1. Hypertension and renovascular hypertension BY Dr. Hayam Hebah Associate professor of Internal Medicine AL Maarefa College

2. In 2000, ¼ of the world‘s population was estimated to have hypertension. It is a risk factor for cardiovascular disease including myocardial infarction and stroke.

3. Definition and stages of hypertension:

5. Types of Hypertension Primary HTN: also known as essential HTN. accounts for 95% cases of HTN. no universally established cause known. Secondary HTN: less common cause of HTN ( 5%). secondary to other potentially rectifiable causes.

6. Primary hypertension

9. Secondary HTN-Clues in Medical History Onset: at age < 30 yrs ( Fibromuscular dysplasia) or > 55 (athelosclerotic renal artery stenosis), sudden onset (thrombus or cholesterol embolism). Severity: Grade II, unresponsive to treatment. Episodic, headache and chest pain/palpitation (pheochromocytoma, thyroid dysfunction). Morbid obesity with history of snoring and daytime sleepiness (sleep disorders)

10. Secondary HTN-Clues on Routine Labs Increased creatinine, abnormal urinalysis ( renovascular and renal parenchymal disease) Unexplained hypokalemia (hyperaldosteronism) Impaired blood glucose ( hypercortisolism) Impaired TFT (Hypo-/hyper- thyroidism)

11. Secondary HTN-Screening Tests www.nhlbi.nih.gov

12. Isolated Systolic Hypertension Not distinguished as a separate entity as far as management is concerned. SBP should be primarily considered during treatment and not just diastolic BP. Systolic BP is more important cardiovascular risk factor after age 50. Diastolic BP is more important before age 50.

13. Hypertensive Crises Hypertensive Urgencies: No progressive target-organ dysfunction. (Accelerated Hypertension) Hypertensive Emergencies: Progressive end- organ dysfunction. (Malignant Hypertension)

14. Hypertensive Urgencies Severe elevated BP in the upper range of stage II hypertension. Without progressive end-organ dysfunction. Examples: Highly elevated BP without severe headache, shortness of breath or chest pain. Usually due to under-controlled HTN.

15. Hypertensive Emergencies Severely elevated BP (>180/120mmHg). With progressive target organ dysfunction. Require emergent lowering of BP. Examples: Severely elevated BP with: Hypertensive encephalopathy Acute left ventricular failure with pulmonary edema Acute MI or unstable angina pectoris Dissecting aortic aneurysm

17. Resistant hypertension Definition: It is blood pressure remaining higher than 140/90 mmHg despite optimal or best tolerated doses of 3 drugs. Confirmed by ABPM Consider add fourth antihypertensive

20. Treatment of hypertension:

24. RENAL ARTERY STENOSIS

25. CAUSES: Atherosclerosis: (85%)more in old patients with atherosclerotic heart disease Fibromuscular dysplasia: (15%)more in young patients especially females Large vessel Vasculitis as Takayasu‘s arteritis and polyarteritis nodosa Thromboembolism Aneurysms of renal artery

26. Mark A. Pohl Pathophysiology:

27. Risk Factors For Renal Artery Stenosis 1.Age- Seen mostly in elderly population of age above 50 years 2.Sex- More common among female patients. 3.Family History Of Vascular Disease- – Hypertension – Coronary artery disease – Peripheral vascular disease – Congestive heart failure 4.Smoking- Patient with history of chronic smoking may suffer with weakness in arterial wall secondary to ischemic changes. 5.Hypertension- Hypertension may be caused by a renal artery stenosis or precedes stenosis. 6.Diabetes- High blood sugar may cause vascular and muscular diseases resulting in renal artery stenosis. 7.High Cholesterol- High cholesterol causes atherosclerosis and plaque formation. High cholesterol is associated with renal artery stenosis. Chronic renal disease

29. Clinical Clues Onset of diastolic hypertension after age 55 Refractory or malignant hypertension Development of resistant hypertension in a previously well-controlled patient Progressive increase in Creatinine, even if still “normal” Presence of atherosclerotic macrovascular disease elsewhere heightens suspicion Left heart failure out-of-proportion to LV dysfunction or ischemic burden Clinically silent RAS

30. Atherosclerotic RAS: Commonest cause of RAS(75-85%). Age >55 years, more in males Characterised by ostial stenosis that is associated with atherosclerosis of aorta and major branches as iliacs. *picture is complicated by small vessel disease in kidnies. *Ischemic nephropathy and renal failure may occur *death may occur from coronary, Cerebral or other vascular disease rather than from renal failure.

31. Fibromuscular dysplasia: More in females, age 15-30 years Uncommon cause of RAS(15-25% of cases). unknown etiology. There is hypertrophy of the media(medial fibroplasia) May be associated with dis- ease in other arteries as carotid artery dissections..irregular narrowing(beading ) in distal renal artery and extends to intrarenal branches

33. Symptoms Of Renal Artery Stenosis Asymptomatic Disease- No Symptoms- The disease is often asymptomatic. Incidental Findings- The Renal Artery Stenosis is often diagnosed during abdominal image studies performed to evaluate other disease causing abdominal symptoms. Non-Specific Symptoms of Renal Artery Stenosis (RAS): Most of the non-specific symptoms are caused by complications like congestive heart failure and hypertension associated with Renal Artery Stenosis. Weakness and fatigue. Somnolence- sleepiness. Loss of appetite.

