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==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 [disease name] 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 toxins associated with [[diabetes]], [[sickle cell disease]], [[urinary tract obstruction]], [[urinary tract infection]] and [[analgesics]] such as [[acetaminophen]] and [[NSAIDS]]. <ref name="pmid12512867">{{cite journal| author=Brix AE| title=Renal papillary necrosis. | journal=Toxicol Pathol | year= 2002 | volume= 30 | issue= 6 | pages= 672-4 | pmid=12512867 | doi=10.1080/01926230290166760 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12512867 }} </ref><ref name="pmid6394414">{{cite journal| author=Sabatini S| title=Pathophysiology of drug-induced papillary necrosis. | journal=Fundam Appl Toxicol | year= 1984 | volume= 4 | issue= 6 | pages= 909-21 | pmid=6394414 | doi=10.1016/0272-0590(84)90229-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6394414 }} </ref> | |||
**[[Medullary cells]] usually produce [[prostaglandins]] and proteoglycans. <ref name="pmid12512867">{{cite journal| author=Brix AE| title=Renal papillary necrosis. | journal=Toxicol Pathol | year= 2002 | volume= 30 | issue= 6 | pages= 672-4 | pmid=12512867 | doi=10.1080/01926230290166760 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12512867 }} </ref> | |||
**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]]. <ref name="pmid12512867">{{cite journal| author=Brix AE| title=Renal papillary necrosis. | journal=Toxicol Pathol | year= 2002 | volume= 30 | issue= 6 | pages= 672-4 | pmid=12512867 | doi=10.1080/01926230290166760 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12512867 }} </ref><ref name="pmid2362779">{{cite journal| author=Burrell JH, Yong JL, Macdonald GJ| title=Experimental analgesic nephropathy: changes in renal structure and urinary concentrating ability in Fischer 344 rats given continuous low doses of aspirin and paracetamol. | journal=Pathology | year= 1990 | volume= 22 | issue= 1 | pages= 33-44 | pmid=2362779 | doi=10.3109/00313029009061423 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2362779 }} </ref> | |||
*Another mechanism is inhibiting [[cyclooxygenase]] enzymes; [[COX I]] and [[COX II]], which play a major role in the [[prostaglandins]] synthesis, following [[NSAIDS]] use. <ref name="pmid11275626">{{cite journal| author=Brater DC, Harris C, Redfern JS, Gertz BJ| title=Renal effects of COX-2-selective inhibitors. | journal=Am J Nephrol | year= 2001 | volume= 21 | issue= 1 | pages= 1-15 | pmid=11275626 | doi=10.1159/000046212 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11275626 }} </ref> | |||
**Multiple [[NSAIDS]] taking and [[hypovolemic]] condition could facilitate development of [[renal papillary necrosis]]. <ref name="pmid12512867">{{cite journal| author=Brix AE| title=Renal papillary necrosis. | journal=Toxicol Pathol | year= 2002 | volume= 30 | issue= 6 | pages= 672-4 | pmid=12512867 | doi=10.1080/01926230290166760 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12512867 }} </ref> <ref name="pmid6394414">{{cite journal| author=Sabatini S| title=Pathophysiology of drug-induced papillary necrosis. | journal=Fundam Appl Toxicol | year= 1984 | volume= 4 | issue= 6 | pages= 909-21 | pmid=6394414 | doi=10.1016/0272-0590(84)90229-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6394414 }} </ref> | |||
[[File:Papillary necrosis-NSAIDS mechanism.PNG|700px|thumb|center]] | |||
==References== | ==References== | ||
Revision as of 08:21, 27 July 2020
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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 [disease name] 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 toxins associated with diabetes, sickle cell disease, urinary tract obstruction, urinary tract infection and analgesics such as acetaminophen and NSAIDS. [1][2]
- 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][3]
- Another mechanism is inhibiting cyclooxygenase enzymes; COX I and COX II, which play a major role in the prostaglandins synthesis, following NSAIDS use. [4]
- Multiple NSAIDS taking and hypovolemic condition could facilitate development of renal papillary necrosis. [1] [2]
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.
- ↑ 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.
[[Category:Disease]