ArticleActa veterinaria Scandinavica2015
Activation of complement system in kidney after ketoprofen-induced kidney injury in sheep.
Article in Acta veterinaria Scandinavica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 12 citations in OpenAlex.
- The complement system in pediatric acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2023Review
- High Expression of Complement Components in the Kidneys of Type 2 Diabetic Rats With Diabetic Nephropathy.Frontiers in endocrinology · 2019Article
- Urinary protein profiles in ketorolac-associated acute kidney injury in patients undergoing orthopedic day surgery.International journal of nephrology and renovascular disease · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-steroidal anti-inflammatory drugs (NSAIDs) are widely used to treat inflammatory pain in humans and animals. An overdose of an NSAID is nephrotoxic and can lead to acute kidney injury (AKI). Complement activation occurs in several types of renal disorders with proteinuria. The aim of this study was to investigate whether complement system becomes activated in kidneys after a high dose of NSAID. Kidney tissue and urine samples were collected from six sheep with ketoprofen-induced AKI and from six healthy control sheep. The localization of complement proteins in kidney tissue was carried out using immunohistochemical stainings, and excretion of C3 was tested by immunoblotting.
resultsThe complement system was found to become activated in the kidney tissue as demonstrated by positive immunostaining for C1q, C3c, C4c, C5, C9 and factor H and by Western blotting analysis of C3 activation products in urine samples in sheep with AKI.
conclusionsOur results thus suggest that the alternative complement pathway is activated, and it may contribute to the acute tubular injury seen in the kidneys of NSAID-induced AKI sheep. Inhibition of complement activation may serve as potential therapeutic target for intervention in drug-induced AKI.
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