RVD

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Reno-vascular diseases

Dr. Abrar Ali KatparResident AKU/Nephrology

Medical DepartmentKing Khalid Hospital

Hail, K.S.A

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Introduction & Definition

Adequate blood supply is essential for renal function.

Any pathology which affect the renal blood vessels directly leads to clinical manifestations of renal disease.• Acute renal failure

• Chronic renal failure

• Secondary hypertension (renovascular hypertension).

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Pathophysiology Narrowing of the renal

arteries usually is cased by one of two pathological entities: • 1) Fibromuscular

disease.

• 2) Atherosclerotic renovascular disease (ARVD).

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Atherosclerosis Is most common

cause of stenosis• Usually in older

patients.

• With other sites for atherosclerosis.

• Specially in lower legs.

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Renal artery stenosis Most likely if

• Hypertension is severe

• Recent onset of HTN

• Difficult to control HTN

• Kidneys are asymmetrical in size

• Evidence of vascular disease elsewhere specially lower legs.

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Mechanism of hypertension Renal ischemia results in a reduction in the pressure in

afferent glomerular arterioles. This leads to an increase in the production and release of

renin from the juxtaglomerular (JG) apparatus with a consequent increase in angiotensin II, a very potent vasoconstructor.

Angiotensin II also causes hypertension by upregulating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme with excessive superoxide generation.

Superoxide chelates nitric oxide (a potent vasodialator) resulting in reduced vasodialator activity and also hypertention.

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Proposed pathogenesis of renovascular hypertension.

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Physiological changes In renal artery stenosis In stenosis, renal perfussion pressure is

reduced & nephron transit time is prolonged on the side of stenosis; salt and water reabsorption is increased.

As a result, urine from the ischemic kidney is concentrated & has a lower Na+ concentration than urine from the contralateral kidney.

Inulin, creatinine and p-aminohippuric acid clearances are decreased on the ischemic side.

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1) Fibromuscular disease of the renal arteries

Fibromuscular disease accounts for 20-40%. Four distinct types: -

• 1- Medial fibroplasia 65-85%.• Usualy folows a benign course & never follows a

progressive course after the age of 40 years

• 2- Peri medial fibroplasia 10-15%.• Progressive course and may lead to total occlusion.

• 3- Intimal fibroplasia 5 -10 %.• Progressive course and may lead to total occlusion.

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• 4- Medial hyperplasia 5%.• A distinct but rare entity accounts for 1%.

• Commonly affects young females, who have: • Elevated blood pressures but with

• Well preserved renal function.

• Angiography revels a characteristic string of beads appearance.

• Angioplasty (occasionally stent insertion) is: • usually successful in improving or even curing

hypertension in affected individuals, & overall prognosis is very good.

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2) Atherosclerotic Renovascular disease

This is a common cause of hypertension and chronic renal failure due to ischemic nephropathy.

Its incidence increases with age, rising from • 5% under 60 years to • 16% over 60 years old.

In most patients the atherosclerotic lesion is ostial (within 1 cm of the origin of the renal artery).

Usually associated with symptomatic atherosclerotic vascular disease elsewhere.

Risk of developing significant renal artery stenosis in:• Patient with peripheral vascular disease (39%),• Coronary artery disease (10-29%),• Congestive cardiac failure (34%) and• Aortic aneurysm (38%).

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Many Pt’s are asymptomatic & are discovered incidentally experience from the USA shows • 11% have significant unilateral stenosis.

• 4% have bilateral disease.

The renal consequences of ARVD are functional.

such as: • Hypertension (present in 50%),

• Sodium retention (ankle and flash pulmonary edema),

• Proteinurea (usually sub-nephrotic range) and

• Decreased GFR.

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The morphological features of affected kidneys include: • Vascular sclerosis,

• Tubular atrophy,

• Interstitial fibrosis with inflammatory cellular infiltrate,

• Atubular glomeruli,

• Cholesterol emboli,

• FSGS changes. Baseline renal function is related to the extent of

renal parenchymal injury rather then to the degree of stenosis.

Improvement in hypertension and renal function is related to revascularization.

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Renovascular disease is easy to miss and should be considered in patients with hypertension and/or CRF.

Other clues to the diagnosis include:• Abdominal audible bruits as well as over carotid

arteries suggestive of generalized arterial disease.

• Ultra sonography showing >1.5 cm renal asymmetry.

• Recurent flash pulmonary edema without cardiopulmonary disease.

• Progressive chronic renal failure in patients with evidence of generalised atherosclerosis.

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Screening for renovascular diseases

Diagnostic flowchart for the workup of renal artery stenosis.

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Radionuclide studies.

These can demonstrate decreased renal perfusion on the affected side.

In unilateral renal artery stenosis, a disproportionate fall in uptake of isotope on the affected side following administration of captopril or aspirin is suggestive of the presence of significant renal artery stenosis.

A completely normal results renders the diagnosis unlikely.

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Doppler ultrasoundThis method is very sensitive but highly operator –dependent

and time –consuming. It generates data about intrarenal vascular resistance, which

can be value able in predicting the success of revascularization procedures.

A resistive index of >_80 is a predictive of poor response following intervention.

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Magnatic resonance angiography

MRA can be used to visualize the renal arteries and there is a good-though not perfect-correlation between MRA findings and those of renal arteriography.

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 Magnetic resonance angiography (MRA) showing renal artery stenosis .Courtesy of Patricia Stoltzfus, West Virginia University.

