Chronic hypertension causes: Difference between revisions

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{{Template:Hypertension}}
{{Chronic hypertension}}


{{CMG}}; '''Assistant Editor-In-Chief: '''[[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]
{{CMG}}; '''Assistant Editor-In-Chief: '''[[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]
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====Refractory Hypertension====
====Refractory Hypertension====
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===Evaluation of Secondary Hypertension===
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{{Familytree/start}}
{{Familytree|boxstyle=text-align: center; font-size: 90%; padding: 0px; width: 50%;| | | | | | A01 | | | | | | | | | |A01=<div style="padding: 15px;">'''''Evaluation of secondary hypertension'''''</div>}}
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'''Investigation should be limited for patients with clues suggestive of potentially correctable causes.'''
❑ Presence of clues for renovascular hypertension (most common potentially correctable cause)?<ref name="pmid16549646">{{cite journal| author=Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL et al.| title=ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. | journal=Circulation | year= 2006 | volume= 113 | issue= 11 | pages= e463-654 | pmid=16549646 | doi=10.1161/CIRCULATIONAHA.106.174526 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16549646  }} </ref><ref name="pmid21963765">{{cite journal| author=Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss LK et al.| title=2011 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Peripheral Artery Disease (updating the 2005 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2011 | volume= 58 | issue= 19 | pages= 2020-45 | pmid=21963765 | doi=10.1016/j.jacc.2011.08.023 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21963765  }} </ref>
: ❑ Onset of hypertension before the age of 30 years
: ❑ Onset of severe hypertension (SBP ≥180 mm Hg and/or DBP ≥120 mm Hg) after the age of 55 years
: ❑ New azotemia or worsening renal function after administration of an ACE inhibitor or ARB agent
: ❑ Unexplained atrophic kidney or size discrepancy between kidneys of greater than 1.5 cm
: ❑ Sudden, unexplained pulmonary edema
: ❑ Accelerated hypertension (sudden and persistent worsening of previously controlled hypertension)
: ❑ Resistant hypertension (failure to achieve goal blood pressure in patients who are adhering to full doses of an appropriate 3-drug regimen that includes a diuretic)
: ❑ Malignant hypertension (hypertension with coexistent evidence of acute end-organ damage, i.e., acute renal failure, acutely decompensated congestive heart failure, new visual or neurological disturbance, and/or advanced [grade III to IV] retinopathy)
: ❑ Unexplained renal failure in the absence of proteinuria or an abnormal urine sediment
: ❑ Multivessel coronary artery disease
: ❑ Unexplained congestive heart failure
: ❑ Refractory angina
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{{Familytree|boxstyle=text-align: center; font-size: 90%; padding: 0px;| | A01 | | | | | | A02 |A01=<div style="padding: 10px; font-weight: bold;">YES</div>|A02=<div style="padding: 10px; font-weight: bold;">NO</div>}}
{{Familytree|boxstyle=text-align: left; font-size: 90%; padding: 0px; border-top: 0px; vertical-align: top; width: 25%;| | A01 | | | | | | A02 |A01=<div style="padding: 10px;">
❑ Perform noninvasive diagnostic studies
: ❑ Duplex ultrasonography
: ❑ Gadolinium-enhanced magnetic resonance angiography
: ❑ Computed tomographic angiography (in individuals with normal renal function)
❑ Consider catheter angiography when noninvasive studies are inconclusive</div>
|A02=<div style="padding: 10px; font-size: 85%;">
Look for findings suggestive of other identifiable causes
❑ Pheochromocytoma
: ❑ Paroxysmal pounding headache
: ❑ Palpitations
: ❑ Profound perspiration
: ❑ Pallor
: ❑ Hand tremor
❑ Hyperaldosteronism
: ❑ Unexplained hypokalemia with urinary potassium wasting
❑ Obstructive sleep apnea
: ❑ Daytime somnolence
: ❑ Snoring
: ❑ Obesity
❑ Hyperparathyroidism
: ❑ Hypercalcemia
❑ Hypothyroidism
: ❑ Elevated TSH
: ❑ Puffy face
❑ Aortic coarctation
: ❑ Diminished or delayed femoral pulses and low or unobtainable blood pressures in the legs</div>}}
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===Common Causes of Secondary Hypertension===
===Common Causes of Secondary Hypertension===
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=====Apnea=====
=====Apnea=====
[[Obstructive sleep apnea]] (OSA) is a respiratory disease characterized by repetitive narrowing or collapse of the upper airway during sleep<ref name="pmid18250206">{{cite journal| author=Eckert DJ, Malhotra A| title=Pathophysiology of adult obstructive sleep apnea. | journal=Proc Am Thorac Soc | year= 2008 | volume= 5 | issue= 2 | pages= 144-53 | pmid=18250206 | doi=10.1513/pats.200707-114MG | pmc=PMC2628457 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18250206  }} </ref> leading to [[apnea]], [[hypopnea]], and a nocturnal decrease in oxygen tension.<ref name="pmid8872797">{{cite journal| author=Silverberg DS, Oksenberg A| title=Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis. | journal=J Hum Hypertens | year= 1996 | volume= 10 | issue= 6 | pages= 353-63 | pmid=8872797 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8872797  }} </ref> Symptoms and signs that might suggest OSA include daytime [[somnolence]], [[obesity]], [[snoring]], and [[morning headache]].<ref name="pmid10593319">{{cite journal| author=Victor LD| title=Obstructive sleep apnea. | journal=Am Fam Physician | year= 1999 | volume= 60 | issue= 8 | pages= 2279-86 | pmid=10593319 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10593319  }} </ref> Diagnosis is made by polysomnography. Treatment relies on maintaining airway patency at night and includes, among others, the use of continuous positive airway pressure (CPAP).
[[Obstructive sleep apnea]] (OSA) is a respiratory disease characterized by repetitive narrowing or collapse of the upper airway during sleep<ref name="pmid18250206">{{cite journal| author=Eckert DJ, Malhotra A| title=Pathophysiology of adult obstructive sleep apnea. | journal=Proc Am Thorac Soc | year= 2008 | volume= 5 | issue= 2 | pages= 144-53 | pmid=18250206 | doi=10.1513/pats.200707-114MG | pmc=PMC2628457 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18250206  }} </ref> leading to [[apnea]], [[hypopnea]], and a nocturnal decrease in oxygen tension.<ref name="pmid8872797">{{cite journal| author=Silverberg DS, Oksenberg A| title=Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis. | journal=J Hum Hypertens | year= 1996 | volume= 10 | issue= 6 | pages= 353-63 | pmid=8872797 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8872797  }} </ref> Symptoms and signs that might suggest OSA include daytime [[somnolence]], [[obesity]], [[snoring]], and [[morning headache]].<ref name="pmid10593319">{{cite journal| author=Victor LD| title=Obstructive sleep apnea. | journal=Am Fam Physician | year= 1999 | volume= 60 | issue= 8 | pages= 2279-86 | pmid=10593319 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10593319  }} </ref> Patients with sleep apnea also tend to have drug resistant hypertension and may retain sodium. Diagnosis is made by polysomnography. Treatment relies on maintaining airway patency at night and includes, among others, the use of continuous positive airway pressure (CPAP).


