Renal Infarct
A renal infarct is an area of the kidney that has lost its blood supply, resulting in tissue death. It most commonly occurs when a blood clot (embolus) travels from the heart or aorta to a renal artery, when a local blood clot forms within a renal artery (thrombosis), or when other vascular processes reduce blood flow to a portion of the kidney. Renal infarcts can affect a small segment of the kidney (segmental infarct) or, less commonly, the entire kidney (global infarct). Acute renal infarction typically causes sudden severe flank pain and can be mistaken for a kidney stone. Chronic changes from a prior infarct—typically a wedge-shaped area of scarring—are often identified incidentally on imaging. Evaluation combines contrast-enhanced imaging, laboratory testing, and, importantly, workup for the underlying cause of the vascular event.
What is it?
The kidneys receive their blood supply from the renal arteries, which arise from the aorta (the main artery from the heart). Within the kidney, the renal arteries branch into progressively smaller vessels that ultimately supply blood to segments of the kidney tissue in a distribution called an end-arterial pattern—meaning that each segmental artery supplies its own distinct portion of the kidney without significant overlap with neighboring segments. When one of these arteries becomes blocked, the tissue it supplies loses its blood supply and can die if the block is not quickly relieved. This area of tissue death is called a renal infarct.
Renal infarcts can be classified by their extent. Segmental infarcts affect a portion of the kidney supplied by one branch of the renal artery and typically appear as wedge-shaped areas with the point (apex) toward the center of the kidney (where the artery enters) and the base at the outer surface. Multiple segmental infarcts can occur simultaneously, particularly in patients with multiple emboli. Global infarct affects the entire kidney and results from complete occlusion of the main renal artery. Global infarction of an entire kidney is much less common than segmental infarction and is a much more serious event, potentially leading to loss of the entire kidney.
Renal infarcts can occur through several mechanisms.
Embolic infarction is the most common cause. In this mechanism, a blood clot (embolus) travels from a distant source through the bloodstream and becomes lodged in a renal artery, blocking blood flow. The most common source of embolism is the heart, particularly in patients with atrial fibrillation (an irregular heart rhythm that predisposes to clot formation in the atria), other cardiac rhythm abnormalities, prior heart attacks (particularly with certain patterns of heart wall dysfunction), heart valve disease (particularly certain types and infected heart valves in endocarditis), and heart chambers with abnormalities that predispose to clot formation. The aorta can also be a source, particularly with cholesterol plaques that break off and become emboli.
Renal artery thrombosis (a blood clot forming locally within the renal artery) is less common but can occur, particularly in patients with underlying vascular disease, hypercoagulable conditions (states that predispose to clotting), trauma to the renal artery, or after certain vascular procedures.
Aortic dissection (a tear in the aortic wall) can extend into or block the origin of a renal artery and cause infarction, and is a serious condition requiring urgent recognition.
Cocaine use is a recognized cause of renal infarction, particularly in younger patients, due to intense vasospasm and other effects on blood vessels.
Vasculitis (inflammation of blood vessels) can affect the renal arteries and cause infarction as part of certain autoimmune and inflammatory conditions.
Certain procedures involving the aorta or renal arteries can occasionally cause renal infarction as a complication.
Renal vein thrombosis (a clot in the vein draining the kidney) is a distinct condition from renal artery infarction but can also affect kidney function and appearance and requires different evaluation.
Acute renal infarction typically presents with sudden severe flank or back pain that develops quickly. The pain can be intense and constant, and is often mistaken for a kidney stone in emergency settings—which is one reason renal infarction is likely underdiagnosed. Nausea and vomiting are common. Blood in the urine (either visible or microscopic) is present in many but not all patients. Fever can develop, sometimes appearing after the initial pain, and can be mistaken for infection. New or worsening high blood pressure may develop and can occasionally be severe. Some patients also experience symptoms of the underlying condition (such as palpitations from atrial fibrillation).
Small renal infarcts may cause few or no symptoms and be identified incidentally on imaging done for other reasons. Chronic (old) infarcts—those that have healed with scarring—typically produce no symptoms and appear on imaging as areas of wedge-shaped scarring or focal atrophy in a segmental distribution.
Diagnosis in the acute setting can be challenging because the presentation overlaps with other conditions, particularly kidney stones. Certain features may raise suspicion for infarction rather than a stone, including underlying risk factors (atrial fibrillation, prior embolic events, hypercoagulable conditions), markedly elevated LDH (a blood test that is often significantly elevated in acute renal infarction—often to a greater degree than in other kidney conditions), and characteristic imaging findings.
Contrast-enhanced CT is the primary imaging test and shows the characteristic wedge-shaped areas of non-enhancement (where the affected tissue is not receiving blood flow and therefore does not take up contrast), often with a thin rim of preserved enhancement along the outer surface of the kidney (called the “rim sign”) in some cases. CT can also identify underlying vascular problems and evaluate for aortic dissection or other causes. MRI provides similar information without ionizing radiation and is an alternative in specific circumstances. Renal artery imaging (CT or MR angiography, or catheter angiography) can further characterize vascular findings and, in some situations, guide intervention. Contrast-enhanced imaging is essential; non-contrast imaging typically cannot identify acute infarction.
Laboratory testing typically includes complete blood count, kidney function (creatinine and estimated glomerular filtration rate), LDH (which is often markedly elevated in acute renal infarction, sometimes several times normal), inflammatory markers, coagulation studies, and urinalysis.
