Hypertensive nephropathy risk factors: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Hypertensive nephropathy}} | {{Hypertensive nephropathy}} | ||
{{CMG}}; {{AE}} {{AN}} | {{CMG}}; {{AE}} {{AN}}{{NN}} | ||
==Risk Factors== | ==Risk Factors== | ||
* High [[systolic blood pressure]] is a very strong risk factor for the development of hypertensive nephrosclerosis. | * High [[systolic blood pressure]] is a very strong risk factor for the development of hypertensive [[nephrosclerosis]]. | ||
* | *African Americans are more likely to develop [[hypertensive nephropathy]]. Firstly, a number of causes had been suggested: | ||
** | **Higher prevalence and severity of hypertension | ||
* The Framingham heart study showed that a combination of [[hypertension]] with mild reduction in [[glomerular filtration rate]] | **Lower socioeconomic status | ||
* [[Diabetes]], [[smoking]], [[obesity]] and high levels of [[low density lipoproteins]] also | **Poor healthcare accessibility. | ||
*However, Ethnic differences related to [[hypertensive nephropathy]] remained after adjusting age, sex, and prevalence of hypertension among ethnic groups, suggesting the presence of genetic predisposition in this population.<ref name="MureaFreedman2010">{{cite journal|last1=Murea|first1=Mariana|last2=Freedman|first2=Barry I|title=Essential hypertension and risk of nephropathy: a reappraisal|journal=Current Opinion in Nephrology and Hypertension|volume=19|issue=3|year=2010|pages=235–241|issn=1062-4821|doi=10.1097/MNH.0b013e3283366344}}</ref> | |||
*Genetic susceptibility | |||
** Non-muscle myosin heavy chain 9 gene (MYH9), which regulates the function of podocyte cytoskeleton, is associated with hypertensive [[ESRD]] in African Americans.<ref name="KoppSmith2008">{{cite journal|last1=Kopp|first1=Jeffrey B|last2=Smith|first2=Michael W|last3=Nelson|first3=George W|last4=Johnson|first4=Randall C|last5=Freedman|first5=Barry I|last6=Bowden|first6=Donald W|last7=Oleksyk|first7=Taras|last8=McKenzie|first8=Louise M|last9=Kajiyama|first9=Hiroshi|last10=Ahuja|first10=Tejinder S|last11=Berns|first11=Jeffrey S|last12=Briggs|first12=William|last13=Cho|first13=Monique E|last14=Dart|first14=Richard A|last15=Kimmel|first15=Paul L|last16=Korbet|first16=Stephen M|last17=Michel|first17=Donna M|last18=Mokrzycki|first18=Michele H|last19=Schelling|first19=Jeffrey R|last20=Simon|first20=Eric|last21=Trachtman|first21=Howard|last22=Vlahov|first22=David|last23=Winkler|first23=Cheryl A|title=MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis|journal=Nature Genetics|volume=40|issue=10|year=2008|pages=1175–1184|issn=1061-4036|doi=10.1038/ng.226}}</ref> | |||
** Solidified [[glomerulosclerosis]] secondary to hypertension in African American is associated with apolipoprotein L1 gene (APOL1)<ref name="RobinsonFreedman2019">{{cite journal|last1=Robinson|first1=Todd W.|last2=Freedman|first2=Barry I.|title=The Impact of APOL1 on Chronic Kidney Disease and Hypertension|journal=Advances in Chronic Kidney Disease|volume=26|issue=2|year=2019|pages=131–136|issn=15485595|doi=10.1053/j.ackd.2019.01.003}}</ref> | |||
** Chromogranin A gene variants, which block secretion of [[catecholamine]], is also contributed to hypertensive [[ESRD]] in African Americans.<ref name="SalemCadman2008">{{cite journal|last1=Salem|first1=Rany M.|last2=Cadman|first2=Peter E.|last3=Chen|first3=Yuqing|last4=Rao|first4=Fangwen|last5=Wen|first5=Gen|last6=Hamilton|first6=Bruce A.|last7=Rana|first7=Brinda K.|last8=Smith|first8=Douglas W.|last9=Stridsberg|first9=Mats|last10=Ward|first10=Harry J.|last11=Mahata|first11=Manjula|last12=Mahata|first12=Sushil K.|last13=Bowden|first13=Donald W.|last14=Hicks|first14=Pamela J.|last15=Freedman|first15=Barry I.|last16=Schork|first16=Nicholas J.|last17=O'Connor|first17=Daniel T.|title=Chromogranin A Polymorphisms Are Associated With Hypertensive Renal Disease|journal=Journal of the American Society of Nephrology|volume=19|issue=3|year=2008|pages=600–614|issn=1046-6673|doi=10.1681/ASN.2007070754}}</ref> | |||
* The Framingham heart study showed that a combination of [[hypertension]] with a mild reduction in [[glomerular filtration rate]] increases the risk of developing [[chronic renal failure]]. | |||
* [[Diabetes]], [[smoking]], [[obesity]] and high levels of [[low density lipoproteins]] also accelerates the progression of renal damage secondary to [[hypertension]]. | |||
==References== | ==References== | ||
Latest revision as of 10:07, 11 June 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]Nasrin Nikravangolsefid, MD-MPH [3]
Risk Factors
- High systolic blood pressure is a very strong risk factor for the development of hypertensive nephrosclerosis.
