Renal Infarction & Renal Vein Thrombosis
When flank pain and hematuria come from a clot, not a stone
Artery clot vs vein clot
Two clots, one disguise. Renal infarction is arterial occlusion, usually by a cardiac embolus, causing ischemic necrosis. Renal vein thrombosis (RVT) is an outflow clot, classically from nephrotic syndrome, producing a swollen, congested kidney. Both present with flank pain and hematuria and are routinely mistaken for a stone or pyelonephritis, so the diagnosis depends on ordering a contrast or venous study and noticing clues such as a disproportionate LDH or a new left varicocele.
| Feature | Renal infarction | Renal vein thrombosis |
|---|---|---|
| Lesion | Renal artery occlusion | Renal vein outflow clot |
| Typical causes | Atrial fibrillation, endocarditis, LV thrombus, dissection | Membranous nephropathy, renal cell carcinoma, infant dehydration |
| Key clue | LDH very high with AST/ALT near normal | Gross hematuria, new left varicocele, pulmonary embolism |
| Diagnosis | Contrast CT: wedge-shaped defects | Doppler ultrasound or CT/MR venography |
| Treatment | Anticoagulate and find the embolic source | Anticoagulate and treat the nephrotic disease |
Renal infarction: causes and presentation
Embolus first. Cardioembolism is the most common mechanism: atrial fibrillation above all, then infective endocarditis, LV thrombus (recent MI, dilated cardiomyopathy), valvular or prosthetic valve disease, and paradoxical embolism from a venous clot through a patent foramen ovale. Emboli elsewhere (stroke, splenic or mesenteric infarction) often coexist.
In situ occlusion. Without an arrhythmia, consider spontaneous or traumatic renal artery dissection (often with fibromuscular dysplasia), hypercoagulable states (antiphospholipid syndrome, HIT), vasculitis (polyarteritis nodosa), cocaine, aortic dissection, and endovascular procedures. A young, otherwise healthy patient with a renal infarct and normal rhythm needs CT angiography of the renal arteries for dissection or FMD plus antiphospholipid antibody testing.
Cholesterol atheroembolism after catheterization is a different disease: subacute AKI with livedo reticularis, blue toes, eosinophilia, and low complement rather than an acute wedge-shaped infarct.
Presentation. Sudden, steady (not colicky) flank or abdominal pain with nausea, vomiting, low-grade fever, and microscopic or gross hematuria. Ischemic parenchyma releases renin, so new or worsened hypertension is common. AKI is unusual unless the infarct is bilateral or the kidney is solitary.
Diagnosing renal infarction
LDH out of proportion. Infarcted kidney releases LDH, which is elevated in nearly all cases and often several-fold, while AST and ALT stay normal or mildly raised. Leukocytosis, a high CRP, and hematuria are common. This pattern separates infarction from stones, pyelonephritis, and liver disease.
| Feature | Renal infarction | Nephrolithiasis | Pyelonephritis |
|---|---|---|---|
| Pain | Sudden and steady | Colicky, radiating to the groin | Constant, with high fever and CVA tenderness |
| Urine | Hematuria without pyuria | Hematuria | Pyuria, WBC casts, bacteriuria |
| LDH | Markedly high | Normal | Normal or mildly raised |
| Noncontrast CT | Normal | Stone, often with hydronephrosis | Often unremarkable |
- Flank pain + hematuriaLooks like a stone.
- Noncontrast CT normalNo stone, no hydronephrosis.
- LDH markedly elevatedAST/ALT near normal.
- Contrast-enhanced CTWedge-shaped perfusion defect confirms the infarct.
Imaging. Contrast-enhanced CT (CT angiography) shows wedge-shaped, peripheral nonenhancing regions, sometimes with a cortical rim sign from preserved capsular collateral flow. MRI or catheter angiography (the gold standard, and also therapeutic) are alternatives.
Managing renal infarction
Anticoagulate. Start heparin, then oral anticoagulation with warfarin or a DOAC, continued indefinitely if the cause is atrial fibrillation.
Hunt the embolic source. Obtain an ECG and prolonged rhythm monitoring for paroxysmal AF, echocardiography (TTE, then TEE with a bubble study for LV thrombus, vegetations, and PFO), and blood cultures if febrile. With no cardiac source, test for antiphospholipid antibodies and image the renal arteries.
Septic emboli from infective endocarditis are treated with antibiotics, not anticoagulation, because of the hemorrhage risk.
Revascularize only when both kidneys are at stake. Endovascular therapy (catheter-directed thrombolysis, thrombectomy, or stenting of a dissection) is reserved for bilateral occlusion, a solitary kidney, or early presentation with threatened renal function. A unilateral infarct with a normal opposite kidney is managed medically: renal parenchyma tolerates warm ischemia poorly, so late revascularization rarely restores function. Control the often renin-driven hypertension.
Renal vein thrombosis: causes and clues
The clot of nephrotic syndrome. Membranous nephropathy carries the highest risk, which climbs as serum albumin falls below ~2–2.5 g/dL. The blood becomes hypercoagulable through several mechanisms:
- Urinary loss of antithrombin and plasminogen
- Lower free protein S
- Hepatic overproduction of fibrinogen and factors V and VIII
Other causes. Renal cell carcinoma characteristically grows as tumor thrombus into the renal vein and IVC. Other adult causes are inherited or acquired thrombophilia, estrogen, pregnancy, trauma, extrinsic compression, and early kidney transplant. In newborns and infants, severe dehydration, perinatal asphyxia, and maternal diabetes predispose; the neonatal triad is a palpable flank mass, gross hematuria, and thrombocytopenia.
Presentation. Acute RVT causes flank pain, gross hematuria, an enlarged kidney, rising creatinine, and worsening proteinuria. Chronic RVT is often silent, sometimes bilateral, until a pulmonary embolism reveals it.
The left gonadal vein drains into the left renal vein, while the right drains directly into the IVC. A new left varicocele, especially one that does not decompress when supine, signals left renal vein obstruction from RVT or a left renal mass.
Renal vein thrombosis: diagnosis and treatment
Image the veins. Doppler ultrasound is the first noninvasive test and the study of choice in infants; CT or MR venography is more accurate in adults.
Anticoagulate. Give heparin followed by warfarin for at least 6–12 months and for as long as the patient remains nephrotic. Catheter-directed thrombolysis is reserved for bilateral RVT with AKI or clot extending into the IVC, and an IVC filter only for patients who cannot be anticoagulated.
Prophylaxis. Consider prophylactic anticoagulation in membranous nephropathy with albumin <2–2.5 g/dL and low bleeding risk.