Symptoms of Renal Artery Infarct
Renal artery infarct presents classically with acute onset of severe flank pain, hematuria (gross or microscopic), and often hypertension, though the diagnosis is frequently missed or delayed because these symptoms can mimic more common conditions like nephrolithiasis or pyelonephritis. 1, 2, 3
Cardinal Clinical Features
The triad of symptoms to recognize includes:
- Severe flank pain on the affected side, typically sudden in onset and the earliest/most prominent symptom 1, 3, 4
- Hematuria (blood in urine), which may be gross or microscopic 1, 4
- Hypertension, often present at presentation 1, 2
Additional Presenting Symptoms
Beyond the classic triad, patients commonly present with:
- Abdominal or chest pain without clear flank localization (occurred in 7 of 17 cases in one series) 4
- Nausea and vomiting (present in approximately half of cases) 4
- Fever (≥37.5°C in approximately 60% of cases) 4
- Flank tenderness on examination (though present in only about half of cases, making its absence unreliable for ruling out the diagnosis) 4
- Decreased urine output (oliguria), though this may be less pronounced with unilateral involvement if the contralateral kidney is healthy 1
Laboratory Abnormalities
Key laboratory findings that support the diagnosis include:
- Elevated serum creatinine (exceeded 1.3 mg/dL in 88% and 4.0 mg/dL in 65% of cases), though rises may be delayed 24-48 hours after the ischemic event 1, 4
- Leukocytosis 4
- Elevated lactate dehydrogenase (LDH) 4
- Elevated liver enzymes (AST, ALT, alkaline phosphatase) 4
- Proteinuria 4
Critical Diagnostic Pitfall
The diagnosis is often delayed because physicians fail to consider renal infarction in the differential diagnosis of flank pain, particularly in patients with cardiac disease or arrhythmias. 3, 4 In one series, 16 of 17 patients had pre-existing cardiac disease or arrhythmias, making this the most important risk factor to recognize. 4
High-Risk Patient Populations
Maintain high clinical suspicion in patients with:
- Cardiac disease or arrhythmias (present in 94% of cases; cardiogenic causes account for 55.7% of all renal infarctions) 2, 4
- Atrial fibrillation (the most common cardiac source of emboli) 2, 3
- Hypercoagulable states (6.6% of cases) 2
- Recent vascular procedures or trauma causing renal artery injury (7.5% of cases) 2
Diagnostic Imaging
IV contrast-enhanced CT with immediate and delayed phases is the gold standard diagnostic test. 1 Key imaging findings include:
- Absence of contrast enhancement in the affected kidney (the definitive finding) 1
- Wedge-shaped parenchymal perfusion defects (single or multiple) 2
- Visualization of thrombus or occlusion in the renal artery 1
- Delayed or absent nephrogram phase on the affected side 1
A critical pitfall is failure to obtain both immediate and delayed phases on CT imaging, which may miss critical findings. 1
Treatment Approach
Acute Management
For patients diagnosed within 24-48 hours of symptom onset, catheter-directed thrombolysis (CDT) should be considered for kidney salvage, even with prolonged ischemia time. 5, 6 Treatment options include:
- Anticoagulation with heparin (used in 78% of cases) followed by warfarin (75% of cases) is the standard approach 2
- Catheter-directed thrombolysis with agents like alteplase or urokinase for complete renal artery occlusion, which achieves complete or partial thrombus resolution in all treated patients 5, 6
- Antiplatelet agents as adjunctive therapy (used in 36% of cases) 2
Revascularization Considerations
In specialized centers, percutaneous revascularization with stent/stentgraft may be considered if warm ischemia time is <240 minutes, though success rates are only 25-35%. 7 For main renal artery injury, angioembolization may be indicated for arterial contrast extravasation or pseudoaneurysms. 7
Long-term Anticoagulation
With long-term anticoagulants, renal function typically returns in patients surviving more than 1 month, even those with bilateral emboli. 4 This makes aggressive anticoagulation the cornerstone of therapy for most patients.
Clinical Outcomes and Prognosis
Despite aggressive treatment, renal infarction carries significant morbidity:
- 5% mortality during initial hospitalization 2
- 20.1% develop acute kidney injury during sentinel hospitalization 2
- 10.9% develop new-onset eGFR <60 mL/min/1.73m² 2
- 2.1% progress to end-stage renal disease requiring dialysis 2
- 2.8% experience recurrent infarction during follow-up 2
For patients treated with CDT, expect a 27% decrease in creatinine clearance at follow-up, with the treated kidney decreasing in size (mean reduction from 10.4 cm to 8.5 cm pole-to-pole), though renal function deterioration stabilizes and does not continue progressively over time. 5
Long-term Monitoring
Monitor for development of renovascular hypertension with periodic blood pressure monitoring for up to a year after the event. 1, 7 In rare instances with uncontrollable hypertension and a functional contralateral kidney, delayed nephrectomy may be necessary. 7
For patients with solitary kidney after infarction, exercise extreme caution with ACE inhibitors or ARBs, as new azotemia after initiation is a Class I indication for renal artery stenosis evaluation. 8 Even when creatinine returns to baseline, significant renal reserve has been permanently lost. 8