Renal infarction and renal-vein thrombosis — Rapid

Synopsis

Distinguish arterial renal infarction from renal-vein thrombosis, obtain time-sensitive vascular imaging, preserve threatened renal tissue and select anticoagulation or intervention according to cause, kidney function and bleeding risk.

Renal infarction is acute loss of arterial perfusion from embolism, in-situ thrombosis, dissection, trauma or a hypercoagulable state; atrial fibrillation is a classic embolic source.
The usual arterial presentation is abrupt unilateral flank or abdominal pain, nausea and new hypertension with microscopic haematuria, proteinuria and a disproportionately raised LDH, but these findings are not individually diagnostic.
A normal non-contrast renal-colic CT can miss infarction. If clinical suspicion persists, obtain contrast-enhanced CT with an arterial phase or CT angiography urgently unless another modality is selected by radiology.
Wedge-shaped cortical hypoenhancement supports segmental infarction; a global non-enhancing kidney or main-artery occlusion raises the urgency of revascularisation discussion, especially early, bilateral or in a solitary kidney.
Renal-vein thrombosis is venous outflow obstruction associated in adults with nephrotic syndrome, renal malignancy, thrombophilia, pregnancy, oestrogen exposure, severe dehydration, trauma and transplantation.
Adult RVT may be silent or cause flank pain, haematuria and kidney impairment. Neonates classically develop haematuria, thrombocytopenia and an enlarged kidney, often after dehydration or critical illness.
Contrast CT or MR venography usually defines native-kidney RVT and caval extension; Doppler ultrasound is useful in neonates and transplants but a technically normal adult scan does not reliably exclude acute thrombosis.
Start anticoagulation promptly for confirmed embolic renal infarction or acute RVT when bleeding risk permits, but agent, dose and duration need renal, vascular or haematology input because evidence is extrapolated and kidney function changes drug handling.
Catheter-directed thrombolysis, thrombectomy, angioplasty or stenting is reserved for selected recent main-artery occlusion, threatened total renal mass, dissection or deterioration, and should never be promised to recover established scar.
Always find and treat the driver: ECG and rhythm monitoring for atrial fibrillation, echocardiography when embolism is plausible, nephrotic and malignancy assessment for RVT, and selective thrombophilia testing at the correct time.

Key red flags

Arterial embolic infarction

Abrupt flank or upper abdominal pain occurs in a patient with atrial fibrillation, recent myocardial infarction, valvular disease, endocarditis or another systemic embolus, with haematuria and new hypertension possible.

Arterial dissection or thrombosis

Severe pain follows trauma or appears with fibromuscular dysplasia, connective-tissue arteriopathy, cocaine exposure or severe atherosclerosis; CTA may show a flap, branch occlusion or renal perfusion defect.

Nephrotic renal-vein thrombosis

A patient with heavy proteinuria and hypoalbuminaemia develops new flank discomfort, visible or microscopic blood, worsening filtration or pulmonary embolism. Membranous nephropathy carries a notable thrombotic association.

Malignancy-associated RVT

Weight loss, visible haematuria, a renal mass or known renal-cell carcinoma accompanies renal-vein filling defect, sometimes extending as tumour thrombus into the inferior vena cava rather than bland clot.

Neonatal RVT

A critically ill or dehydrated neonate develops an enlarged flank mass or kidney, haematuria and thrombocytopenia, with possible AKI if disease is bilateral or the other kidney is abnormal.

Investigation priorities

FBC, creatinine, electrolytes, LDH, liver profile and CRPFirst step

Measure renal impact, anaemia, thrombocytopenia, inflammation and the tissue-injury signal that supports infarction.

Management branches

Acute arterial suspicionDo not stop at renal-colic imaging

Sudden flank pain, embolic risk, high LDH or new hypertension persists without an explanatory stone.

Stabilise, document exact symptom onset, give kidney-safe analgesia and send renal, blood-count, coagulation, LDH, urine and pregnancy tests without postponing definitive imaging.
Ask radiology for urgent contrast-enhanced arterial imaging to define main or branch occlusion, infarct extent, dissection and viable parenchyma.
Contact renal and vascular or interventional teams immediately for bilateral, solitary-kidney, transplant or main-artery disease so anticoagulation and a revascularisation window are considered together.

Key medicines

Unfractionated or low-molecular-weight heparinUse a therapeutic weight-based local protocol, choosing agent and adjustment from current creatinine clearance and bleeding risk.Check baseline FBC, coagulation and renal function; severe renal impairment favours controllable strategies, while active bleeding, thrombocytopenia, recent surgery, neuraxial procedures and suspected heparin-induced thrombocytopenia require specialist modification.

Vitamin K antagonistStart warfarin with parenteral anticoagulation for at least five days and until therapeutic INR criteria are met under local policy.Individualise target and duration, monitor INR and interactions closely, provide counselling and avoid in pregnancy; initial protein C reduction makes unbridged loading unsafe for acute thrombosis.

Open full textbook →Answer 2 questions