RENOVASCULAR HYPERTENSION POWERPOINT PRESENTATION

Ppt on renovasular hypertension

1. RENOVASCULAR HYPERTENSION DR. ANEES PUTHAWALA UROLOGY DEPT SAVEETHA MEDICAL COLLEGE

2. INTRODUTION Renovascular disease - states in which reduced perfusion of the kidney exist (with or without hypertension) Ischemic nephropathy reduced GFR associated with reduced renal blood flow beyond levels of renal auto-regulatory compensation Renovascular hypertension is a clinical syndrome marked by a rise in arterial pressure with or without associated ischemic and hypertensive renal injury

3. Partial or complete occlusion of one or both renal arteries – renal ischemia - Renovascular hypertension MC reason : Renal Artery Stenosis (RAS) Defined as narrowing of the renal artery by more than 50% of its natural luminal diameter MC form of secondary & potentially curable hypertension

4. Epidemiology : 5% of hypertensives 10% to 20% of the ESRD population Moderate to severe hypertension (very less mild cases) 10% to 45% : Malignant hypertension India: 0.8% of urban population (Indian journal of Nephrology) uncertain whether the correction of an underlying vascular lesion results in long-term BP control or preservation of renal function

5. Etio -pathogenesis Main Etiology : Atherosclerosis (70 %) and fibromuscular dysplasia (30%)

6. Atherosclerosis M>F 40-70 yrs Involves proximal 1/3rd of renal artery/ ostium 70-80% plaque impinging on the renal ostium 30%: non ostial narrowing, 1-3 cm away from ostium Fibromuscular dysplasia Younger Caucasian women B/L Distal segments of renal arteries Medial fibroplasia is the most common and least likely to progress over time

7. Other causes Endovascular aortic stent migration Post renal trauma Extrinsic compression Aortic dissection extending into renal artery

8. Medial fibroplasia Medial fibroplasia occurs almost exclusively in women between 25 and 50 years of age. This lesion has the characteristic “ string of beads ” appearance on angiography. The lesions involve the distal half of the main renal artery and may extend into the branches. Patients are not likely to progress to complete occlusion, nor are they likely to experience a decrease in their overall renal function. Types of fibromuscular dysplasia: medial fibroplasia(30%), perimedial fibroplasia (5%), intimal fibroplasia (5%).

9. Perimedial fibroplasia • Girlie disease -15 to 30yrs • Affects only the renal A. • The collagen is deposited in the outer border of the media • the aneurysmal “beads” in perimedial fibroplasia that never exceed the diameter of the main renal artery. • If left untreated, perimedial fibroplasia often progresses to renal occlusion and loss of renal function

10. Intimal fibroplasia • Intimal fibroplasia predominantly in children and younger adults. • May result in dissection, arterial wall hematoma, and renal infarction. • The lesions are usually in the proximal renal artery; however, they may also occur in the mid or distal renal artery. • Without intervention are likely to progress and result in loss of renal function.

11. PATHOPHYSIOLOGY OF RENOVASCULAR HYPERTENSION The classical experiments on RVH were performed by Goldblatt and colleagues who demonstrated that hypertension could be produced by constricting the renal artery in the dog The two-kidney, one-clip (2K,1C) model, in which one renal artery is clipped and the contralateral kidney is normal, One-kidney, one-clip (1K,1C) model, in which one renal artery is clipped and the contralateral kidney is removed. RVH results in both models, but the evolution and the pathophysiologic mechanisms are different

12. Two-Kidney, One-Clip Model (2k –1C) Two-kidney, one-clip model is characterized by the unilateral release of renin from the ischemic kidney accompanied by contralateral suppression of renin release from the normal kidney Sodium retention by the stenotic kidney, and excretion by the contralateral kidney; euvolemia ; Hypertension dependent on ANGIOTENSIN-II-induced vasoconstriction Unclipping of the ischemic kidney, ACE inhibitors, or A-II antagonists result in a marked decrease in blood pressure

13. Vasoconstrictor hypertensive model managed with reversal of the RAS, with ACE inhibition, or with angiotensin receptor blockade

