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RENOVASCULAR HYPERTENSION

بسم الله الرحمن الرحيم. RENOVASCULAR HYPERTENSION . NAIF ALQARNI. PHYSIOLOGY OF R.A.A.S Angiotensinogen The source of all angiotensins . The liver is the primary site of synthesis, which is not stored but secreted directly after production.

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RENOVASCULAR HYPERTENSION

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  1. بسم الله الرحمن الرحيم RENOVASCULAR HYPERTENSION NAIF ALQARNI

  2. PHYSIOLOGY OF R.A.A.S Angiotensinogen • The source of all angiotensins. • The liver is the primary site of synthesis, which is not stored but secreted directly after production. • Several hormones stimulate angiotensinogen synthesis by the liver, including estrogens, glucocorticoids .Stress-full stimuli. • Feedback control through AII and renin.

  3. Renin The kidney is the major site of renin production. mechanisms affect the secretion A–Macula Densa Mechanism Reduction of salt delivery stimulates renin secretion and vice versa B–Baroreceptor Mechanism Diminished cell stretch as a result of renal hypoperfusion ,hyperpolarizes the juxtaglomerular cells.

  4. C–Neural Mechanism β-adrenergic ; and Dopamine. D–Endocrine and Paracrine Mechanisms Prostaglandin E2 and I2 E–Intracellular Mechanisms Agents that increase cyclic AMP.

  5. Angiotensin-Converting Enzyme pulmonary endothelial ACE is presumed to be the major site of ACE.

  6. Angiotensin II Effect of AngiotensinII on • GlomerularCirculation. • Tubular Effects. • Medullary Effects. • Vascular Effects. • Adrenal Effects. • Central Nervous Effect. • GonadalEffect.

  7. Angiotensin II Receptor Subtypes • Angiotensinreceptor subtypes, named AT1 and AT2. • In the kidneys, AT1 receptors are located predominantly in the glomeruli and tubulointerstitium, whereas AT2 receptors are located in the large cortical blood vessels.

  8. PATHOLOGY AND NATURAL HISTORY OF RVH

  9. PATHOLOGY AND NATURAL HISTORY OF RVH Atherosclerosis • Approximately 70% of all renovascular lesions are caused by atherosclerosis. • Atherosclerotic stenosis usually occurs in the proximal 2 cm of the renal artery. • The lesion involves the intima of the artery and, in two thirds of the cases, arises as an eccentric plaque.

  10. Atherosclerosis • Seen predominantly in males and usually in older age groups. • progressive arterial obstruction occurs in 42% to 53% of patients with atherosclerotic renal artery disease, often within the first 2 years of radiographic follow-up.

  11. Atherosclerosis The incidence of progression to complete renal artery occlusion in the most wide study has ranged from 9% to 16%, and this has occurred more often in arteries that initially showed high degrees of stenosis.

  12. Atherosclerosis Atherosclerotic renal artery disease progresses in many patients and that loss of functioning renal parenchyma is a common sequela of such progression. And artery obstruction can eventuate in end-stage renal disease (ESRD).

  13. PATHOLOGY AND NATURAL HISTORY OF RVH Fibrous dysplasia IntimalFibroplasia • Primary intimalfibroplasia occurs in children and in young adults and constitutes approximately 10% of the total number of fibrous lesions. • characterized by a circumferential accumulation of collagen inside the internal elastic lamina.

  14. PATHOLOGY AND NATURAL HISTORY OF RVH Fibrous dysplasia Medial Fibroplasia Medial fibroplasia is the most common of the fibrous lesions, constituting 75% to 80% of the total number. It tends to occur in women between the ages of 25 and 50 years and often involves both renal arteries.

  15. PATHOLOGY AND NATURAL HISTORY OF RVH Fibrous dysplasia PerimedialFibroplasia Perimedialfibroplasia occurs predominantly in young women between the ages of 15 and 30 years and has therefore been referred to, rather crudely, as girlie disease. It constitutes about 10% to 15% of the total number of fibrous lesions.

