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Evaluation and treatment of renal hypertension

Evaluation and treatment of renal hypertension. Dr. Scope. Renal hypertension Introduction Causes ARAS, FMD Takayasu’s arteritis Pathophysiology Clinical features Diagnosis Imaging Management Conclusions. Renovascular hypertension (RVH). Renal Hypertension or RVH: Defined as

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Evaluation and treatment of renal hypertension

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  1. Evaluation and treatment of renal hypertension Dr.

  2. Scope • Renal hypertension • Introduction • Causes • ARAS, FMD • Takayasu’s arteritis • Pathophysiology • Clinical features • Diagnosis • Imaging • Management • Conclusions

  3. Renovascular hypertension (RVH) • Renal Hypertension or RVH: • Defined as • The presence of systemic hypertension due to a stenotic or obstructive lesion within the renal artery • Form of secondary hypertension, accounting for an estimated 0.5% to 4% of cases in unselected hypertensive patients US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  4. RVH: Introduction • The simultaneous presence of renal artery stenosis (RAS) and systemic hypertension should not lead to the conclusion that • The patient has RVH; • Strictly speaking, the definitive diagnosis of RVH can only be made retrospectively • When hypertension improves upon correction of the stenosis US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  5. RVH: Introduction (Contd) • In practice, obtaining complete “reversal” of hypertension is rarely possible • Important to recognize that renovascular disease • Often accelerates preexisting hypertension, • Can ultimately threaten the viability of the post-stenotic kidney and • Impair sodium excretion in subjects with congestive heart failure Med Clin North Am. 2009 May ; 93(3): 717, available in PMC 2010 May 1.

  6. RVH: Causes • The two most common causes of RVH are 1. Atherosclerotic renal artery stenosis (ARAS) 2. Fibromuscular dysplasia (FMD) Med Clin North Am. 2009 May ; 93(3): 717, available in PMC 2010 May 1.

  7. RVH: Causes (Contd) • Takayasu’s arteritis (TA) • Although TA has a worldwide distribution, it is observed frequently in Asia than in North America • The most common cause of RVH in • India • China • Korea • Japan and other countries of South East Asia Eur J Vasc Endovasc Surg 2007;33, 578-82

  8. RVH: Indian studies • TA • In one study from Chandigarh by Sharma et al Takayasu’s arteritis was found as the leading cause of hypertension in hospitalised patients • Involvement: 50% cases bilateral and in 28% unilateral • Indicating that this condition must be kept in mind as one of the important causes, especially in northern India, whenever one is considering RVH Angiology 1985; 36: 370-8

  9. RVH: Indian studies (Contd) • Study at PGI Chandigarh • 205 patients with hypertension were shown to have a renovascular aetiology over 16 years. Of these, • 125 (61 %) Takayasu's arteritis, • 58 (28.3 %) fibromuscular dysplasia, • 16 (7.8 %) atherosclerosis, • five (2.4 %) polyarteritis nodosa and • one (0.5 %) renal artery aneurysm Q J Med. 1992;85:833-43.

  10. RVH: Indian studies (Contd) • Study at PGI Chandigarh (Contd) • Among patients with TA, males were affected as commonly as females • The mean age of these patients at the time of detection was 26.8 +/- 8.6 years (range 5-52 years) • Type I arteritis in nine (7.2 %), • Type II in 40 (32 %) and • Type III in 76 (60.8 %) patients • The abdominal aorta was involved in 117 (93.3 %) patients • TA was associated with ulcerative colitis in two patients and with renal amyloidosis and focal segmental glomerulosclerosis with a nephrotic syndrome in one patient each Q J Med. 1992;85:833-43.

  11. RVH: Indian studies (Contd) • Seth GS Medical College & KEM Hospital, Parel, Mumbai • Medical records of 54 patients with RVH showed • Aortoarteritis 44 (81.5%), • Atherosclerotic disease 7 (31.5%) and • Fibromuscular dysplasia 3 (5.6%) as etiologies of RVH 32nd Annual Conference ofIndian Society of Nephrology September, 2001

  12. TA • TA is a chronic vasculitis involving mainly the aorta and its branches, as well as the pulmonary and coronary arteries • Classical definition of TA is that of • Chronic, progressive, inflammatory, occlusive disease of the aorta and its branches Eur J Vasc Endovasc Surg 2007;33, 578-82

  13. TA: Aetiology • Remains enigmatic • Various mechanisms such as post-infective, autoimmune, ethnic susceptibility and a genetic predisposition have been postulated • Autoimmunity appears to be the most plausible mechanism Eur J Vasc Endovasc Surg 2007;33, 578-82

  14. ARAS • Most common and problematic cause of RVH • 90% of cases of RVH due to ARAS • Mainly in older men • Lesion at the ostium or proximal third of the renal artery as an extension of an aortic plaque • Bilateral in approx. 1/3 of cases Med Clin North Am. 2009 May ; 93(3): 717, available in PMC 2010 May 1.