14. One-Kidney, One-Clip Model One-kidney, one-clip model, one renal artery is clipped and the contralateral kidney is removed The solitary kidney secretes renin, activating the RAAS and resulting in systemic hypertension. Stenotic kidney avidly conserves sodium and fluid, producing volume expansion. The elevation of blood pressure, sodium retention, and volume expansion gradually suppress renin release from the ischemic kidney. Hypertension in the one-kidney, one-clip model is largely maintained by volume and sodium excess in the presence of normal circulating A-II levels , ACE inhibitors or AII antagonists do not result in a marked decrease of blood pressure

15. Volume hypertensive model Plasma renin levels normal

16. Who to suspect? 1.Severe or refractory hypertension with evidence of grade III or IV hypertensive retinopathy (particularly in Caucasians) 2. Abrupt onset of moderate to severe hypertension, particularly in a normotensive or previously well-controlled hypertensive 3. Onset of hypertension before age 20 (early onset) or after age 50 (late onset), particularly in those without a family history of hypertension 4. Unexplained worsening of renal function with or without hypertension or in association with the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) or with a reduction of blood pressure (BP) to the current accepted norm with the use of other antihypertensive agents

17. 5. Paradoxic worsening of hypertension with the use of diuretics 6. Unexplained recurrent episodes of heart failure —“flash” pulmonary edema 7. The presence of a systolic-diastolic abdominal bruit that radiates to both flanks 8. The presence of diffuse vascular disease and/or evidence of cholesterol embolization

18. Noninvasive screening tests : • Magnetic resonance angiography (MRA) • Spiral (helical) computed tomography (CT) • Duplex Doppler ultrasonography Invasive screening tests: CAPTOPRIL RENOGRAPHY Investigations for Renovascular Hypertension

19. Magnetic resonance angiography (MRA) Sensitive non-invasive screening test Sensitivity of 100% ( main renal artery); specificity of 71% to 96% Lesions involving the distal,intrarenal , and accessory arteries can be missed Risk of NSF (GFR< 30)

20. Spiral Ct Angiography Sensitivity of 98% and a specificity of 94% for detecting renovascular lesions Limited in renal insufficiency dye induced nephrotoxicity increases (for creatinine>1.7mg/dl or↑)

21. Duplex doppler Demonstrates bilateral disease Does not require the discontinuation of antihypertensive therapy or the exposure to potentially nephrotoxic contrast Accurate for those with renal failure Disadvantage: Time consuming, highly operator dependent, and is a technically difficult test to perform. Difficult to adequately visualize renal arteries in obese patients and in those with overlying intestinal gas

22. RENAL DOPPLER Usually seven readings are taken from one kidney- origin, proximal, mid and distal main renal artery and upper, midpolar and lower segmental arteries. Spectral waveforms are captured from each artery and PSV, RI are calculated. Normal PSV of renal arteries is 60-100 cm/sec. Normal renal artery waveforms demonstrate rapid systolic upstroke and persistent forward flow in diastole.

23. Findings of hemodynamically significant renal artery stenosis Include - PSV at the site of stenosis of greater than 180-200 cm/ sec. -Renal artery to aortic ratio exceeding 3.3 or 3.5

24. Angiography & intra-arterial DSA Gold standard Indicated if clinical index of suspicion is high and intervention is contemplated Intra-arterial DSA allows less radiocontrast to be administered (25 to 50 mL vs. 100 ml for conventional angio

25. CAPTOPRIL RENOGRAPHY Oral captopril 25-50 mg is given, prior to isotope injection Determines rate of isotope uptake and washout Intrinsic renal abnormalities limit the washout and curve characteristics(serum creat >2mg/dl)

26. Major criteria for positive test .  Decreased relative uptake with one kidney accounting for <40% of total GFR.  Delayed peak uptake of the isotope 10-11 min.  Slower washout in stenotic kidney.  ( > 5 min. delay)

27. Renal vein renin measurements:- May help predict the BP response to renal revascularization. Previous studies indicated that lateralization of renal vein levels (>1.5 : 1 stenotic nonstenotic kidney ratio) predicts a favorable BP response for more than 90% of patients. Some clinicians use these measurements to verify the role of a pressor kidney before undertaking nephrectomy

28. Management  Medical therapy  Angioplasty with or without stenting  Surgery

29. Medical therapy Control of BP : 90% by medication Mainly ACE inhibitors and ARB’s As monotherapy , ACE inhibitors may control BP in 80% of patients Combined with a diuretic , control may be increased to almost 90% Atherosclerotic renal artery lesions may progress with time 40% to 60% of patients have progression of their atherosclerotic renal artery lesions throughout 7 years, with half of these progressing within 2 years.