=====Aldosterone=====
=====Aldosterone=====
Primary (hyporeninemic) and secondary (hyperreninemic) [[hyperaldosteronism]] result in excess sodium and water retention with excretion of [[potassium]].<ref name="pmid9854120">{{cite journal| author=Ganguly A| title=Primary aldosteronism. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 25 | pages= 1828-34 | pmid=9854120 | doi=10.1056/NEJM199812173392507 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9854120  }} </ref>  Common symptoms of hyperaldosteronism include fatigue, headache, hypertension, intermittent paralysis, muscle weakness, and numbness.  The most common cause of [[primary hyperaldosteronism]] is an aldosterone-producing adenoma, i.e. [[Conn’s Syndrome]]. [[Secondary hyperaldosteronism]] is due to an overactive [[RAAS]], as seen in renin-secreting tumors, [[renal artery stenosis]], [[pheochromocytoma]], and other syndromes.  The diagnosis is made by measuring the ratio of plasma aldosterone to plasma renin activity.<ref name="pmid7923898">{{cite journal| author=Gordon RD, Stowasser M, Tunny TJ, Klemm SA, Rutherford JC| title=High incidence of primary aldosteronism in 199 patients referred with hypertension. | journal=Clin Exp Pharmacol Physiol | year= 1994 | volume= 21 | issue= 4 | pages= 315-8 | pmid=7923898 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7923898  }} </ref> It is elevated in [[primary hyperaldosteronism]] and decreased/normal with elevated [[renin]] in [[secondary hyperaldosteronism]].  Treatment depends upon the underlying etiology: surgery to resect an adenoma causing [[primary hyperaldosteronism]] and [[spironolactone]], an aldosterone antagonist to treat [[secondary hyperaldosteronism]].
Primary (hyporeninemic) and secondary (hyperreninemic) [[hyperaldosteronism]] result in excess sodium and water retention with slight [[hypernatremia]] along with excretion of [[potassium]] resulting in [[hypokalemia]] in one half of patients.<ref name="pmid9854120">{{cite journal| author=Ganguly A| title=Primary aldosteronism. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 25 | pages= 1828-34 | pmid=9854120 | doi=10.1056/NEJM199812173392507 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9854120  }} </ref>  Common symptoms of hyperaldosteronism include drug resistant hypertension, [[fatigue]], [[headache]], intermittent [[paralysis]], [[muscle weakness]], and [[numbness]].  The most common cause of [[primary hyperaldosteronism]] is an aldosterone-producing [[adenoma]] (an "[[aldosteronoma]]"), i.e. [[Conn’s Syndrome]]. [[Secondary hyperaldosteronism]] is due to an overactive [[RAAS]], as seen in renin-secreting tumors, [[renal artery stenosis]], [[pheochromocytoma]], and other syndromes.  The diagnosis is made by measuring the ratio of plasma aldosterone to plasma renin activity.<ref name="pmid7923898">{{cite journal| author=Gordon RD, Stowasser M, Tunny TJ, Klemm SA, Rutherford JC| title=High incidence of primary aldosteronism in 199 patients referred with hypertension. | journal=Clin Exp Pharmacol Physiol | year= 1994 | volume= 21 | issue= 4 | pages= 315-8 | pmid=7923898 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7923898  }} </ref> It is elevated in [[primary hyperaldosteronism]] and decreased/normal with elevated [[renin]] in [[secondary hyperaldosteronism]].  It should be noted that obesity can also cause [[aldosterone]] levels to be elevated.  Treatment depends upon the underlying etiology: surgery to resect an adenoma causing [[primary hyperaldosteronism]] and [[spironolactone]], an aldosterone antagonist to treat [[secondary hyperaldosteronism]].


===== Bruit=====
===== Bruit=====
[[Renovascular hypertension]] is due to decreased blood supply to the [[kidneys]] secondary to renal artery stenosis and it is the most common correctable cause of secondary hypertension.  [[Atherosclerosis]] of the renal artery ([[renal artery stenosis]]) in older patients above 50 years of age<ref name="pmid12196346">{{cite journal| author=Chade AR, Rodriguez-Porcel M, Grande JP, Krier JD, Lerman A, Romero JC et al.| title=Distinct renal injury in early atherosclerosis and renovascular disease. | journal=Circulation | year= 2002 | volume= 106 | issue= 9 | pages= 1165-71 | pmid=12196346 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12196346  }} </ref> and [[fibromuscular dysplasia]] in younger patients are the most common etiologies.  
[[Renovascular hypertension]] is due to decreased blood supply to the [[kidneys]] secondary to renal artery stenosis and it is the most common correctable cause of secondary hypertension.  [[Atherosclerosis]] of the renal artery ([[renal artery stenosis]]) in older patients above 50 years of age<ref name="pmid12196346">{{cite journal| author=Chade AR, Rodriguez-Porcel M, Grande JP, Krier JD, Lerman A, Romero JC et al.| title=Distinct renal injury in early atherosclerosis and renovascular disease. | journal=Circulation | year= 2002 | volume= 106 | issue= 9 | pages= 1165-71 | pmid=12196346 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12196346  }} </ref> and [[fibromuscular dysplasia]] in younger patients are the most common etiologies.  


The ACC / AHA Guidelines state that you should suspect renal artery stenosis in the following scenarios<ref name="pmid16549646">{{cite journal| author=Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL et al.| title=ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. | journal=Circulation | year= 2006 | volume= 113 | issue= 11 | pages= e463-654 | pmid=16549646 | doi=10.1161/CIRCULATIONAHA.106.174526 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16549646 }} </ref>:
According to the 2013 ACC/AHA Guidelines for the Management of PAD<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117  }} </ref>, diagnostic work-up for renal artery stenosis is indicated in the following conditions:
 
* Severe hypertension (systolic blood pressure > 180 mm Hg or diastolic blood pressure > 120 mm Hg) in a patient over the age of 55. If only mild hypertension is present, then renal artery stenosis is the underlying cause in only 1% of patients <ref name="pmid3872106">{{cite journal| author=Lewin A, Blaufox MD, Castle H, Entwisle G, Langford H| title=Apparent prevalence of curable hypertension in the Hypertension Detection and Follow-up Program. | journal=Arch Intern Med | year= 1985 | volume= 145 | issue= 3 | pages= 424-7 | pmid=3872106 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3872106  }} </ref>, but if the blood pressure is markedly elevated, then the risk of renal artery stenosis goes up 10 to 50 fold.
====Class I Recommendations<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>====
* Severe hypertension in the presence of polyvascular disease (coronary artery disease or peripheral arterial disease)
*Hypertension of any stage before the age of 30
* Severe hypertension and an atrophic kidney that is 1.5 cm smaller than the other. If the kidney is < 9 cm in size, there is a 75% chance that renal artery stenosis is present.
*Stage II hypertension (severe hypertension systolic blood pressure > 180 mm Hg or diastolic blood pressure > 120 mm Hg) in patients older than 55 years. If only mild hypertension is present, then renal artery stenosis is the underlying cause in only 1% of patients <ref name="pmid3872106">{{cite journal| author=Lewin A, Blaufox MD, Castle H, Entwisle G, Langford H| title=Apparent prevalence of curable hypertension in the Hypertension Detection and Follow-up Program. | journal=Arch Intern Med | year= 1985 | volume= 145 | issue= 3 | pages= 424-7 | pmid=3872106 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3872106  }} </ref>, but if the blood pressure is markedly elevated, then the risk of renal artery stenosis goes up 10 to 50 fold.
* Severe hypertension, impaired renal function, and recurrent flash [[pulmonary edema]]
*Accelerated condition of previously controlled hypertension
* A 50% rise in [[creatinine]] that is sustained within one week of starting an [[ACE inhibitor]] or an [[ARB]]
*[[Resistant hypertension]]
*[[Malignant hypertension]]
*New [[azotemia]] (50% rise in [[creatinine]] that is sustained) within one week after administration of an [[Angiotensin Converting Enzyme]] ([[ACE]])inhibitor or [[ARB]]
*Unexplained atrophic kidney or asymmetric kidneys that differ by > 1.5 cm. If the kidney is < 9 cm in size, there is a 75% chance that renal artery stenosis is present.
*Severe hypertension, impaired renal function, and recurrent flash [[pulmonary edema]]
 
====Class IIa Recommendations<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117  }} </ref>====
*Unexplained renal failure including patients starting renal replacement therapy
 
====Class IIb Recommendations<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117  }} </ref>====
*Presence of multi vessel [[CAD]] and no clinical clues of ARAS or PAD
*Unexplained [[CHF]] or [[refractory angina]]
 
