Renal infarct is ischemic necrosis of renal parenchyma resulting from acute occlusion of the renal artery or its branches. Most commonly embolic in origin: atrial fibrillation, cardiac thrombus, aortic atheromatous plaque fragments, or renal artery dissection. Presents with acute-onset flank pain, hematuria, elevated LDH, and leukocytosis. Contrast-enhanced CT typically shows a wedge-shaped, cortical-based, non-enhancing area. Cortical rim sign (preserved subcapsular perfusion) is characteristic. Early diagnosis and treatment within 24-48 hours is crucial — reperfusion therapy (anticoagulation, thrombolysis) should be considered.
Age Range
40-80
Peak Age
60
Gender
Equal
Prevalence
Uncommon
Acute occlusion of the renal artery or segmental branches interrupts parenchymal blood flow. The kidney is an end-artery organ — each segmental artery supplies a specific parenchymal territory with limited collateral circulation. Ischemia begins within minutes of occlusion, and irreversible cell injury develops within 60-90 minutes. Coagulative necrosis causes the parenchyma to lose viability. The subcapsular region is supplied by capsular arteries that originate independently from the inferior phrenic, adrenal, and gonadal arteries. Therefore, while central parenchyma becomes necrotic, the thin subcapsular rim preserves its perfusion — this is the anatomical basis of the cortical rim sign. In the late phase, flip-flop enhancement occurs: disrupted capillary permeability in necrotic tissue allows contrast to seep in late, producing delayed enhancement.
Thin subcapsular enhancing rim surrounding the infarct area. Subcapsular parenchyma supplied by capsular arteries preserves its perfusion while deep parenchyma supplied by the renal artery has become necrotic. Most prominent in the acute-subacute period.
Wedge-shaped non-enhancing hypodense area with base facing the renal capsule and apex pointing toward the hilum in corticomedullary phase. Borders are sharp with marked density difference from surrounding normal parenchyma. Single wedge is seen in small segmental infarcts, while multiple wedge areas may be visible in multiple emboli. In global infarction, the entire kidney fails to enhance.
Report Sentence
Wedge-shaped, cortical-based, non-enhancing area in the left/right kidney on corticomedullary phase, consistent with acute renal infarction.
A thin (1-3 mm) enhancing rim is observed in the subcapsular region at the periphery of the infarct area. This rim corresponds to subcapsular parenchyma supplied by capsular arteries that maintain perfusion independently of the renal artery. The cortical rim sign becomes apparent after the first 8 hours of acute infarction and is best seen in the subacute period. The nephrographic phase best demonstrates this finding.
Report Sentence
A thin subcapsular enhancing rim along the periphery of the infarct area (cortical rim sign) indicates preserved capsular artery perfusion.
On delayed phase (5-10 minutes later), contrast accumulation is observed in the previously non-enhancing infarct area — flip-flop enhancement. The infarct area that was hypodense in early phases becomes isodense or slightly hyperdense in the late phase. Simultaneously, normal parenchyma loses contrast and becomes isodense or hypodense. This reversal of contrast behavior (flip-flop) confirms subacute infarction.
Report Sentence
Contrast accumulation is observed in the previously non-enhancing infarct area on delayed phase (flip-flop enhancement), consistent with subacute renal infarction.
CT angiography may reveal filling defect or abrupt cutoff in the main renal artery or segmental branches. The embolus appears as a low-density intraluminal filling defect. In renal artery dissection, intimal flap and double lumen may be present. In-situ thrombosis may be superimposed on pre-existing atherosclerotic stenosis.
Report Sentence
CT angiography demonstrates an intraluminal filling defect in the segmental branch of the left/right renal artery, consistent with embolic occlusion.
The infarct area shows high signal on DWI and low signal on ADC map (restricted diffusion). This finding is most prominent in the acute phase (first 24-48 hours) and reflects cellular swelling during the cytotoxic edema period. DWI is particularly sensitive for detecting subclinical or small segmental infarcts in renal infarction. Diffusion restriction decreases as the infarct becomes chronic.
Report Sentence
A wedge-shaped area of restricted diffusion is observed in the kidney on DWI, consistent with acute renal infarction.
No blood flow is observed in the infarct area on color Doppler US. A focal avascular area is detected compared to normal kidney parenchyma. On B-mode US, the infarct area may appear normal or slightly hypoechoic in early stage; the hypoechoic area becomes more prominent and cortical retraction develops later. Doppler US can provide early diagnostic clues but requires confirmation with CT angiography.
Report Sentence
A focal avascular area is observed in the kidney on color Doppler US, consistent with renal infarction; correlation with CT angiography is recommended.
Criteria
Occlusion of segmental artery or branches. Single wedge-shaped infarct area. Remainder of the kidney shows normal perfusion.
Distinct Features
Most common type. Usually embolic in origin. Treated with anticoagulation. Functional loss is limited.
Criteria
Complete occlusion of the main renal artery. Entire kidney fails to enhance. Only thin subcapsular rim may be preserved.
Distinct Features
Emergency reperfusion or thrombolysis indication. Risk of complete kidney function loss. Seen in renal artery dissection or large emboli.
Criteria
Occlusion of multiple segmental arteries. Multiple wedge-shaped infarct areas. May be unilateral or bilateral.
Distinct Features
Suggests shower embolism — cardiac source (AF, endocarditis), aortic atheroma fragments. Bilateral involvement strongly supports embolic source. Echocardiography is mandatory.
Distinguishing Feature
Focal pyelonephritis can show a wedge-shaped hypodense area but striated nephrogram (alternating enhancing and non-enhancing striations) is characteristic of pyelonephritis. Fever and pyuria are prominent in pyelonephritis, LDH is usually normal. Cortical rim sign is positive in infarct but not expected in pyelonephritis.
Distinguishing Feature
Renal abscess shows a round-oval rim-enhancing collection, not wedge-shaped. Marked restricted diffusion on DWI (pus) is seen in abscess. Abscess presents with infectious clinical features (high fever, leukocytosis). Infarct is wedge-shaped, cortical-based, and cortical rim sign is positive.
Distinguishing Feature
RCC typically appears as a round enhancing mass; infarct presents as a wedge-shaped non-enhancing area. Marked heterogeneous enhancement is typical of RCC, while no enhancement in the infarct area in early phases. Clinically, infarct has acute onset; RCC shows a more insidious course.
Urgency
emergentManagement
medicalBiopsy
Not NeededFollow-up
specialist-referralRenal infarction requires emergent diagnosis and treatment. Irreversible damage begins within the first 90 minutes. Treatment involves embolic source control and anticoagulation (heparin → warfarin/DOAC). Endovascular thrombolysis or thrombectomy may be considered for global infarction or main artery occlusion. Embolic source investigation (echocardiography, arrhythmia monitoring, aortic evaluation) is mandatory. Long-term anticoagulation is required for atrial fibrillation. Renal function monitoring (creatinine, GFR) should be performed.
Renal infarct is an emergent vascular event. Early diagnosis and treatment (anticoagulation, thrombectomy/thrombolysis) can preserve renal function. Underlying causes such as atrial fibrillation, endocarditis, and vasculitis should be investigated.