  16. PATHOLOGY AND NATURAL HISTORY OF RVH Fibrous dysplasia Fibromuscular Hyperplasia Fibromuscular hyperplasia is an extremely rare disease, constituting only 2% to 3% of fibrous lesions, and tends to occur in children and young adults.

  17. PATHOLOGY AND NATURAL HISTORY OF RVH Miscellaneous: Renal artery aneurysms, middle aortic syndrome, periarterial fibrosis, and post-traumatic intimal or medial disease. Variable in location and obstruction; occurs in diverse clinical settings.

  18. PATHOPHYSIOLOGY OF RVH Two-Kidney, One-Clip Model ischemia of the clipped kidney RAAS is activated generalized vasoconstriction and systemic hypertension

  19. PATHOPHYSIOLOGY OF RVH Two-Kidney, One-Clip Model contralateral kidney higher than normal perfusion pressure suppression of renin secretion excreting higher than normal levels of sodium and water

  20. PATHOPHYSIOLOGY OF RVH One-Kidney, One-Clip Model solitary ischemic kidney secretes renin activating the RAAS and resulting in systemic hypertension No contralateral kidney No excretion of Na and water

  21. Stages in the development of renovascular hypertension • Acute stage • Transitional stage Days to weeks, in solitary kidney No contralateral kidney no dauiresis and natuiresis hyper vlemia AII and hypervolemia maintain renal perfusion decrease renin level So, in this case hypertension depend on volume expansion.

  22. So, In patients with renovascular disease, particularly those with bilateral RAS or those with a stenotic renal artery to a single kidney, ACE inhibitors or AII antagonist may cause a deterioration of renal function and azotemia.

  23. Stages in the development of renovascular hypertension In nmormalcontralateral kidney volume expansion is avoided renin levels remain high So, HTN is due to RAAS.

  24. Stages in the development of renovascular hypertension Chronic stage If blood flow is restored during these first 2 stages and renal perfusion is reinstated, blood pressure soon returns to a normal level. If renal hypoperfusion persists and stage 3 is reached, restoration of renal blood flow may not normalize blood pressure, presumably because of secondary irreversible vascular or renal parenchymal disease.

  25. ISCHEMIC NEPHROPATHY This is a clinical syndrome that occurs through different pathophysiologic mechanisms, is distinct from RVH, and can occur in the absence of elevated blood pressure. IN is the result of chronic hypoperfusion of the total functioning renal mass.

  26. ISCHEMIC NEPHROPATHY • Renal autoregulation fails to maintain the GFR when renal perfusion decreases below 70 to 80 mm Hg. • This occurs when the luminal diameter of the renal artery is stenosed by more than 70% of the original size. • At this point, the stenosis becomes hemodynamically significant, resulting in a gradual deterioration of the GFR with an accompanying rise in the serum creatinine level.

  27. ISCHEMIC NEPHROPATHY This injury is not simply cell death related to a lack of oxygen and nutrients ? because; • The oxygen demand of the kidney never exceeds the supply. • kidney needs only about 10% of its blood flow to maintain its oxygen requirement. So, the cellular mechanisms by which a decrease in renal size and IN develop are not well understood.

  28. ISCHEMIC NEPHROPATHY mechanisms play a role, including vascular mediators (endothelin, thromboxane, prostacyclin, and nitric oxide), calcium accumulation in or ATP depletion of the ischemic cells, production of oxygen free radicals, or disruption of cellular membrane polarity ( Textor, 1994 ).

  29. ISCHEMIC NEPHROPATHY HISTOPATHOLOGY • Tubular necrosis and atrophy. • Glomeruli decrease in size with wrinkling of the glomerular tuft and thickening of Bowman's capsule. • Localized or global glomerular sclerosis . • Hypercellularity of the juxtaglomerular apparatus is commonly seen.

  30. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Clinical Clues • The onset of hypertension. • A family history. • Sudden onset and shorter duration. • Hypertension that is difficult to control • Malignant hypertension or hypertensive crises. • Smoking.