====Other Indications====
* Severe hypertension in the presence of polyvascular disease ([[coronary artery disease]] or [[peripheral arterial disease]])
* A unilateral systolic-diastolic [[abdominal bruit]]. Although a bruit is infrequent in documented renal artery stenosis (the sensitivity is only 40% percent) if it is auscultated, it is associated with a very high specificity of 99%.<ref name="pmid7563536">{{cite journal| author=Turnbull JM| title=The rational clinical examination. Is listening for abdominal bruits useful in the evaluation of hypertension? | journal=JAMA | year= 1995 | volume= 274 | issue= 16 | pages= 1299-301 | pmid=7563536 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7563536  }} </ref>
* A unilateral systolic-diastolic [[abdominal bruit]]. Although a bruit is infrequent in documented renal artery stenosis (the sensitivity is only 40% percent) if it is auscultated, it is associated with a very high specificity of 99%.<ref name="pmid7563536">{{cite journal| author=Turnbull JM| title=The rational clinical examination. Is listening for abdominal bruits useful in the evaluation of hypertension? | journal=JAMA | year= 1995 | volume= 274 | issue= 16 | pages= 1299-301 | pmid=7563536 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7563536  }} </ref>
*The association of race with renal artery stenosis is not clear. Reports that it is observed more often in white patients may be due to reporting bias.<ref name="pmid2022411">{{cite journal| author=Svetkey LP, Kadir S, Dunnick NR, Smith SR, Dunham CB, Lambert M et al.| title=Similar prevalence of renovascular hypertension in selected blacks and whites. | journal=Hypertension | year= 1991 | volume= 17 | issue= 5 | pages= 678-83 | pmid=2022411 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2022411  }} </ref>
*The association of race with renal artery stenosis is not clear. Reports that it is observed more often in white patients may be due to reporting bias.<ref name="pmid2022411">{{cite journal| author=Svetkey LP, Kadir S, Dunnick NR, Smith SR, Dunham CB, Lambert M et al.| title=Similar prevalence of renovascular hypertension in selected blacks and whites. | journal=Hypertension | year= 1991 | volume= 17 | issue= 5 | pages= 678-83 | pmid=2022411 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2022411  }} </ref>
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=====Cushing’s Syndrome=====
=====Cushing’s Syndrome=====
[[Cushing's syndrome]] is an endocrine disorder caused by prolonged exposure to high endogenous or exogenous [[cortisol]] levels.  Hypertension in [[Cushing’s syndrome]] has been classically attributed to the [[mineralocorticoid]] effects of cortisol. It manifests as an absent fall of nocturnal [[blood pressure]] physiologically seen in normotensive subjects with associated disturbance in the adrenocorticotropic hormone-glucocorticoid system.<ref name="pmid3397172">{{cite journal| author=Imai Y, Abe K, Sasaki S, Minami N, Nihei M, Munakata M et al.| title=Altered circadian blood pressure rhythm in patients with Cushing's syndrome. | journal=Hypertension | year= 1988 | volume= 12 | issue= 1 | pages= 11-9 | pmid=3397172 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3397172  }} </ref>  Symptoms of Cushing's syndrome include  rapid [[obesity|weight gain]], particularly of the trunk and face with sparing of the limbs ([[central obesity]]), a round face often referred to as a "[[moon face]]", excess [[sweating]], [[insomnia]], reduced [[libido]], [[impotence]], [[amenorrhoea]], [[infertility]] and psychological disturbances, ranging from [[Euphoria (emotion)|euphoria]] to [[psychosis]]. [[clinical depression|Depression]] and [[anxiety]].<ref>{{cite book |title=The American Psychiatric Publishing Textbook of Neuropsychiatry and Behavioral Neurosciences |last=Yudofsky |first=Stuart C. |coauthors=Robert E. Hales |edition=5th |year=2007 |publisher=American Psychiatric Pub, Inc. |isbn=1585622397 }}</ref> Although an ideal diagnostic test is not considered yet available, clinicians often assess the 24-hour urinary [[cortisol]] excretion<ref name="pmid3958132">{{cite journal| author=Contreras LN, Hane S, Tyrrell JB| title=Urinary cortisol in the assessment of pituitary-adrenal function: utility of 24-hour and spot determinations. | journal=J Clin Endocrinol Metab | year= 1986 | volume= 62 | issue= 5 | pages= 965-9 | pmid=3958132 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3958132  }} </ref>, a low-dose [[dexamethasone suppression test]]<ref name="pmid14315650">{{cite journal| author=NUGENT CA, NICHOLS T, TYLER FH| title=Diagnosis of Cushing’s Syndrome; Single Dose Dexamethasone Suppression Test. | journal=Arch Intern Med | year= 1965 | volume= 116 | issue=  | pages= 172-6 | pmid=14315650 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14315650  }} </ref>, late evening serum or salivary cortisol<ref name="pmid9709931">{{cite journal| author=Raff H, Raff JL, Findling JW| title=Late-night salivary cortisol as a screening test for Cushing's syndrome. | journal=J Clin Endocrinol Metab | year= 1998 | volume= 83 | issue= 8 | pages= 2681-6 | pmid=9709931 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9709931  }} </ref>, and a [[CRH]] a following a [[dexamethasone suppression test]] to establish the diagnosis.<ref name="pmid8386285">{{cite journal| author=Yanovski JA, Cutler GB, Chrousos GP, Nieman LK| title=Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states. | journal=JAMA | year= 1993 | volume= 269 | issue= 17 | pages= 2232-8 | pmid=8386285 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8386285  }} </ref>
[[Cushing's syndrome]] is an endocrine disorder caused by prolonged exposure to high endogenous or exogenous [[cortisol]] levels.  Hypertension in [[Cushing’s syndrome]] has been classically attributed to the [[mineralocorticoid]] effects of cortisol. It manifests as an absent fall of nocturnal [[blood pressure]] physiologically seen in normotensive subjects with associated disturbance in the adrenocorticotropic hormone-glucocorticoid system.<ref name="pmid3397172">{{cite journal| author=Imai Y, Abe K, Sasaki S, Minami N, Nihei M, Munakata M et al.| title=Altered circadian blood pressure rhythm in patients with Cushing's syndrome. | journal=Hypertension | year= 1988 | volume= 12 | issue= 1 | pages= 11-9 | pmid=3397172 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3397172  }} </ref>  Symptoms of Cushing's syndrome include  rapid [[obesity|weight gain]], particularly of the trunk and face with sparing of the limbs ([[central obesity]]), a round face often referred to as a "[[moon face]]" along with central obesity, excess [[sweating]], [[proximal muscle weakness]], [[ecchymoses]], [[insomnia]], reduced [[libido]], [[impotence]], [[amenorrhoea]], [[infertility]] and psychological disturbances, ranging from [[Euphoria (emotion)|euphoria]] to [[psychosis]]. [[clinical depression|Depression]] and [[anxiety]].<ref>{{cite book |title=The American Psychiatric Publishing Textbook of Neuropsychiatry and Behavioral Neurosciences |last=Yudofsky |first=Stuart C. |coauthors=Robert E. Hales |edition=5th |year=2007 |publisher=American Psychiatric Pub, Inc. |isbn=1585622397 }}</ref> Although an ideal diagnostic test is not considered yet available, clinicians often assess the 24-hour urinary [[cortisol]] excretion<ref name="pmid3958132">{{cite journal| author=Contreras LN, Hane S, Tyrrell JB| title=Urinary cortisol in the assessment of pituitary-adrenal function: utility of 24-hour and spot determinations. | journal=J Clin Endocrinol Metab | year= 1986 | volume= 62 | issue= 5 | pages= 965-9 | pmid=3958132 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3958132  }} </ref>, a low-dose [[dexamethasone suppression test]]<ref name="pmid14315650">{{cite journal| author=NUGENT CA, NICHOLS T, TYLER FH| title=Diagnosis of Cushing’s Syndrome; Single Dose Dexamethasone Suppression Test. | journal=Arch Intern Med | year= 1965 | volume= 116 | issue=  | pages= 172-6 | pmid=14315650 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14315650  }} </ref>, late evening serum or salivary cortisol<ref name="pmid9709931">{{cite journal| author=Raff H, Raff JL, Findling JW| title=Late-night salivary cortisol as a screening test for Cushing's syndrome. | journal=J Clin Endocrinol Metab | year= 1998 | volume= 83 | issue= 8 | pages= 2681-6 | pmid=9709931 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9709931  }} </ref>, and a [[CRH]] a following a [[dexamethasone suppression test]] to establish the diagnosis.<ref name="pmid8386285">{{cite journal| author=Yanovski JA, Cutler GB, Chrousos GP, Nieman LK| title=Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states. | journal=JAMA | year= 1993 | volume= 269 | issue= 17 | pages= 2232-8 | pmid=8386285 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8386285  }} </ref>


