Renal Arterial occlusion

Partial renal artery occlusion may be caused by arteriosclerotic disease or fibromuscular which may lead to hypertension or ischemic nephropathy as a result of progressive atherosclerotic arterial stenosis.

Renal artery occlusion may also occur as a result of thrombotic or embolic phenomena. Thrombosis may result from blunt trauma or dissection of the renalartery or may complicate procedures such as renal angioplasty, stent placement, or surgical procedures. In ammatory conditions such as Takayasu’s syndrome, systemic vasculitis, and obliterans may also be associated with renal arterial thrombosis. However, embolization is more common than thrombosis, and in 90% of the cases it originates from the heart.

The causes of embolic disease of cardiac origin include atrial fibrillation, valvular heart disease, bacterial or nonbacterial endocarditis, and atrial myxoma. Clinical symptoms associated with occlusion of a primary or secondary branch of the renal artery depend on the presence of collateral circulation. Acute renal infarction is associated with lumbar or flank pain, abdominal pain, nausea, vomiting, and fever. If infarction occurs, leukocytosis will develop and levels of serum enzymes such as serum aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase will be elevated. Microscopic hematuria may also be seen. Significant renal dysfunction may be associated with bilateral renal infarction or infarction of a solitary kidney. It is frequently associated with acute onset of hypertension owing to the activation of the system. Radiologic evaluation is necessary to establish the diagnosis of renal Radionuclide imaging with technetium-DTPA(diethylenetriamine pentaacetic acid) or DMSA(dimercaptosuccinic acid) will show nonprofusion of the kidney. Enhanced co and duplex Doppler studies have shown improved diagnostic accuracy. However, the diagnosis is more reliably established by renal arteriography The goal of management is to restore blood flow to the ischemic kidney promptly to avoid irreversible damage. Therefore, rapid diagnosis and localization of the thrombus is critical. Traumatic renal artery thrombosis can lead to irreversible renal damage unless surgical thrombectomy is performed within 4 to 6 hours.

In acute atheroembolic disease, early diagnosis and revascularization within hours has the highest success in preserving renal function. In contrast, in chronic ischemic renal disease and in the presence of collateral circulation the return of renal function may occur even when diagnosis and treatment are delayed. Return of ren function has been documented after surgical treatment for up to 6 weeks after thrombosis.

Therapeutic options include anticoagulation, intravenous or intra-artenal thrombolytic therapy, percutaneous angioplasty, clot extraction by a percutaneous catheter, and surgical thrombectomy.

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