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Renal Infarction

Causes

Most common caused - renal artery embolism secondary to  mitral stenosis.  Other causes includes infective endocarditis, atrial fibrillation, microthrombi in the left ventricle, rheumatic valvular disease, or recent myocardial infarction.
May also be caused by  atherosclerosis with or without thrombus formation, thrombus from flank trauma, sickle cell anemia, scleroderma, and arterionephrosclerosis.

Signs and symptoms

• Patient can be asymptomatic
• Upper abdominal pain
• Fever
• Nausea and/or vomiting
• Anorexia

Renovascular hypertension, a frequent complication that may occur several days after infarction, results from reduced blood flow, which stimulates the renin-angiotensin mechanism.

Diagnosis

A history of predisposing cardiovascular disease or other factors in a patient with typical clinical features strongly suggests renal infarction. A firm diagnosis requires the appropriate laboratory tests:

• Urinalysis reveals proteinuria and microscopic hematuria.
• Urine enzyme levels, especially lactate dehydrogenase (LD) and alkaline phosphatase, are often elevated as a result of tissue destruction.
• Blood studies may reveal elevated serum enzyme levels, especially aspartate aminotransferase, alkaline phosphatase, and LD. Blood studies may also reveal leukocytosis and an increased erythrocyte sedimentation rate.
• Excretory urography shows diminished or absent excretion of contrast dye, indicating vascular occlusion or urethral obstruction.
• Isotopic renal scan, a noninvasive technique, demonstrates absent or reduced blood flow to the kidneys.
• Renal arteriography provides absolute proof of an existing infarction but is used as a last resort because it's a high­risk procedure.

Treatment

Infection in the infarcted area or significant hypertension may require surgical repair of the occlusion or nephrectomy. Surgery to establish collateral circulation to the area can relieve renovascular hypertension.

Persistent hypertension may respond to antihypertensives and a low-sodium diet. Additional treatments may include administration of intra-arterial streptokinase, lysis of blood clots, catheter embolectomy, and heparin therapy.