=====Drugs=====
=====Drugs=====
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|-bgcolor="LightSteelBlue"
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
| '''Drug Side Effect'''
|bgcolor="Beige"| [[almotriptan]], [[dihydroergotamine]], [[ergotamine]], [[frovatriptan]], [[isometheptene]], [[rizatriptan]], [[sumatriptan]], [[zolmitriptan]], [[amitriptyline]], [[cyclosporine]], [[desipramine]], [[doxepin]], [[ephedrine]], [[glucocorticoid resistance ]], [[imipramine]], [[monoamine oxidase inhibitor]]s, [[nasal decongestants]], [[nortriptyline]], [[NSAIDs]], [[combined oral contraceptive pill]], [[phencyclidine]], [[phenylpropanolamine]], [[protriptyline]], [[pseudoephedrine]], [[sedative dependence]], [[serotonin toxicity]], [[steroid abuse]], [[cocaine]]
|bgcolor="Beige"| [[almotriptan]], [[amitriptyline]],  [[Asenapine maleate]], [[Atropine]], [[Beractant]], [[Betamethasone valerate]], [[Benzphetamine]], [[Betamethasone dipropionate]], [[Butorphanol]], [[Cidofovir]], [[cocaine]], [[combined oral contraceptive pill]], [[cyclosporine]], [[caspofungin acetate]], [[desipramine]], [[Desmopressin]], [[Desogestrel and Ethinyl Estradiol]], [[Diethylpropion]], [[dihydroergotamine]], [[diflunisal]], [[Dimercaprol]], [[Dipivefrine]], [[doxepin]], [[Drospirenone and Ethinyl estradiol]], [[Eculizumab]], [[Eletriptan]], [[ephedrine]], [[ergotamine]], [[Erythropoietin]], [[Estropipate]], [[etodolac]], [[febuxostat]], [[Florbetapir F-18]], [[formoterol]], [[frovatriptan]], [[gadoterate]], [[glucocorticoid resistance ]], [[gadopentetate]], [[Hydrocortisone]], [[Hydroxocobalamin]], [[Indomethacin]], [[imipramine]], [[interferon alfacon-1]], [[isometheptene]], [[Ketorolac tromethamine]], [[Lanreotide]], [[Leuprolide]], [[Levalbuterol]], [[Medroxyprogesterone]], [[Mefenamic acid]], [[Megestrol]], [[Meloxicam]],  [[Meloxicam]], [[Meropenem]], [[Metipranolol]], [[Methylene blue]], [[Methylphenidate]], [[Methylprednisolone]],  [[Metoclopramide]], [[Methoxy polyethylene glycol-epoetin beta]], [[Mifepristone]], [[Milnacipran hydrochloride]], [[Mirabegron]], [[monoamine oxidase inhibitor]]s, [[Nabilone]], [[Naphazoline]] , [[nasal decongestants]], [[Naproxen and esomeprazole magnesium]], [[Norethindrone acetate and Ethinyl estradiol]], [[Norgestimate and Ethinyl estradiol]], [[Norgestrel and Ethinyl estradiol]],  [[nortriptyline]], [[NSAIDs]], [[Oxaprozin]], [[Oxcarbazepine]], [[Pentamidine Isethionate]], [[Pergolide]], [[phencyclidine]], [[Phendimetrazine]], [[phenylpropanolamine]], [[Pilocarpine]], [[Piroxicam]], [[Pralidozxime]], [[protriptyline]], [[pseudoephedrine]], [[prednisolone]], [[Prednisone]], [[Ramucirumab]], [[Rasagiline]], [[Repaglinide and Metformin hydrochloride]],  [[rizatriptan]], [[Rotigotine]], [[sedative dependence]], [[serotonin toxicity]], [[Sertraline]], [[Sipuleucel-T]], [[Sorafenib]], [[steroid abuse]], [[Sulindac]], [[sumatriptan]], [[Sunitinib]], [[Thalidomide]], [[Tiagabine]], [[Tocilizumab]], [[Tolmetin]], [[Travoprost]], [[Triamcinolone]], [[Valganciclovir hydrochloride]], [[zolmitriptan]], [[Zolmitriptan]], [[Zonisamide]]
|-
|-
|-bgcolor="LightSteelBlue"
|-bgcolor="LightSteelBlue"
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==Causes in Alphabetical Order==
==Causes in Alphabetical Order==
{{MultiCol}}
{{MultiCol}}
* [[Abdominal obesity metabolic syndrome ]]
* [[Abdominal obesity metabolic syndrome ]]
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* [[Asphyxia ]]
* [[Asphyxia ]]
* [[Atheroma]]
* [[Atheroma]]
*[[Atropine]]
* Atypical [[Hemolytic uremic syndrome]]
* Atypical [[Hemolytic uremic syndrome]]
* [[Autoimmune Vasculitis ]]
* [[Autoimmune Vasculitis ]]
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* [[Avasthey syndrome ]]
* [[Avasthey syndrome ]]
* [[Bartter's Syndrome]]
* [[Bartter's Syndrome]]
*[[Betamethasone valerate]]
*[[Betamethasone dipropionate]]
* Bilateral [[Renal artery stenosis ]]
* Bilateral [[Renal artery stenosis ]]
* [[Binswanger's Disease ]]
* [[Binswanger's Disease ]]
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* [[Bright's Disease ]]
* [[Bright's Disease ]]
* [[Bronchopulmonary dysplasia]]
* [[Bronchopulmonary dysplasia]]
*[[Butorphanol]]
* [[Cadmium poisoning]]
* [[Cadmium poisoning]]
* [[Carcinoid Syndrome]]
* [[Carcinoid Syndrome]]
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* [[Chronic kidney disease ]]
* [[Chronic kidney disease ]]
* [[Chronic pyelonephritis]]
* [[Chronic pyelonephritis]]
*[[Cidofovir]]
* [[Cocaine]]
* [[Cocaine]]
* [[Cockayne syndrome ]]
* [[Cockayne syndrome ]]
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* [[Cyclosporine]]
* [[Cyclosporine]]
* [[Desipramine]]
* [[Desipramine]]
*[[Desmopressin]]
*[[Desogestrel and Ethinyl Estradiol]]
* [[Dexamethasone sensitive hypertension]]
* [[Dexamethasone sensitive hypertension]]
* [[Diabetes]]
* [[Diabetes]]
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* [[Eclampsia ]]
* [[Eclampsia ]]
* [[Ecstasy]] abuse
* [[Ecstasy]] abuse
* [[Eculizumab]]
{{ColBreak}}
{{ColBreak}}
* [[Eisenmenger's Syndrome ]]
* [[Eisenmenger's Syndrome ]]
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* [[Hereditary nephritis]] (X-linked)
* [[Hereditary nephritis]] (X-linked)
* [[Hereditary sensory and autonomic neuropathy 3 ]]
* [[Hereditary sensory and autonomic neuropathy 3 ]]
*[[Hydroxocobalamin]]
* [[Hyperadrenalism ]]
* [[Hyperadrenalism ]]
* [[Hypereosinophilic syndrome ]]
* [[Hypereosinophilic syndrome ]]
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* [[Increased salt intake]]
* [[Increased salt intake]]
* Indian [[Tobacco]] [[Poisoning ]]
* Indian [[Tobacco]] [[Poisoning ]]
*[[Infliximab]]
* [[Irradiation]]
* [[Irradiation]]
* [[Isolated secretion of 18-hydroxy-deoxycorticosterone]]
* [[Isolated secretion of 18-hydroxy-deoxycorticosterone]]
Line 393: Line 481:
* [[Lupus nephritis ]]
* [[Lupus nephritis ]]
* [[Lymphomatoid granulomatosis ]]
* [[Lymphomatoid granulomatosis ]]
* [[Medroxyprogesterone]]
* [[Meloxicam]]
* [[Meningitis]]
* [[Meningitis]]
* [[Meropenem]]
* [[Metabolic syndrome]]
* [[Metabolic syndrome]]
* [[Methylphenidate]]
* [[Mifepristone]]
* [Milnacipran hydrochloride]]
* [[Mineralocorticoid excess]]
* [[Mineralocorticoid excess]]
* [[Monoamine oxidase inhibitor]]s
* [[Monoamine oxidase inhibitor]]s
* [[MSBD syndrome ]]
* [[MSBD syndrome ]]
* [[Mucopolysaccharidosis]] type I [[Hurler syndrome]]
* [[Mucopolysaccharidosis]] type I [[Hurler syndrome]]
* Multicentric [[Reticulohistiocytosis ]]
* Multicentric [[Reticulohistiocytosis]]
* [[Multiple endocrine neoplasia type 1]]
* [[Multiple endocrine neoplasia type 1]]
* [[Mustard tree poisoning ]]
* [[Mustard tree poisoning ]]
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* [[Nicotine addiction ]]
* [[Nicotine addiction ]]
* [[Nipah virus encephalitis ]]
* [[Nipah virus encephalitis ]]
* [[Norgestrel and Ethinyl estradiol]]
* [[Nortriptyline]]
* [[Nortriptyline]]
* [[NSAIDs]]
* [[NSAIDs]]
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* [[Oral contraceptive pill]]
* [[Oral contraceptive pill]]
* [[Ovarian dysgenesis]]
* [[Ovarian dysgenesis]]
*[[Oxaprozin]]
* [[Paget's disease of bone ]]
* [[Paget's disease of bone ]]
* [[Pain]]
* [[Pain]]
* [[Pancreatitis]]
* [[Pancreatitis]]
* [[Patent ductus arteriosus]]
* [[Patent ductus arteriosus]]
*[[Pergolide]]
* [[PCOS]]
* [[PCOS]]
* [[Pheochromocytoma]]
* [[Pheochromocytoma]]
Line 433: Line 530:
* [[Pierre Robin's sequence ]]
* [[Pierre Robin's sequence ]]
* [[Pierson syndrome ]]
* [[Pierson syndrome ]]
*[[Pilocarpine]]
* [[Piroxicam]]
* [[Pituitary Cancer ]]
* [[Pituitary Cancer ]]
* [[Poliomyelitis]]
* [[Poliomyelitis]]
Line 441: Line 540:
* [[Post streptococcal glomerulonephritis ]]
* [[Post streptococcal glomerulonephritis ]]
* [[Post-exercise]]
* [[Post-exercise]]
*[[Pralidoxime]]
* [[Pregnancy toxemia /hypertension ]]
* [[Pregnancy toxemia /hypertension ]]
* [[Primary aldosteronism]]
* [[Primary aldosteronism]]
Line 455: Line 555:
* [[Pulmonary Lymphangiomatosis]]
* [[Pulmonary Lymphangiomatosis]]
* [[Quadriplegia]]
* [[Quadriplegia]]
*[[Ramucirumab]]
* [[Renal artery thrombosis]]
* [[Renal artery thrombosis]]
* [[Renal artery stenosis]]
* [[Renal emboli]]
* [[Renal emboli]]
* [[Renal segmental hypoplasia-induced Hypertension ]]
* [[Renal segmental hypoplasia-induced Hypertension ]]
Line 476: Line 578:
* [[Silicosis ]]
* [[Silicosis ]]
* [[Simple kidney cysts ]]
* [[Simple kidney cysts ]]
*[[Sipuleucel-T]]
* [[Skull fracture ]]
* [[Skull fracture ]]
* [[Sneddon Syndrome ]]
* [[Sneddon Syndrome ]]
*[[Sorafenib]]
* [[Steroid abuse]]
* [[Steroid abuse]]
* [[Stress-induced hypertension ]]
* [[Stress-induced hypertension ]]
* [[Sumatriptan]]
* [[Sumatriptan]]
* [[Sunitinib]]
* [[Systemic lupus erythematosus]]
* [[Systemic lupus erythematosus]]
* [[Takayasu arteritis ]]
* [[Takayasu arteritis ]]
Line 487: Line 592:
* [[Thromboembolism ]]
* [[Thromboembolism ]]
* [[Thrombotic thrombocytopenic purpura]]
* [[Thrombotic thrombocytopenic purpura]]
*[[Tiagabine]]
* [[Toxic mushrooms -- Psychedelic ]]
* [[Toxic mushrooms -- Psychedelic ]]
* [[Transfusion of large blood volumes]]
* [[Transfusion of large blood volumes]]
Line 497: Line 603:
* [[Urinary tract infections ]]
* [[Urinary tract infections ]]
* [[Urinary tract obstruction]]
* [[Urinary tract obstruction]]
* [[Valganciclovir hydrochloride]]
* [[Vasculitis ]]
* [[Vasculitis ]]
* [[Vater-like syndrome, with pulmonary hypertension, abnormal ears and growth deficiency ]]
* [[Vater-like syndrome, with pulmonary hypertension, abnormal ears and growth deficiency ]]