  15. ARAS (Contd) Aortogram demonstrating high-grade stenosis affecting the left renal artery Quantitative measurements indicated more than 86% lumen obstruction Med Clin North Am. 2009 May ; 93(3): 717, available in PMC 2010 May 1.

  16. ARAS (Contd) • Risk factors • Identical to those associated with systemic atherosclerosis, i.e., • Advanced age, male sex, smoking, • Diabetes mellitus, hypertension, • Positive family history, and • Dyslipidemia US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  17. ARAS (Contd) • Generally believed that • ARAS slowly progresses over time, but the rate of progression is variable • Atherosclerotic renovascular disease is associated with accelerated and more severe target organ injury than essential HT US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49 HT- Hypertension

  18. FMD • 10% of cases of RVH are due to FMD • Mainly in younger women • Bilateral renal artery involvement with extension into the distal portion of the artery and its branches is common US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  19. RVH: Pathophysiology Safian & Textor. NEJM 344:6;

  20. RVH: Pathophysiology (Contd) • Widely believed that • The obstructing lesion in the renal artery has to reach a “critical level” of about 75% to cause any clinically significant hemodynamic effects US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  21. RVH: Pathophysiology (Contd) US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  22. RVH: Pathophysiology (Contd) • Bilateral RAS, or unilateral RAS in a functionally impaired or absent contralateral kidney, • The increased renin produced by both kidneys is responsible for the increased salt and water retention and subsequent HT US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  23. RVH: Pathophysiology (Contd) • Unilateral RAS with a normal contralateral kidney, • HT is caused by the increased renin produced in the ischemic kidney while • The nonischemic kidney has its renin production suppressed US Nephrology 2009;5(2):56–59, Proc (Bayl Univ Med Cent) 2010;23(3):246–49

  24. RVH: Diagnosis • Mere presence of RAS and hypertension does not establish the diagnosis of RVH • Three-step approach to the diagnosis of RVH has been suggested Curr Cardiol Rep 2005;7(6):405–11.

  25. RVH: Diagnosis (Contd) • First step: • An appropriate selection of patients who are more likely to have RVH • Second step: • The patients’ renal arteries are imaged to demonstrate RAS • Third step: • Resolution or improvement in blood pressure control occurs with reversion of the stenosis Curr Cardiol Rep 2005;7(6):405–411.

  26. RVH: Diagnosis (Contd) • Clinical findings associated with RVH N Engl J Med 2001;344(6):431–42.; Curr Cardiol Rep 2005;7(6):405–11; Kidney Int 2006;70(9):1543–1547

  27. RVH: Diagnosis (Contd) • Clinical findings associated with RVH(Contd) ACE: angiotensin-converting enzyme; ARBs: angiotensin II receptor blockers; RAS: renal artery stenosis N Engl J Med 2001;344(6):431–42.; Curr Cardiol Rep 2005;7(6):405–11; Kidney Int 2006;70(9):1543–1547

  28. RVH: Diagnosis (Contd) • Clinical findings associated with RVH (Contd) AAA: abdominal aortic aneurysm; CAD, coronary artery disease; PAD:peripheral arterial disease N Engl J Med 2001;344(6):431–42.; Curr Cardiol Rep 2005;7(6):405–11; Kidney Int 2006;70(9):1543–47

  29. RVH: Imaging • Intra-arterial angiography • The gold standard • Invasive and carries the risk of contrast-induced nephropathy • Not used routinely unless • Concurrent therapy with angioplasty, with/without stenting, is being considered

  30. RVH: Imaging (Contd) • Digital subtraction angiography (DSA) • Uses less dye than a conventional arteriogram but is still invasive • The quality of images with DSA is not as good as with conventional angiogram

  31. RVH: Imaging (Contd) • Captopril-enhanced renography and scintigraphy • Noninvasive test and the ability to assess renal functional status • Use is limited in patients with bilateral RAS and in patients with significant renal insufficiency • Provide a basis for functional, not anatomical, diagnosis of RAS, as there is no direct visualization of the renal arteries

  32. RVH: Imaging (Contd) • Duplex ultrasound imaging • Direct visualization of the renal vascular tree while assessing blood flow velocity and pressure wave forms • Limitations include interoperator variability and the need for expertise in obtaining and interpreting the images

