disease 2, UMOD-Associated Kidney Disease, Uromodulin Kidney Disease Anthony J Bleyer, MD, MS, P Suzanne Hart, PhD, and Stanislav Kmoch, PhD.
  8. Biodegradation of Polyethers (Polyethylene Glycol, Polypropylene Glycol, Polytetramethylene glycol, and Others) Part 9. Miscellaneous Biopolymers and Biodegradation of Polymers Prof. Dr. Fusako Kawai. 2005.
  9. Perinpam M, Enders FT, Mara KC, Vaughan LE, Mehta RA, et al. Plasma oxalate in relation to eGFR in patients with primary hyperoxaluria, enteric hyperoxaluria and urinary stone disease. Clin Biochem. 2017; 50: 1014-1019. PubMed: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705406/

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