Latest revision as of 14:01, 17 May 2017

Chronic Hypertension Microchapters

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2017 ACC/AHA Hypertension Guidelines

Patient Information

Overview

Definition

Classification

Pathophysiology

Causes

Differentiating Hypertension from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Blood Pressure Measurement

Physical Examination

Laboratory Findings

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ETT

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor-In-Chief: Yazan Daaboul, Serge Korjian

Overview

Secondary hypertension is only responsible for 5% of cases of chronic hypertension whereas primary hypertension (also known as essential hypertension where no identifiable cause is identified) is responsible for 95% of cases.[1] Common causes of secondary hypertension include obstructive sleep apnea, hyperaldosteronism, kidney diseases, excess catecholamines, coarctation of the arota, cushing syndrome among other diseases.


 
 
Chronic hypertension
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Primary hypertension
(also known as essential hypertension)
(95% of the cases)
 
Secondary hypertension

(5% of the cases)


Primary Hypertension

When a full evaluation yields no clear etiology for the elevated blood pressure, the latter is identified as primary hypertension. Primary or essential hypertension is considered a chronic disease requiring lifelong treatment and follow-up. If an underlying disease is identifiable as the cause, secondary hypertension is diagnosed. Secondary hypertension is a potentially curable condition in most cases.[2] In comparison, the prevalence of primary hypertension is significantly higher than secondary hypertension, where only 5-10% of patients have a secondary etiology[1] Classically, the common age range for the presentation of primary hypertension is 30 to 55 years[3], but age alone should never warrant a diagnosis of primary hypertension without a proper work-up.

Secondary Hypertension

When to Suspect Secondary Hypertension

It is not cost effective to evaluate all hypertensive patients for secondary hypertension. [2] There are certain clinical scenarios, though, that should prompt further evaluation.

Early Onset Hypertension Under Age 30

Primary hypertension generally first occurs between 30 and 55 years. Onset of hypertension before puberty and before age 30 in the absence of risk factors should raise suspicion for secondary hypertension.

