Acute renal failure following oxalic acid poisoning: a case report

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Oxalic acid poisoning is being recognized as an emerging epidemic in the rural communities of Sri Lanka as it is a component of locally produced household laundry detergents. Herein we describe a case of a 32 year old female, presenting after direct ingestion of oxalic acid. She then went on to develop significant metabolic acidosis and acute renal failure, requiring dialysis. Renal biopsy revealed acute tubulointerstitial nephritis associated with diffuse moderate acute tubular damage with refractile crystals in some of the tubules. The patient symptomatically improved with haemodialysis and renal functions subsequently returned to normal.

Related collections

Most cited references 8

Record: found
Abstract: found
Article: not found

Mechanism of calcium oxalate renal stone formation and renal tubular cell injury.

M Tsujihata (2008)

Formation of calcium oxalate stones tends to increase with age and begins from the attachment of a crystal formed in the cavity of renal tubules to the surface of renal tubular epithelial cells. Though most of the crystals formed in the cavity of renal tubules are discharged as is in the urine, in healthy people, crystals that attach to the surface of renal tubular epithelial cells are thought to be digested by macrophages and/or lysosomes inside of cells. However, in individuals with hyperoxaluria or crystal urine, renal tubular cells are injured and crystals easily become attached to them. Various factors are thought to be involved in renal tubular cell injury. Crystals attached to the surface of renal tubular cells are taken into the cells (crystal-cell interaction). And then the crystal and crystal aggregates grow, and finally a stone is formed.

0 comments Cited 58 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Diagnosis and management of acute interstitial nephritis.

Archana Kudrimoti, Charles M Kodner (2003)

Acute interstitial nephritis is an important cause of acute renal failure resulting from immune-mediated tubulointerstitial injury, initiated by medications, infection, and other causes. Acute interstitial nephritis may be implicated in up to 15 percent of patients hospitalized for acute renal failure. Clinical features are essentially those of acute renal failure from any cause, and apart from a history of new illness or medication exposure, there are no specific history, physical examination, or laboratory findings that distinguish acute interstitial nephritis from other causes of acute renal failure. Classic findings of fever, rash, and arthralgias may be absent in up to two thirds of patients. Diagnostic studies such as urine eosinophils and renal gallium 67 scanning provide suggestive evidence, but they are unable to reliably confirm or exclude the diagnosis of acute interstitial nephritis. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending agent or medication. The time until removal of such agents, and renal biopsy findings, provide the best prognostic information for return to baseline renal function. Corticosteroids appear to provide some benefit in terms of clinical improvement and return of renal function, but no controlled clinical trials have been conducted to confirm this.

0 comments Cited 31 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Are calcium oxalate crystals involved in the mechanism of acute renal failure in ethylene glycol poisoning?

K McMartin (2009)

Ethylene glycol (EG) poisoning often results in acute renal failure, particularly if treatment with fomepizole or ethanol is delayed because of late presentation or diagnosis. The mechanism has not been established but is thought to result from the production of a toxic metabolite. A literature review utilizing PubMed identified papers dealing with renal toxicity and EG or oxalate. The list of papers was culled to those relevant to the mechanism and treatment of the renal toxicity associated with either compound. ROLE OF METABOLITES: Although the "aldehyde" metabolites of EG, glycolaldehyde, and glyoxalate, have been suggested as the metabolites responsible, recent studies have shown definitively that the accumulation of calcium oxalate monohydrate (COM) crystals in kidney tissue produces renal tubular necrosis that leads to kidney failure. In vivo studies in EG-dosed rats have correlated the severity of renal damage with the total accumulation of COM crystals in kidney tissue. Studies in cultured kidney cells, including human proximal tubule (HPT) cells, have demonstrated that only COM crystals, not the oxalate ion, glycolaldehyde, or glyoxylate, produce a necrotic cell death at toxicologically relevant concentrations. COM CRYSTAL ACCUMULATION: In EG poisoning, COM crystals accumulate to high concentrations in the kidney through a process involving adherence to tubular cell membranes, followed by internalization of the crystals. MECHANISM OF TOXICITY: COM crystals have been shown to alter membrane structure and function, to increase reactive oxygen species and to produce mitochondrial dysfunction. These processes are likely to be involved in the mechanism of cell death. Accumulation of COM crystals in the kidney is responsible for producing the renal toxicity associated with EG poisoning. The development of a pharmacological approach to reduce COM crystal adherence to tubular cells and its cellular interactions would be valuable as this would decrease the renal toxicity not only in late treated cases of EG poisoning, but also in other hyperoxaluric diseases such as primary hyperoxaluria and kidney stone formation.

0 comments Cited 20 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): J Occup Med Toxicol

Journal ID (iso-abbrev): J Occup Med Toxicol

Title: Journal of Occupational Medicine and Toxicology (London, England)

Publisher: BioMed Central

ISSN (Electronic): 1745-6673

Publication date Collection: 2012

Publication date (Electronic): 14 September 2012

Volume: 7

Page: 17

Affiliations

[1 ]Department of Clinical Medicine, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka

Article

Publisher ID: 1745-6673-7-17

DOI: 10.1186/1745-6673-7-17

PMC ID: 3527234

PubMed ID: 22978510

SO-VID: 2207b996-16f0-4239-a764-45f41ef197e4

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Acute renal failure following oxalic acid poisoning: a case report

Read this article at

Abstract

Related collections

ScienceOpen Clinical Case Reports Collection

Most cited references 8

Mechanism of calcium oxalate renal stone formation and renal tubular cell injury.

Diagnosis and management of acute interstitial nephritis.

Are calcium oxalate crystals involved in the mechanism of acute renal failure in ethylene glycol poisoning?

Author and article information

Journal

Affiliations

Article

History

Categories

Comments

Comment on this article

Similar content 258

Cited by 2

Most referenced authors 86