  31. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Peripheral Plasma Renin Activity • To diagnose overactivity of the RAAS. • Antihypertensive medications should be discontinued for 2 weeks. • Blood should be collected 4 hours after the patient's ambulation.

  32. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Peripheral Plasma Renin Activity • Sensitivity of 80% • Specificity 84%. • 16% of patients with essential hypertension have elevated PRA, whereas up to 20% of patients with RVH have normal PRA. • No anatomic information and has no value for diagnosing IN

  33. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Captopril Test • Measurement of peripheral PRA before and after an oral dose of captopril. • All diuretics and ACE inhibitors need to be discontinued for at least 1 week before the test. • A normal- or high-salt diet is needed • Blood should be drawn with the patient in the same position before and after captopril administration. • An oral dose of 25 mg of captopril is used, and blood is drawn again 1 hour after the dose.

  34. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Captopril Test Positive when; • postcaptopril PRA greater than 12 ng/mL/hr • an absolute increase in PRA greater than 10 ng/mL/hr, • 400% increase in baseline PRA (150% increase if the baseline PRA was more than 3 ng/mL/hr). • sensitivity 74%. • specificity is around 89% .

  35. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Renal Vein Renins • Subtracting the renin value in the arterial blood to the kidney (inflow) from the renin value in the venous blood from the kidney (outflow). • Hypersecretion of renin from the ischemic kidney (>50% of PRA) confirms the diagnosis of RVH. • Contralateral suppression of renin secretion (i.e. renal vein - IVC renin = 0) indicates an appropriate response of the normal contralateral kidney to the elevated blood pressure and predicts a cure of hypertension after revascularization. • Increasing severity of stenosis reduces blood flow to the ischemic kidney, resulting in an increased RVR increment

  36. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION CaptoprilRenography • Oral captopril (25 to 50 mg) is usually used, although IV enalapril (0.04 mg/kg) • MAG3 befor and after one hour ACE inhibitor asymmetry of renal size and function specific captopril-induced changes in the renogram normally less than 0.3, a 0.15 change is considered significant • sensitivity 90% to 93%, specificity 93% to 98%

  37. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Duplex Ultrasonography • Normal renal PSV averages 100 ± 25 cm/sec • The ratio of the renal PSV to the aortic PSV (renal PSV/aortic PSV) is called the renal aortic ratio (RAR). A ratio of 3.5 or more indicates severe (>60%) stenosis • sensitivity 89.5%. • specificity 90.7%.

  38. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Magnetic Resonance Angiography Only the proximal parts of the main renal arteries are visualized without the ability to image the distal arterial tree.

  39. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Computed Tomography Angiography Spiral CTA lacks the ability to define disease distal to the main stem renal artery, and a relatively large volume of IV iodinated contrast material is required to perform the study.

  40. CLINICAL FEATURES OF RENOVASCULAR HYPERTENSION Contrast Arteriography • Gold standard for diagnosing renal artery disease. • Combined diagnostic and therapeutic procedure. • Carbon dioxide has been introduced as a contrast agent for intra-arterial injection in an effort to reduce contrast nephrotoxicity from iodinated contrast material.

  41. Angiography in primary intimalfibroplasia reveals a smooth, fairly focal stenosis, usually involving the proximal or midportion of the vessel or its branches.

  42. Angiographically, medial fibroplasia demonstrates a typical “string of beads” appearance involving the distal two thirds of the main renal artery and branches.

  43. SELECTION OF PATIENTS FOR SURGICAL OR ENDOVASCULAR THERAPY atherosclerotic RVH • Medical management • Intervention with surgery or endovascular therapy is best reserved for patients whose hypertension cannot be adequately controlled or when renal function is threatened by advanced vascular disease.

  44. SELECTION OF PATIENTS FOR SURGICAL OR ENDOVASCULAR THERAPY Fibrous dysplasia • Because loss of renal function from progressive obstruction is uncommon in medial type, medical management is the best choice. • Intimal or perimedialfibroplasia generally progresses and often eventuates in ischemic renal atrophy so, early interventional therapy in these patients is therefore indicated.

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