Abrupt Onset of Hypertension in A Normotensive Patient

Rapidly Progressive Hypertension or a Hypertensive Emergency or Urgency

Refractory Hypertension

Evaluation of Secondary Hypertension

 
 
 
 
 
Evaluation of secondary hypertension
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Investigation should be limited for patients with clues suggestive of potentially correctable causes.

❑ Presence of clues for renovascular hypertension (most common potentially correctable cause)?[4][5]

❑ Onset of hypertension before the age of 30 years
❑ Onset of severe hypertension (SBP ≥180 mm Hg and/or DBP ≥120 mm Hg) after the age of 55 years
❑ New azotemia or worsening renal function after administration of an ACE inhibitor or ARB agent
❑ Unexplained atrophic kidney or size discrepancy between kidneys of greater than 1.5 cm
❑ Sudden, unexplained pulmonary edema
❑ Accelerated hypertension (sudden and persistent worsening of previously controlled hypertension)
❑ Resistant hypertension (failure to achieve goal blood pressure in patients who are adhering to full doses of an appropriate 3-drug regimen that includes a diuretic)
❑ Malignant hypertension (hypertension with coexistent evidence of acute end-organ damage, i.e., acute renal failure, acutely decompensated congestive heart failure, new visual or neurological disturbance, and/or advanced [grade III to IV] retinopathy)
❑ Unexplained renal failure in the absence of proteinuria or an abnormal urine sediment
❑ Multivessel coronary artery disease
❑ Unexplained congestive heart failure
❑ Refractory angina
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
YES
 
 
 
 
 
NO
 

❑ Perform noninvasive diagnostic studies

❑ Duplex ultrasonography
❑ Gadolinium-enhanced magnetic resonance angiography
❑ Computed tomographic angiography (in individuals with normal renal function)
❑ Consider catheter angiography when noninvasive studies are inconclusive
 
 
 
 
 

Look for findings suggestive of other identifiable causes

❑ Pheochromocytoma

❑ Paroxysmal pounding headache
❑ Palpitations
❑ Profound perspiration
❑ Pallor
❑ Hand tremor

❑ Hyperaldosteronism

❑ Unexplained hypokalemia with urinary potassium wasting

❑ Obstructive sleep apnea

❑ Daytime somnolence
❑ Snoring
❑ Obesity

❑ Hyperparathyroidism

❑ Hypercalcemia

❑ Hypothyroidism

❑ Elevated TSH
❑ Puffy face

❑ Aortic coarctation

❑ Diminished or delayed femoral pulses and low or unobtainable blood pressures in the legs

Common Causes of Secondary Hypertension

Common causes of secondary hypertension are often memorized by the mnemonic ABCDE:

Letter Causes of Secondary Hypertension
A Accuracy, Apnea, Aldosteronism
B Bruit, Bad Kidneys
C Catecholamines, Coarctation, Cushing’s Syndrome
D Drugs, Diet
E Erythropoitin, Endocrine Disorders
Accuracy

An accurate assessment and re-assessment of blood pressures is an essential first step when a patient presents with high blood pressure. The accuracy of home BP measurements should be confirmed by calibrating the patient's measurement technique with that obtained in the doctor's office.

Apnea

Obstructive sleep apnea (OSA) is a respiratory disease characterized by repetitive narrowing or collapse of the upper airway during sleep[6] leading to apnea, hypopnea, and a nocturnal decrease in oxygen tension.[7] Symptoms and signs that might suggest OSA include daytime somnolence, obesity, snoring, and morning headache.[8] Patients with sleep apnea also tend to have drug resistant hypertension and may retain sodium. Diagnosis is made by polysomnography. Treatment relies on maintaining airway patency at night and includes, among others, the use of continuous positive airway pressure (CPAP).

Aldosterone

Primary (hyporeninemic) and secondary (hyperreninemic) hyperaldosteronism result in excess sodium and water retention with slight hypernatremia along with excretion of potassium resulting in hypokalemia in one half of patients.[9] Common symptoms of hyperaldosteronism include drug resistant hypertension, fatigue, headache, intermittent paralysis, muscle weakness, and numbness. The most common cause of primary hyperaldosteronism is an aldosterone-producing adenoma (an "aldosteronoma"), i.e. Conn’s Syndrome. Secondary hyperaldosteronism is due to an overactive RAAS, as seen in renin-secreting tumors, renal artery stenosis, pheochromocytoma, and other syndromes. The diagnosis is made by measuring the ratio of plasma aldosterone to plasma renin activity.[10] It is elevated in primary hyperaldosteronism and decreased/normal with elevated renin in secondary hyperaldosteronism. It should be noted that obesity can also cause aldosterone levels to be elevated. Treatment depends upon the underlying etiology: surgery to resect an adenoma causing primary hyperaldosteronism and spironolactone, an aldosterone antagonist to treat secondary hyperaldosteronism.

Bruit

Renovascular hypertension is due to decreased blood supply to the kidneys secondary to renal artery stenosis and it is the most common correctable cause of secondary hypertension. Atherosclerosis of the renal artery (renal artery stenosis) in older patients above 50 years of age[11] and fibromuscular dysplasia in younger patients are the most common etiologies.

According to the 2013 ACC/AHA Guidelines for the Management of PAD[12], diagnostic work-up for renal artery stenosis is indicated in the following conditions:

Class I Recommendations[12]

  • Hypertension of any stage before the age of 30
  • Stage II hypertension (severe hypertension systolic blood pressure > 180 mm Hg or diastolic blood pressure > 120 mm Hg) in patients older than 55 years. If only mild hypertension is present, then renal artery stenosis is the underlying cause in only 1% of patients [13], but if the blood pressure is markedly elevated, then the risk of renal artery stenosis goes up 10 to 50 fold.
  • Accelerated condition of previously controlled hypertension
  • Resistant hypertension
  • Malignant hypertension
  • New azotemia (50% rise in creatinine that is sustained) within one week after administration of an Angiotensin Converting Enzyme (ACE)inhibitor or ARB
  • Unexplained atrophic kidney or asymmetric kidneys that differ by > 1.5 cm. If the kidney is < 9 cm in size, there is a 75% chance that renal artery stenosis is present.
  • Severe hypertension, impaired renal function, and recurrent flash pulmonary edema

Class IIa Recommendations[12]

  • Unexplained renal failure including patients starting renal replacement therapy

Class IIb Recommendations[12]

Other Indications

  • Severe hypertension in the presence of polyvascular disease (coronary artery disease or peripheral arterial disease)
  • A unilateral systolic-diastolic abdominal bruit. Although a bruit is infrequent in documented renal artery stenosis (the sensitivity is only 40% percent) if it is auscultated, it is associated with a very high specificity of 99%.[14]
  • The association of race with renal artery stenosis is not clear. Reports that it is observed more often in white patients may be due to reporting bias.[15]

Definitive diagnosis is made by magnetic resonance angiography (MRA) and renal arteriography.[16] Other diagnostic methods include duplex ultrasound scanning[17], and captopril-augmented radio-isotopic renogram[18]. Treatment is based upon the underlying etiology.

Bad Kidney (Chronic Renal Failure)

Renal parenchymal disease blunts the kidney’s physiological ability to maintain appropriate blood pressure. Notably, hypertension is both a cause and a consequence of renal parenchymal disease; the two are closely associated and may potentiate each other.[19] The diagnosis is made by demonstration of a decreased GFR. The mechanisms by which renal parenchymal disease leads to the development of hypertension are numerous and include activation of the local RAAS, release of vasoconstrictor cytokines, and inappropriate natriuresis for any given blood pressure.

