Renal papillary necrosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]
Overview
Renal papillary necrosis is a significant kidney disorder, which is associated with ischemia of the inner renal medulla and papilla due to chronic conditions such as diabetes, sickle cell disease, urinary tract obstruction, urinary tract infection and long term use of analgesics. Decreased prostaglandin synthesis and subsequent reduced renal blood flow is an important mechanism for developing renal papillary necrosis.
Pathogenesis
- The exact pathogenesis of renal papillary necrosis is not fully understood.
- It is thought that Renal papillary necrosis is the result of damage to interstitial medullary and papillary cells due to direct effect of diseases such as diabetes, sickle cell disease, urinary tract obstruction, renal vein thrombosis, upper urinary tract infection, tuberculosis, vasculitis, renal transplant rejection and long term analgesics use such as acetaminophen and NSAIDS. [1][2]
- Renal medullary and papillary cells are susceptible to ischemia. [4]
- Medullary cells usually produce prostaglandins and proteoglycans. [1]
- Damage of medullary cells leads to changes in renal matrix and vessels due to decreased production of prostaglandins that causes vasoconstriction, reduced renal perfusion, ischemia and necrosis. [1][5]
- Another mechanism is inhibiting cyclooxygenase enzymes; COX I and COX II, which play a major role in the prostaglandins synthesis, following NSAIDS use. [6]
- Multiple NSAIDS taking and hypovolemic condition could facilitate development of renal papillary necrosis. [1] [2]
- Accumulation of sickle-shaped RBCs in patients with sickle cell disease can lead to intravascular obstruction, blood stasis and thrombosis that results in ischemic necrosis of renal papillary and medullary cells.[7]
References
- ↑ 1.0 1.1 1.2 1.3 Brix AE (2002). "Renal papillary necrosis". Toxicol Pathol. 30 (6): 672–4. doi:10.1080/01926230290166760. PMID 12512867.
- ↑ 2.0 2.1 Sabatini S (1984). "Pathophysiology of drug-induced papillary necrosis". Fundam Appl Toxicol. 4 (6): 909–21. doi:10.1016/0272-0590(84)90229-x. PMID 6394414.
- ↑ By BruceBlaus. When using this image in external sources it can be cited as:Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. - Own work, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=31118599
- ↑ Jung DC, Kim SH, Jung SI, Hwang SI, Kim SH (2006). "Renal papillary necrosis: review and comparison of findings at multi-detector row CT and intravenous urography". Radiographics. 26 (6): 1827–36. doi:10.1148/rg.266065039. PMID 17102053.
- ↑ Burrell JH, Yong JL, Macdonald GJ (1990). "Experimental analgesic nephropathy: changes in renal structure and urinary concentrating ability in Fischer 344 rats given continuous low doses of aspirin and paracetamol". Pathology. 22 (1): 33–44. doi:10.3109/00313029009061423. PMID 2362779.
- ↑ Brater DC, Harris C, Redfern JS, Gertz BJ (2001). "Renal effects of COX-2-selective inhibitors". Am J Nephrol. 21 (1): 1–15. doi:10.1159/000046212. PMID 11275626.
- ↑ Henderickx MMEL, Brits T, De Baets K, Seghers M, Maes P, Trouet D; et al. (2017). "Renal papillary necrosis in patients with sickle cell disease: How to recognize this 'forgotten' diagnosis". J Pediatr Urol. 13 (3): 250–256. doi:10.1016/j.jpurol.2017.01.020. PMID 28341428.
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