- African Americans are more likely to develop hypertensive nephropathy. Firstly, a number of causes had been suggested:
- Higher prevalence and severity of hypertension
- Lower socioeconomic status
- Poor healthcare accessibility.
- However, Ethnic differences related to hypertensive nephropathy remained after adjusting age, sex, and prevalence of hypertension among ethnic groups, suggesting the presence of genetic predisposition in this population.[1]
- Genetic susceptibility
- Non-muscle myosin heavy chain 9 gene (MYH9), which regulates the function of podocyte cytoskeleton, is associated with hypertensive ESRD in African Americans.[2]
- Solidified glomerulosclerosis secondary to hypertension in African American is associated with apolipoprotein L1 gene (APOL1)[3]
- Chromogranin A gene variants, which block secretion of catecholamine, is also contributed to hypertensive ESRD in African Americans.[4]
- The Framingham heart study showed that a combination of hypertension with a mild reduction in glomerular filtration rate increases the risk of developing chronic renal failure.
- Diabetes, smoking, obesity and high levels of low density lipoproteins also accelerates the progression of renal damage secondary to hypertension.
References
- ↑ Murea, Mariana; Freedman, Barry I (2010). "Essential hypertension and risk of nephropathy: a reappraisal". Current Opinion in Nephrology and Hypertension. 19 (3): 235–241. doi:10.1097/MNH.0b013e3283366344. ISSN 1062-4821.
- ↑ Kopp, Jeffrey B; Smith, Michael W; Nelson, George W; Johnson, Randall C; Freedman, Barry I; Bowden, Donald W; Oleksyk, Taras; McKenzie, Louise M; Kajiyama, Hiroshi; Ahuja, Tejinder S; Berns, Jeffrey S; Briggs, William; Cho, Monique E; Dart, Richard A; Kimmel, Paul L; Korbet, Stephen M; Michel, Donna M; Mokrzycki, Michele H; Schelling, Jeffrey R; Simon, Eric; Trachtman, Howard; Vlahov, David; Winkler, Cheryl A (2008). "MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis". Nature Genetics. 40 (10): 1175–1184. doi:10.1038/ng.226. ISSN 1061-4036.
- ↑ Robinson, Todd W.; Freedman, Barry I. (2019). "The Impact of APOL1 on Chronic Kidney Disease and Hypertension". Advances in Chronic Kidney Disease. 26 (2): 131–136. doi:10.1053/j.ackd.2019.01.003. ISSN 1548-5595.
- ↑ Salem, Rany M.; Cadman, Peter E.; Chen, Yuqing; Rao, Fangwen; Wen, Gen; Hamilton, Bruce A.; Rana, Brinda K.; Smith, Douglas W.; Stridsberg, Mats; Ward, Harry J.; Mahata, Manjula; Mahata, Sushil K.; Bowden, Donald W.; Hicks, Pamela J.; Freedman, Barry I.; Schork, Nicholas J.; O'Connor, Daniel T. (2008). "Chromogranin A Polymorphisms Are Associated With Hypertensive Renal Disease". Journal of the American Society of Nephrology. 19 (3): 600–614. doi:10.1681/ASN.2007070754. ISSN 1046-6673.