30. Medical therapy may reduce BP below a critical level and induce ongoing renal ischemia distal to the arterial lesion Results in tubular atrophy, interstitial fibrosis, glomerulosclerosis , and progressive loss of function in the affected kidney Renal function should be closely monitored Serum creatinine concentration and estimated GFR or creatinine clearance, renal sizes and cortical blood flow velocity by duplex scanning should be assessed

31. Percutaneous Transluminal Renal artery Angioplasty (PTRA) BEST RESULTS : Less than 10 mm in length , partially occluded, and do not involve the ostium Improvement in BP may be seen as quickly as 4 to 6 hours after the procedure but is more commonly seen after 48 hours Results better in - fibromuscular dysplasia - recent onset of hypertension -those with poorly controlled hypertension despite medical therapy - unable to tolerate medical therapy - Evidence of ischemic nephropathy Success rate of PTRA in experienced hands ranges from 87% to 100% Restenosis rate of up to 27% may be seen

32. PTRA-Unilateral atherosclerotic RAS Technical success rates may be as low as 70% Long term improvement not consistent Improvement of hypertension was seen in 86% of patients with unilateral non- ostial lesions as compared with 46% with unilateral ostial lesions ( Canzanello et al, 1989) Thrombosis, perforation, or dissection of the renal arteries and/or diffuse athero -embolism occurring in 15% undergoing the procedure

33. PTRA-B/L Atherosclerotic lesions Disappointing results Difficult to dilate High complication rates Unsuccessful in 60% pts Cure rates of HTN : 8 %; improvement of BP: 43% (Ramsay and Waller, 1990) The restenosis rate following PTRA is significant (30% for nonostial and 50% for ostial lesions)

34. Angioplasty with stenting Successful stenting can be achieved in 100% patients Restenosis rate: 15-25 % 88% success rate vs 57 % (with no stent) [Van et al, 1999] But no statistically significant difference in BP Can be used after an unsuccessful PTRA Mainly important in atherosclerotic patients

35. 5% to 15% complication rate may be seen with PTRA or stenting. Hematoma formation at the puncture site renal spasm - severe renal artery spasm may result in local thrombosis and renal infarction Reversible acute renal failure-20% Renal artery perforation, occlusion, dissection, and irreversible acute renal failure resulting from atheroembolization are less frequent (<5%)

36. ACC/AHA GUIDELINES (before coral study) PTRA is a reasonable option for 1. Patients with a hemodynamically significant RAS and accelerated hypertension or malignant hypertension 2. Hypertension with an unexplained unilateral small kidney 3. Hypertension with intolerance to medication 4. Renal stent placement that is indicated for ostial lesions that meet the clinical criteria for intervention “ Window of opportunity” defined by a serum creatinine level between 1.5 mg/ dL and 3 mg/ dL for most interventions to be successful

37. Surgical treatment RAS with concomitant aneurysmal or occlusive aortic ds (where surgery is indicated) Macroaneurysms of the renal artery (>4cm; risk of rupture is high) Malignant or accelerated hypertension (with or without acute renal failure) Who did not respond or cannot tolerate medical therapy Transluminal angioplasty is technically impossible to accomplish

38. Criteria that will ensure the best outcome of surgical revascularization of a renal artery a kidney greater than 8 cm in length; retrograde filling of the distal renal artery by collateral vessels on radiographic or scintigraphic imaging studies patency of the distal renal artery viability of the involved kidney on isotopic renography minimal glomerular sclerosis and well-preserved tubules on renal biopsy Aorto renal bypass : preferred technique (when abdominal aorta is not diseased) Spleno renal bypass , hepato renal bypass , ileo renal bypass Use of the supraceliac or lower thoracic aorta for the bypass as these are usually less involved by atherosclerotic disease

39. Thank you