Catecholamines

Catecholamine excess occurs in several non-disease states, such as acute stress, the administration of medications with sympathomimetic activity, and illicit drug use such as cocaine and these conditions can be ruled out by thorough history taking. Pheochromocytoma, a tumor of the adrenal gland leading to excess secretion of epinephrine, should be considered in young patients with the triad of intermittent hypertensive episodes causing headache, sweating, and tachycardia. However, pheochromocytoma in older adults or a presentation with sustained hypertension is not uncommon. Diagnostic studies to evaluate pheochromocytoma include measurement of plasma free metanephrines and urinary fractionated metanephrines. The diagnostic value of plasma and urinary catecholamines is of limited value given the very short half-life of catecholamines. Treatment is usually by surgical resection of the secreting tumor with appropriate adrenergic blockade.[20]

Coarctation

Coarctation of the aorta is a congenital heart defect, caused by a narrowing in a segment of the ascending or descending aorta. The diagnosis is often made in a neonate or an infant as a result of a weak femoral pulse or asymmetric brisk brachial pulses. Hypertension occurs as a result of a reduction in the effective circulation at the level of the kidneys which respond by increasing plasma volume which in turn causes hypertension in the upper extremities. Diagnosis is by CT angiography, but can also be made in neonates and infants by ultrasound of the heart and the great vessels. Definitive treatment is by surgical correction and or stenting.

Cushing’s Syndrome

Cushing's syndrome is an endocrine disorder caused by prolonged exposure to high endogenous or exogenous cortisol levels. Hypertension in Cushing’s syndrome has been classically attributed to the mineralocorticoid effects of cortisol. It manifests as an absent fall of nocturnal blood pressure physiologically seen in normotensive subjects with associated disturbance in the adrenocorticotropic hormone-glucocorticoid system.[21] Symptoms of Cushing's syndrome include rapid weight gain, particularly of the trunk and face with sparing of the limbs (central obesity), a round face often referred to as a "moon face" along with central obesity, excess sweating, proximal muscle weakness, ecchymoses, insomnia, reduced libido, impotence, amenorrhoea, infertility and psychological disturbances, ranging from euphoria to psychosis. Depression and anxiety.[22] Although an ideal diagnostic test is not considered yet available, clinicians often assess the 24-hour urinary cortisol excretion[23], a low-dose dexamethasone suppression test[24], late evening serum or salivary cortisol[25], and a CRH a following a dexamethasone suppression test to establish the diagnosis.[26]

Drugs

An extensive list of drugs can be associated with hypertension. The most common agents include immunosuppressive agents, non-steroidal anti-inflammatory drugs, oral contraceptive pills, some weight loss agents, stimulants, monoamine oxidase inhibitors, triptans, ergotamines, and sympathomimetics.[1]

Diet

In addition to the association of obesity with hypertension, the 2001 study “Effects on Blood Pressure of Reduced Dietary Sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet” concluded that a high sodium diet above the recommended 100 mmol per day (2.4 g of sodium or 6 g of sodium chloride salt) is associated with hypertension. As a result, reduction of sodium levels below 100 mmol per day and following the DASH diet (rich in vegetables, fruits, with low-fat dairy products) can significantly lower BP.[27] Ingestion of excessive amounts of liquorice can lead to elevation in the blood pressure.

Erythropoietin

Elevated erythropoietin is typically seen in COPD patients who have functional anemia due to chronic hypoxia and in hematologic disorders such as polycythemia. The pathogenesis of erythropoietin-induced hypertension includes increased hematocrit and blood viscosity, altered sensitivity to vasopressors, dysregulated vasodilatory factors, and vascular cell growth causing arterial remodeling and changes in arterial smooth musculature.[28] Diagnosis and treatment are etiology-dependent.

Endocrine

In addition to the more common endocrine causes of hypertension such as hyperaldosteronism, Cushing’s syndrome, and pheochromocytoma, several other endocrine changes can cause hypertension. Both hypothyroidism and hyperthyroidism can cause hypertension by volume retention and by increased cardiac output, respectively. Also, hyperparathyroidism and hypovitaminosis D can cause hypertension due to poorly understood mechanisms, where parathyroidectomy seems to significantly decrease blood pressure in patients with parathyroid disease and elevated BP.[29] Acromegaly can also be a cause of hypertension.