34. Specific Symptoms of Renal Artery Stenosis (RAS): Uncontrolled Hypertension- – Headache – Tinnitus – Vertigo – Lightheadedness – Palpitation Congestive Heart Failure- – dyspnea – Edema – Ascites End Stage Renal Disease- – Hematuria – Proteinuria – Edema feet

35.  Clinical syndrome most important in patient selection When there is a suspicion of a Renal Artery Stenosis, investigative tests may be ordered for confirmatory diagnosis, which may include: Urine Examination- Hematuria Proteinuria Blood Examination- Hyperkalemia (high serum potassium) hyponatremia Screening for Renovascular Disease

36.  Various diagnostic modalities: – Serologic markers – Duplex ultrasound - in experienced hands can predict with great accuracy the presence or absence of significant RAS – Captopril renal scan - 10-25% false negative – MR angiography - rare false negatives / common false positives. Equipment/experience dependent – Contrast angiography

39. Approach: The preferred imaging method for a patient suspected of having RAS is controversial Non invasive sonography: accurate identification can be difficult,because they provide only indirect evidence of the presence of RAS. Invasive techniques : much more accurate BUT have the potential of nephrotoxicity. They can cause deterioration of renal function and procedure-related complications at the site of arterial puncture or catheter-induced embolism.

40. When the history is highly suggestive and no risk of radiocontrast-mediated renal injury is present-------  intra-arterial digital subtraction angiography (DSA) or conventional angiography in the form of renal arteriography (the current standard) is the appropriate initial test. In patients at risk-----  carbon dioxide angiography can determine the presence of a stenosis, and the risk associated with radiocontrast angiography is imposed only on those individuals most likely to benefit. When a moderate suspicion of exists----  spiral (CT), (MRA), or duplex ultrasonography should be performed, depending on availability and local experience. A negative test result indicates that RAS is highly unlikely, whereas a positive test result can be followed up by means of renal arteriography.

41. Assessment of Renin Release The baseline plasma renin activity (PRA) is elevated in 50-80% of patients with RVHT. Measuring the rise in the PRA 1 hour after administering 25-50 mg of captopril can increase the predictive value of the test. Patients with RAS have an exaggerated increase in PRA, perhaps due to removal of the normal suppressive effect of high angiotensin II levels on renin secretion in the stenotic kidney.

42. The sensitivity and specificity of studies of the captopril renin test are 75-100% and 60-95%, respectively. Limitations include the need to discontinue antihypertensive medications that can affect the PRA (eg, ACE inhibitors, beta-blockers, and diuretics), the low sensitivity, and the somewhat decreased predictive value when compared to a renogram after ACE inhibition. Although elevation of peripheral or renal vein PRA has been used to diagnose unilateral renal disease and predict surgical curability, an elevated plasma renin level does not establish the cause of hypertension, and levels that are within the reference range do not rule out renovascular disease.

43. Renal vein renin ratio Renal vein renin measurements compare renin release from the 2 kidneys and are used to predict the potential success of surgical revascularization.

44. Angiography The standard diagnostic study of RAS is renal arteriography. It is necessary whenever surgery or percutaneous transluminal angioplasty is anticipated. Some consider intra-arterial DSA to be equally acceptable as a standard. It requires one half the volume of dilute contrast medium that standard arteriography requires. MRA, CT angiography, and spiral angiography are newer studies that hold considerable promise for diagnosis and evaluation of RVHT

45. Complication of angiography Bleeding at puncture site. Thrombus formation. Embolus formation ( plaque dislodged). Dissection of vessel. Puncture site infection(contamination) Contrast reaction. Renal impairment due to ATN.

49. Treatment and management Optimal blood pressure control plays an essential role in the therapeutic management of renovascular hypertension (RVHT); Definitive therapy for the underlying cause must be considered in order to avoid the development of ischemic nephropathy

50. Pharmacologic Therapy RVHT is often refractory to medical treatment. Because current approaches to renal artery dilation and surgical revascularization yield excellent results, these procedures are generally considered the treatments of choice in preference to life-long antihypertensive medication. the most effective therapy is with an angiotensin- converting enzyme (ACE) inhibitor In patients without hemodynamically significant renal artery disease, a serum creatinine increase of up to 35% above baseline with an ACE or an ARB is considered acceptable and is not a reason to withhold treatment unless hyperkalemia develops.

51. Percutaneous Transluminal Angioplasty PTA is cheaper and less invasive than surgical revascularization and can be performed at the time of angiography. If patients are refractory to treatment or if restenosis develops, surgical revascularization can still be performed. PTRA is most effective against midvessel stenosis. Lesions involving segmental arteries or the ostia of renal arteries and lesions in patients with neurofibromatosis are especially refractory to balloon angioplasty Primary renal artery stenting in patients with atherosclerotic RAS has a high rate of technical success and a low rate of complications

52. Surgical Revascularization more than 90% of patients are cured or experience improvement of their hypertension with surgical revascularization In patients with FMD, the cure rate is as high as 80%, and morbidity is low; however, these results are not significantly better than what can be achieved by means of PTRA with less morbidity, mortality, cost, and inconvenience. In patients with diffuse atherosclerosis, the complication rate is relatively high with surgical revascularization, as with angioplasty; thus medical therapy may be preferable

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