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Helical (spiral) CT scanning.

This permits non invasive immaging of the renal arteries .

Advantage:• Much less expensive then MRI

Disadvantages:• Exposes the patient to ionizing radiation

• Exposes to contrast injection

• Less reliable then MRI.

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Renal Arteriography.

Remains the

‘ GOLD STANDARD’ investigation in the diagnosis of renal arterial disease.

Required to start treatment.

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Angiogram showing bilateral renal artery stenosis. Courtesy of Henry Ford Hospital.

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After percutaneous transluminal angioplasty (right renal artery). Courtesy of Department of Radiology, Henry Ford Hospital.

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After percutaneous transluminal angioplasty & stent placement ,Lt. renal artery .

Courtesy of Department of Radiology, Henry Ford Hospital.

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Treatment

Medical• The aim of treatment is

• To correct hypertention

• To improve renal perfusion

• To improve excreatory function.

Renal artery stenosis can progress to occlusion, particularly in patients with stenosis, >75% as shown by serial angiography necessitating revascularization in AVRD.

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Procedures (Revascularization) • The options include:

• Transluminal angioplasty to dilate the stenotic region.

• Insertion of stents across the stenosis.

( some times only endoscopic option when the stenosis occurs close to the origin of the renal artery from the aorta, rendering angioplasty technically difficult or impossible)

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Surgical• Reconstructive surgery.

• Nephrectomy.

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Revascularization is indicated in • Vessels with stenosis >75% and recurrent

flash pulmonary oedema.

• Drug resistant severe hypertension.

• ARVD affecting solitary functioning kidney.

• Patients with cardiac failure needing ACE inhibitors,

• Unexplained progressive renal failure

• Dialysis dependent renal failure.

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Selection

With good selection of patients• Hypertension is cured or improved by

intervention in >then 50%.

• Occasionally dramatic improvements in renal function ensue but results are generally disappointing.

• All Pt’s with ARVD should be treated with a combination of asprin, statins and optimal BP control as prophylaxsis against progression of atherosclerosis.

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Mortality

Mortality is high because of other associated co-morbidities, and ARVD patients have generalized endothelial dysfunction.

ARVD patients with ESRF have high rates then those with good renal functions.

Five-year survival is only 18% in patients with ESRF due to ARVD.

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ACE-Inhibitor Augmented Scintigraphy

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(1) Left, Sonograms of the kidneys on a 57-year-old woman with difficult-to-control hypertension shows kidneys of uneven sizes: The left kidney is 96 mm, and the right kidney is 63 mm. Top right, Isotopic renogram (obtained with technetium MAG3) after captopril shows a markedly depressed renal function in the right kidney. Bottom right, Analogous images show negligible activity in the right kidney. Note that this pattern is more typical for DTPA than MAG3 (as DTPA depends on the glomerular filtration rate for uptake which is decreased after captopril in renovascular hypertension [RVHT]). In severe cases of RVHT, MAG3 uptake can be decreased, as in this case. However, typically, uptake is preserved with decreased cortical excretion.

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(2) Sonograms of the kidneys on a 46-year old woman with difficult to control hypertension showing uneven sizes of the kidneys the right kidney is 2.5 cm smaller in size. An isotope renogram obtained with technetium mercaptoacetyltriglycine (Tc-MAG3) shows a markedly depressed renal function in the right kidney (purple)

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(3) Left, Flush aortogram in a 63-year-old man with hypertension shows marked stenosis of the right renal artery and complete occlusion of the left renal artery. Note the extensive atheroma in the aorta and iliac arteries. Right, nephrogram-phase image shows a significantly smaller left kidney with a faint nephrogram. Some blood supply to the left kidney is retained via collaterals (see image on the left).

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(4) Digital subtraction flush aortogram in a 77-year-old normotensive man shows marked left renal artery stenosis and diffuse aortic atheroma. The patient presented with lower-limb claudication.

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(5) Digital subtraction flush aortogram in an 83-year-old mildly hypertensive man shows complete occlusion of the left renal artery; only a stub of the artery is visualized. Note the diffuse aortic atheroma. The patient presented with lower-limb claudication.

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(6) Three-dimensional phase-contrast MRA images of normal renal arteries.

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(7) Dynamic gadolinium-enhanced MRA shows normal renal arteries.

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(8) Flush aortogram in a 32-year-old man with familial hypercholesterolemia and difficult-to-control hypertension. Radiograph shows complete occlusion of right renal artery & marked stenosis of the left renal artery.

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(9) Left, A balloon angioplasty catheter is seen in situ across the left renal artery stenosis. Right, After angioplasty, an excellent anatomic (and functional) result was achieved.

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(10) Technetium mercaptoacetyltriglycine (Tc-MAG3) isotopic renogram shows curves before and after angioplasty.

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Captopril renogram

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(11) Digital subtraction flush aortogram in a patient with a right iliac fossa transplanted kidney. Image shows stenosis at the anastomotic site associated with post-stenotic dilatation.

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(12) Digital subtraction flush aortogram in a patient with a left iliac fossa transplanted kidney. Image shows an intrarenal branch stenosis associated with post-stenotic dilatation.

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(13) Selective right renal angiogram shows standing waves in an intralobar artery. Standing waves in the renal arteries show as multiple serrated indentations that are symmetrically distributed at evenly spaced intervals. These of no pathologic significance and may represent arterial spasm. They may also affect intrarenal branches, as in this case.

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