Once renal infarction is diagnosed, evaluation for the underlying cause is essential. This typically includes cardiac evaluation with an echocardiogram (to look for sources of embolism, including atrial abnormalities, cardiac clots, valve disease, or vegetation from endocarditis) and rhythm monitoring for atrial fibrillation and other arrhythmias (which may require prolonged monitoring in some patients if not immediately identified). Blood tests for hypercoagulable conditions may be appropriate in selected patients. Evaluation of the aorta and vascular system is important. Evaluation for cocaine or other drug use, vasculitis, or other causes is guided by the clinical context.
Important to Know
Management of renal infarction depends on the timing (acute vs. chronic), the extent of infarction, the underlying cause, and patient factors. Care is typically coordinated by emergency medicine clinicians (in acute presentations), nephrologists, cardiologists (given the frequent cardiac sources), interventional radiologists or interventional vascular specialists (when procedures are considered), hematologists (for hypercoagulable causes), and, when relevant, other specialists.
For acute renal infarction, initial care focuses on stabilizing the patient, controlling pain and blood pressure, and identifying and treating the underlying cause. Anticoagulation with heparin or similar medications is typically started when a cardioembolic or thrombotic cause is suspected, in preparation for long-term anticoagulation. Pain control is important. Blood pressure control may require intravenous medications initially, particularly if severe hypertension is present.
For patients with large renal infarcts (particularly those affecting most of the kidney) identified early, catheter-based interventions—such as catheter-directed thrombolysis (delivery of clot-dissolving medication directly to the clot through a catheter), mechanical thrombectomy (physical removal of the clot), or, less commonly, surgical revascularization—may be considered in selected patients if the diagnosis is made early enough for meaningful recovery of kidney tissue to be possible. The benefit of these interventions depends on how quickly they can be performed after the onset of infarction, the extent of infarction, and other factors. Not all patients are candidates for these interventions, and the decision is highly individualized.
For patients with smaller infarcts or those diagnosed later in the course, the initial infarct itself cannot be reversed, and treatment focuses on preventing recurrence, managing blood pressure and kidney function, and treating the underlying cause. Long-term anticoagulation is typically continued for cardiac or hypercoagulable causes—for example, direct oral anticoagulants (such as apixaban, rivaroxaban, dabigatran, or edoxaban) or warfarin for atrial fibrillation, with the choice depending on patient factors and indications. For patients with atrial fibrillation who cannot tolerate anticoagulation, alternative approaches (such as left atrial appendage closure) may be considered.
Treatment of the source of embolism is essential. For atrial fibrillation, this typically includes long-term anticoagulation for stroke and systemic embolism prevention, along with rate or rhythm control. For heart valve disease or endocarditis, treatment follows established principles for the specific condition. For cocaine-related infarction, addiction treatment and cessation are essential.
For patients with hypercoagulable conditions, long-term anticoagulation and, when appropriate, additional workup (such as evaluation for underlying malignancy or specific inherited hypercoagulable conditions) is important. Coordination with hematology is often beneficial.
For vasculitis-related infarction, treatment of the underlying vasculitis (typically with immunosuppressive medications) is essential. Coordination with rheumatology is important.
For aortic dissection or other vascular emergencies, urgent evaluation and treatment by vascular specialists is essential.
Management of blood pressure is important both acutely and long term. New high blood pressure that develops after renal infarction is often related to the infarct itself (particularly with larger infarcts) and typically requires ongoing treatment. ACE inhibitors or ARBs may be considered, though care is needed when overall kidney function is affected.
Management of kidney function is important. Small infarcts often do not significantly affect overall kidney function, particularly with a normal opposite kidney. Larger infarcts, bilateral infarction (rare), or infarction in a solitary kidney can significantly affect function. Monitoring of kidney function over time is essential.
Long-term follow-up is important. For patients with atrial fibrillation, adherence to anticoagulation is critical to prevent further embolic events (including potentially devastating strokes). For patients with hypercoagulable conditions or vasculitis, ongoing management of the underlying condition is important. Regular monitoring of blood pressure and kidney function is standard.
Chronic (old) renal infarcts identified incidentally on imaging typically do not require specific treatment for the infarct itself but do warrant evaluation for the underlying cause if not already known. This may include cardiac evaluation, evaluation for atrial fibrillation, and, in selected cases, evaluation for other conditions. In many cases, incidental chronic infarcts prompt reevaluation of overall cardiovascular risk and preventive measures.
Care during pregnancy in patients with a history of renal infarction requires special attention. Some anticoagulation options (particularly warfarin) have implications for the fetus, and coordination with obstetrics, maternal-fetal medicine, cardiology, and hematology is essential.
Care is typically coordinated by nephrologists, cardiologists, and other specialists depending on the underlying cause. Imaging and laboratory findings are interpreted alongside the patient’s symptoms, examination, past medical history, and broader clinical context rather than in isolation.
Patient education plays an important role. Understanding the diagnosis, the underlying cause when identified, the rationale for the treatment plan (including long-term anticoagulation when needed), the importance of medication adherence, warning signs of complications or recurrent events (including stroke), and, when relevant, lifestyle changes and preventive measures all contribute to better outcomes.
Red flag symptoms include severe flank or back pain, sudden severe abdominal pain (particularly if it radiates to the back, which may suggest aortic dissection), sudden severe headache, sudden weakness or numbness (particularly one-sided, which may suggest stroke), sudden speech difficulty or vision changes (which may suggest stroke), sudden severe chest pain, severe difficulty breathing, significant decrease in urine output, severe hypertension not controlled with medications, high fever with chills, symptoms of sepsis, or rapid clinical deterioration. These warrant immediate emergency evaluation, as they may indicate stroke, aortic dissection, additional embolic events, severe hypertension, or other life-threatening conditions.