Causes by Organ System

Cardiovascular Aortic regurgitation, aortic dissection, acute severe vascular damage, adams Nance syndrome , aneurysm, aortic coarctation , aortic stenosis, arterial occlusive disease, progressive - -- heart defects -- bone fragility -- brachysyndactyly , arteriosclerosis, atheroma, avasthey syndrome , carotid paraganglioma ,Congenital mitral stenosis , eisenmenger's Syndrome , fibromuscular dysplasia of arteries , grange syndrome , hemangiomatosis (familial pulmonary capillary disease), hypertensive heart disease , pulmonary artery agenesis , vasculitis , patent ductus arteriosus, third degree AV block
Chemical / poisoning Acetaldehyde , aristolochic acid poisoning , arizona Bark Scorpion poisoning , black widow spider envenomation , cadmium poisoning, cocaine, ecstasy abuse , ginseng , heavy metal poisoning, Indian tobacco poisoning, jimsonweed poisoning , lead poisoning , lockwood-Feingold syndrome , mustard tree poisoning , nicotine addiction , pseudoephedrine poisoning , silicosis , toxic mushrooms -- Psychedelic , lobelia poisoning
Dermatologic No underlying causes
Drug Side Effect almotriptan, amitriptyline, Asenapine maleate, Atropine, Beractant, Betamethasone valerate, Benzphetamine, Betamethasone dipropionate, Butorphanol, Cidofovir, cocaine, combined oral contraceptive pill, cyclosporine, caspofungin acetate, desipramine, Desmopressin, Desogestrel and Ethinyl Estradiol, Diethylpropion, dihydroergotamine, diflunisal, Dimercaprol, Dipivefrine, doxepin, Drospirenone and Ethinyl estradiol, Eculizumab, Eletriptan, ephedrine, ergotamine, Erythropoietin, Estropipate, etodolac, febuxostat, Florbetapir F-18, formoterol, frovatriptan, gadoterate, glucocorticoid resistance , gadopentetate, Hydrocortisone, Hydroxocobalamin, Indomethacin, imipramine, interferon alfacon-1, isometheptene, Ketorolac tromethamine, Lanreotide, Leuprolide, Levalbuterol, Medroxyprogesterone, Mefenamic acid, Megestrol, Meloxicam, Meloxicam, Meropenem, Metipranolol, Methylene blue, Methylphenidate, Methylprednisolone, Metoclopramide, Methoxy polyethylene glycol-epoetin beta, Mifepristone, Milnacipran hydrochloride, Mirabegron, monoamine oxidase inhibitors, Nabilone, Naphazoline , nasal decongestants, Naproxen and esomeprazole magnesium, Norethindrone acetate and Ethinyl estradiol, Norgestimate and Ethinyl estradiol, Norgestrel and Ethinyl estradiol, nortriptyline, NSAIDs, Oxaprozin, Oxcarbazepine, Pentamidine Isethionate, Pergolide, phencyclidine, Phendimetrazine, phenylpropanolamine, Pilocarpine, Piroxicam, Pralidozxime, protriptyline, pseudoephedrine, prednisolone, Prednisone, Ramucirumab, Rasagiline, Repaglinide and Metformin hydrochloride, rizatriptan, Rotigotine, sedative dependence, serotonin toxicity, Sertraline, Sipuleucel-T, Sorafenib, steroid abuse, Sulindac, sumatriptan, Sunitinib, Thalidomide, Tiagabine, Tocilizumab, Tolmetin, Travoprost, Triamcinolone, Valganciclovir hydrochloride, zolmitriptan, Zolmitriptan, Zonisamide
Ear Nose Throat Nephrosis -- deafness -- urinary tract -- digital malformation , Fitzsimmons-Walson-Mellor syndrome
Endocrine Carcinoid Syndrome, acromegaly , adrenal incidentaloma , alcohol-induced pseudo-Cushing syndrome , apparent mineralocorticoid excess , congenital adrenal hyperplasia due to 11-Beta-hydroxylase deficiency, congenital adrenal hyperplasia due to 17-alpha-hydroxylase deficiency, Conn's syndrome, cushing's disease, cushing's syndrome , diabetes, Familial cushing syndrome , graves disease , hyperadrenalism , hyperparathyroidism , hyperpituitarism , hyperthyroidism, hypothyroidism, isolated secretion of corticosterone, isolated secretion of deoxycorticosterone, mineralocorticoid excess, multiple endocrine neoplasia type 1, myxoedema, pheochromocytoma, primary aldosteronism, primary cortisol resistance, pseudohyperaldosteronism , pseudohypoaldosteronism , Schroeder syndrome 1 , hyperthyroidism, hypoglycemia, isolated secretion of 18-hydroxy-deoxycorticosterone, renin-secreting tumors, dexamethasone sensitive hypertension
Environmental No underlying causes
Gastroenterologic Hepatorenal tyrosinemia , pancreatitis, retroperitoneal Fibrosis
Genetic Congenital adrenal hyperplasia due to 11-Beta-hydroxylase deficiency, congenital adrenal hyperplasia due to 17-alpha-hydroxylase deficiency, cockayne syndrome , down Syndrome , Fabry's Disease , isolated secretion of 18-hydroxy-deoxycorticosterone, Pierre Robin's sequence , Senior-Loken Syndrome, Turner Syndrome , Vater-like syndrome, with pulmonary hypertension, abnormal ears and growth deficiency , Von Hippel-Lindau Disease , Werner syndrome , Williams Syndrome , Gaucher disease type 3 , mucopolysaccharidosis type I Hurler syndrome
Hematologic Anemia, Atypical Hemolytic uremic syndrome, Catastrophic antiphospholipid syndrome , Essential mixed cryoglobulinemia , Faye-Petersen-Ward-Carey syndrome , hemolytic uremic syndrome , hypereosinophilic syndrome , Liddle's syndrome, Multicentric reticulohistiocytosis , polycythemia , thromboembolism , thrombotic thrombocytopenic purpura
Iatrogenic No underlying causes
Infectious Disease Poliomyelitis, meningitis, post streptococcal glomerulonephritis , renal tuberculosis, nipah virus encephalitis
Musculoskeletal / Ortho Acrodynia , Allain Babin Demarquez syndrome , familial osteodysplasia - Anderson type, Paget's disease of bone , Grange syndrome , Faye-Petersen-Ward-Carey syndrome , oculo skeletal renal syndrome , Thieffry and Sorrell Dejerine syndrome
Neurologic Guillain-Barre Syndrome, autonomic dysreflexia syndrome , Binswanger's Disease , Brain stem encephalitis, central sleep apnea , choroideremia -- hypopituitarism , disequilibrium syndrome , dysautonomia , hereditary sensory and autonomic neuropathy 3 , increased intracranial pressure, neurofibromatosis syndrome Type II , neurogenic hypertension , nipah virus encephalitis , obstructive sleep apnea , Sneddon Syndrome , upper spinal cord lesions, Wolfram's disease, meningitis, polyradiculitis, quadriplegia, Adams Nance syndrome , glycine encephalopathy - classical neonatal form, pituitary Cancer , Fitzsimmons-Walson-Mellor syndrome
Nutritional / Metabolic Abdominal obesity metabolic syndrome , acute intermittent porphyria , congenital hepatic porphyria , Gaucher disease type 3, glycine encephalopathy - classical neonatal form, glycine synthase deficiency , gouty nephropathy, liquorice, metabolic syndrome, tyrosinemia , Von Gierke disease IB, increased salt intake, mucopolysaccharidosis type I Hurler syndrome, Fabry's Disease , vitamin D -- adverse effects
Obstetric/Gynecologic Eclampsia , Fowler-Christmas-Chapple syndrome , gestational hypertension, HELLP syndrome , ovarian dysgenesis, PCOS, pregnancy toxemia /hypertension , twin-twin transfusion syndrome
Oncologic Endothelin producing tumor, adrenal Cancer , familial adrenal adenoma , renal Cancer , neuroblastoma

pituitary Cancer , renin-secreting tumors, rhabdoid tumor , Wilms' tumor , adrenal incidentaloma , familial renal cell carcinoma

Opthalmologic Isolated Ectopia lentis, oculo skeletal renal syndrome
Overdose / Toxicity Amphetamine abuse, almotriptan, dihydroergotamine, ergotamine, frovatriptan, isometheptene, rizatriptan, sumatriptan, zolmitriptan, amitriptyline, cyclosporine, desipramine, dexamethasone sensitive hypertension, doxepin, ephedrine, glucocorticoid resistance , imipramine, nasal decongestants, nortriptyline, combined oral contraceptive pill, phencyclidine, phenylpropanolamine, protriptyline, serotonin toxicity, steroid abuse, pseudoephedrine, cocaine
Psychiatric Anxiety
Pulmonary Asphyxia , bronchopulmonary dysplasia, COPD , Goodpasture syndrome , pulmonary cystic lymphangiectasis , pulmonary embolism , pulmonary fibrosis /granuloma , pulmonary veno-occlusive disease , pulmonary lymphangiomatosis, respiratory acidosis , respiratory failure , unilateral pulmonary agenesis , hyperventilation, obstructive sleep apnea , Wegener's granulomatosis
Renal / Electrolyte Bartter's Syndrome, dissection of the renal arteries, acid-base imbalance , acute renal failure , albuminuria , analgesic nephropathy syndrome , autosomal dominant polycystic kidney disease , autosomal recessive polycystic kidney disease , bilateral renal artery stenosis , Bright's Disease , chronic kidney disease , chronic pyelonephritis, congenital membranous glomerulonephritis, congenital stenosis of renal artery, congenital hydronephrosis, diffuse mesangial sclerosis, familial renal cell carcinoma , Fitzsimmons-Walson-Mellor syndrome , glomerulonephritis , hereditary nephritis (X-linked), hypoplastic kidney, IgA nephropathy , kidney arteriovenous fistula , Kimmelstiel-Wilson disease, lupus nephritis , nephrocalcinosis , nephrosclerosis , nephrosis -- deafness -- urinary tract -- digital malformation , nephrotic syndrome , oculo skeletal renal syndrome , Pierson syndrome , Severe infantile polycystic kidneys with tuberous sclerosis , post streptococcal glomerulonephritis , renal artery thrombosis, renal artery stenosis, renal emboli, renal segmental hypoplasia-induced Hypertension , renal tuberculosis, Salcedo syndrome , simple kidney cysts , Thieffry and Sorrell Dejerine syndrome , urinary tract infections , urinary tract obstruction, vesicoureteral reflux , Wegener's granulomatosis , Gitelman's Syndrome, hepatorenal tyrosinemia , Atypical hemolytic uremic syndrome, gouty nephropathy, Goodpasture syndrome
Rheum / Immune / Allergy Autoimmune Vasculitis , systemic lupus erythematosus, diffuse systemic sclerosis , polyarteritis nodosa , Takayasu arteritis
Sexual No underlying causes
Trauma Electrical burns , head injury, skull fracture
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Acquired total lipodystrophy , following kidney transplantation, aging, alcohol intake, alcohol withdrawal, amyloidosis , bone cement implantation syndrome, brachydactyly with hypertension, Carnevale-Canun-Mendoza syndrome , codeine withdrawal , collagen disease, essential hypertension, fever, Gram's syndrome , hypothermia, irradiation, Kashani-Strom-Utley syndrome , lymphomatoid granulomatosis , MSBD syndrome , neuroleptic malignant syndrome , obesity, physical inactivity , Selye syndrome , serotonin syndrome , shaken baby syndrome , stress-induced hypertension , type A personality, Wagener syndrome , pain, post-exercise, transfusion of large blood volumes, white coat hypertension

Causes in Alphabetical Order


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