  33. RVH: Imaging (Contd) • Spiral computed tomography angiography • Enables a three-dimensional reconstruction of the vascular tree • Excellent sensitivity and specificity to visualize RAS • However, requires up to 150 cc of iodinated contrast, which may be nephrotoxic

  34. RVH: Imaging (Contd) • Magnetic resonance angiography (MRA) • Noninvasive imaging technique and results in excellent visualization of the renal vasculature • Gadolinium is used as the radio-contrast in the phase contrast technique • Drawbacks • High cost • Potential for nephrogenic systemic fibrosis in patients with renal insufficiency

  35. TA: Diagnostic criteria • Following table mentions • Sensitivity and specificity for the various diagnostic criteria Eur J Vasc Endovasc Surg 2007;33, 578-82

  36. TA: Diagnostic criteria Modified diagnosis criteria for TA: Sharma et al Eur J Vasc Endovasc Surg 2007;33, 578-82

  37. TA: Diagnostic criteria (Contd) Modified diagnosis criteria for TA: Sharma et al (Contd) Eur J Vasc Endovasc Surg 2007;33, 578-82

  38. TA: Diagnostic criteria (Contd) • Type I is limited to the aortic arch and its branches • Type II affects the descending thoracic and abdominal aorta • Type III is extensive form involving the arch and the thoracic and abdominal aorta • Type IV is designated to those cases with pulmonary involvement in addition to the features of type I, II, or III Eur J Vasc Endovasc Surg 2007;33, 578-82

  39. TA: Clinical features • TA classically progresses through 3 stages: • An early systemic illness usually associated with constitutional symptoms and fever • A vascular inflammatory phase • The inflammation settles down or burns out Eur J Vasc Endovasc Surg 2007;33, 578-82

  40. TA: Clinical features (Contd) Eur J Vasc Endovasc Surg 2007;33, 578-82

  41. RVH: Management • Treatment options include • Pharmacological therapy with various antihypertensive medications, • Percutaneous angioplasty with or without stent placement, and • Surgical revision of RAS

  42. RVH: Management (Contd) • Availability of potent antihypertensive drugs and the advances in endovascular techniques, as well as stents, have made surgical treatment rarely necessary

  43. RVH: Management (Contd)

  44. RVH: TA Management • Besides management of hypertension and its complications, • Steroids and immunosuppressive agents like methotrexate and cyclophosphamide are used to suppress disease activity • Response to therapy is faster and better in children with a higher rate of remission • Anti-platelet agents like aspirin and dipyridamole have been used especially in patients with transient neurological symptoms Eur J Vasc Endovasc Surg 2007;33, 578-82

  45. RVH: TA Management (Contd) • Percutaneous transluminal angioplasty (PCTA) is the commonest palliative procedure performed with a success rate varying from 56-80% • All lesions are not amenable to PCTA and surgical bypass procedures become imperative when stenosis exceeds 70% Eur J Vasc Endovasc Surg 2007;33, 578-82

  46. RVH: TA Management (Contd) • Irrespective of the surgical procedures undertaken, the outcome appears to be favorable when the disease is quiescent • Surgical procedures are required for total aortic occlusion, severe aortic incompetence, critical central nervous system ischemia, aneurysms, renovascular hypertension, ostial lesions, tight stenosis, extensive renal segmental artery involvement, poorly functioning renal units, renal failure and, occasionally, in case of failure of angioplasty Eur J Vasc Endovasc Surg 2007;33, 578-82

  47. RVH: TA Management (Contd) • Surgery for TA should be deferred in the active phase of the disease, which is characterized by an increased ESR, increased C-reactive protein and symptoms of fever, malaise or pain over the major arteries, or signs of progressive vascular involvement on angiography as the chances of thrombosis increase • Surgery is often difficult in the active disease period due to more bleeding, friable tissue and the high chance of thrombosis Eur J Vasc Endovasc Surg 2007;33, 578-82

  48. RVH: FMD Management • FMD • Percutaneous angioplasty is the treatment of choice, • Often resulting in relief of the stenosis and marked improvement (or cure) of the hypertension • Stents may be used • In patients with suboptimal results with angioplasty alone • Surgery is considered to be the last option, particularly • For patients for whom endovascular procedures have failed

  49. RVH: FMD Case • CT angiogram obtained in a 45 y.o. woman presenting with new onset RVH • Aneurysmal dilation and vascular occlusion beyond a fibromuscular lesion is present in the right kidney associated with loss of perfusion to the entire upper pole of the kidney • Antihypertensive therapy in this instance can be achieved using agents that block the RAS • While such cases are unusual, they underscore the broad range of lesions that can produce the syndrome of RVH

  50. Fibromuscular Dysplasia, before and after PTRA Atherosclerotic RAS before and after stent Safian & Textor. NEJM 344:6;

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