Renal infarction

Renal blood vessel occlusion results in renal infarction — the formation of a coagulated, necrotic area in one or both kidneys. The location and size of the infarction depend on the site of vascular occlusion. Most commonly, infarction affects the renal cortex but it can extend into the medulla. (See Sites of renal infarction.) Residual renal function after infarction depends on the extent of the damage from the infarction.

Causes

In 75% of patients, renal infarction results from renal artery embolism secondary to mitral stenosis, infective endocarditis, atrial fibrillation, micro-thrombi in the left ventricle, rheumatic valvular disease, or a recent myocardial infarction.

The embolism reduces the rate of blood flow to renal tissue and leads to ischemia. The rate and degree of blood flow reduction determine whether the insult will be acute or chronic as arterial narrowing progresses.

Less common causes of renal infarction are atherosclerosis, with or without thrombus formation; and thrombus from flank trauma, sickle cell anemia, scleroderma, or arterionephrosclerosis.

Signs and symptoms

Although renal infarction may be asymptomatic, typical signs and symptoms include severe upper abdominal pain or gnawing flank pain and tenderness, costovertebral tenderness, fever, anorexia, nausea, and vomiting. When arterial occlusion causes infarction, the affected kidney is small and nonpalpable.

Renovascular hypertension, a common 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 signs and symptoms 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 typically 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 high-risk 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 antihypertensive therapy and a low-sodium diet. Additional treatments include administration of intra-arterial streptokinase, lysis of blood clots, catheter embolectomy, and heparin therapy.

Special considerations

❑ Assess the degree of renal function, and offer supportive care to maintain homeostasis.

❑ Monitor intake and output, vital signs (particularly blood pressure), electrolyte levels, and daily weight.

CLINICAL TIP: Watch for signs of fluid overload, such as dyspnea, tachycardia, pulmonary edema, and electrolyte imbalances.

❑ Carefully explain all diagnostic procedures.

❑ Provide reassurance and emotional support for the patient and family.

❑ Encourage the patient to return for a follow-up examination, which usually includes excretory urography or a renal scan to assess regained renal function.

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Book Source Details

• Book Title: Handbook of Diseases
• Author(s): Springhouse
• Year of Publication: 2003
• Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.

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Copyright Details: Handbook of Diseases, Copyright © 2008 Williams & Wilkins.

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More About This Book: Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5

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