Renal infarction and renal-vein thrombosis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Arterial and venous renal occlusion share pain, haematuria and kidney dysfunction but have different mechanisms. An arterial embolus creates abrupt cortical ischaemia and activates renin, while venous obstruction raises interstitial pressure and reduces perfusion secondarily. Segmental arterial loss may leave creatinine unchanged because the other kidney compensates; conversely bilateral RVT or disease in a transplant or solitary kidney can cause rapid renal failure.

Diagnosis is often delayed because pyelonephritis and ureteric stone are more common. LDH elevation with little liver injury is a clue to infarction, but imaging is decisive. Non-contrast CT is appropriate for many colic presentations yet cannot safely close the case when embolic risk, persistent severe pain, absent stone or new hypertension points to vascular disease. Venous-phase imaging is required when nephrotic syndrome, tumour or caval extension makes RVT likely.

Treatment evidence for these uncommon sites is less robust than for leg DVT or stroke. Immediate decisions therefore depend on time from onset, vascular anatomy, preserved renal tissue, cause, bleeding risk and total functioning renal mass. General NICE VTE and atrial-fibrillation principles and British unusual-site thrombosis guidance inform care, but the definitive regimen must be agreed locally with specialist teams.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Arterial embolism

Atrial fibrillation, cardiac thrombus, valvular disease or aortic plaque can send emboli into main or segmental renal arteries.

In-situ arterial occlusion

Renal artery thrombosis, dissection, trauma and hypercoagulable states can abruptly interrupt flow without a distant embolic source.

Nephrosis, malignancy and thrombophilia

Severe nephrosis, renal malignancy and thrombophilia promote renal-vein clot through hypercoagulability, local compression and altered venous flow.

Additional thrombotic risk states

Pregnancy, oestrogen exposure, severe dehydration, critical illness, trauma and transplantation create additional venous or arterial risk in the appropriate setting.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Arterial perfusion loss
Occlusion abruptly deprives downstream cortex of oxygen, creating wedge-shaped segmental or global ischaemic necrosis depending on vessel level.
2
Ischaemic renin response
Ischaemic renal tissue activates renin, contributing to acute pain, hypertension and a rise in markers of tissue injury such as LDH.
3
Renal venous congestion
Venous thrombus raises capillary and interstitial pressure, reducing perfusion gradient and causing kidney swelling, haemorrhage and impaired filtration.
4
Loss of functioning renal mass
Bilateral events, a solitary kidney or extensive main-vessel involvement can cause severe AKI, while smaller events heal with focal atrophy.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Arterial embolic infarctionRed flag

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 thrombosisRed flag

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 thrombosisRed flag

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 RVTRed flag

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 RVTRed flag

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.

Common mimics

Stone, pyelonephritis, renal abscess, aortic pathology, splenic infarction and musculoskeletal pain can resemble renal vascular occlusion. Fever or pyuria does not completely exclude infarction or infected embolism.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
FBC, creatinine, electrolytes, LDH, liver profile and CRPFirst step
Why
Measure renal impact, anaemia, thrombocytopenia, inflammation and the tissue-injury signal that supports infarction.
Interpretation and limitations
A marked LDH rise with relatively modest transaminase change supports renal infarction but is non-specific. Creatinine may stay normal in unilateral segmental disease and must not delay imaging.
02
Urinalysis, culture and quantified urine protein
Why
Identify haematuria, exclude infection and detect nephrotic syndrome as a venous-thrombotic driver.
Interpretation and limitations
Microscopic blood or protein occurs in both entities. Obtain ACR or PCR and serum albumin when RVT is possible; culture pyuria before assuming the vascular finding is infection.
03
Contrast CT with CT angiography
Why
Show arterial occlusion, dissection, wedge or global perfusion defects and competing abdominal emergencies.
Interpretation and limitations
Coordinate arterial and nephrographic phases with radiology. Contrast risk is weighed against losing a time-sensitive diagnosis; a previous non-contrast colic scan does not answer the vascular question.
04
CT or MR venography
Why
Confirm renal-vein clot, determine laterality and identify IVC extension, tumour invasion or collateralisation.
Interpretation and limitations
Distinguish bland thrombus from enhancing tumour thrombus with specialist radiology. MR avoids ionising radiation but takes longer and has motion, availability and device constraints.
05
Renal Doppler ultrasound
Why
Assess venous and arterial flow at the bedside, particularly in neonates, pregnancy and kidney transplants.
Interpretation and limitations
An enlarged kidney, abnormal venous signal or reversed diastolic arterial flow can support venous obstruction. Native adult sensitivity is limited by habitus and operator factors.
06
ECG, telemetry and echocardiography
Why
Find atrial fibrillation, ventricular or valvular thrombus and endocardial sources after arterial infarction.
Interpretation and limitations
One sinus-rhythm ECG does not exclude paroxysmal AF. Select transthoracic, transoesophageal and rhythm-monitoring duration according to embolic probability and specialist advice.
07
Cause-directed thrombosis and renal work-up
Why
Identify nephrotic disease, cancer, antiphospholipid syndrome, myeloproliferative disease or another persistent risk factor.
Interpretation and limitations
Use serum albumin, protein quantification and age-appropriate malignancy assessment first. Acute thrombosis and anticoagulants distort several thrombophilia assays, so haematology should choose tests and timing.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Renal colic

A calculus commonly causes colicky pain and obstruction on non-contrast CT, whereas persistent suspicion after a normal stone study warrants contrast vascular imaging.

Acute pyelonephritis

Fever, pyuria, positive culture and infectious imaging changes favour pyelonephritis, though infarction can also provoke fever and inflammatory markers.

Aortic or mesenteric vascular disease

Pulse deficit, abdominal catastrophe, bowel symptoms or more extensive vascular imaging abnormalities suggest dissection or mesenteric ischaemia involving more than the kidney.

Musculoskeletal or retroperitoneal pain

Movement-related tenderness or an alternative imaging lesion without haematuria, hypertension or vascular risk lowers the probability of renal vessel occlusion.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Acute arterial suspicionDo not stop at renal-colic imagingFirst stepSudden flank pain, embolic risk, high LDH or new hypertension persists without an explanatory stone.

1DefinitiveStabilise, document exact symptom onset, give kidney-safe analgesia and send renal, blood-count, coagulation, LDH, urine and pregnancy tests without postponing definitive imaging.
2Ask radiology for urgent contrast-enhanced arterial imaging to define main or branch occlusion, infarct extent, dissection and viable parenchyma.
3Contact 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.

02Confirmed infarctionTreat the vessel and the sourceCTA demonstrates renal infarction from embolus, thrombosis or dissection.

1Define mechanism, bleeding risk, onset and total threatened renal mass; begin specialist-agreed anticoagulation when embolic or thrombotic disease is likely and no contraindication exists.
2Use ECG, telemetry, echocardiography and cause-directed testing to find AF, cardiac thrombus, aortic plaque, endocarditis, FMD, malignancy or thrombophilia.
3Arrange BP, renal-function and anticoagulation follow-up, and let the MDT determine finite or extended therapy and whether follow-up vascular imaging will change care.

03Confirmed RVTAnticoagulate and remove venous riskVenous imaging shows acute bland renal-vein thrombosis with or without IVC extension.

1Assess haemodynamic stability, active bleeding, platelet count, eGFR, pregnancy, PE symptoms and clot extent, then start renal-adjusted parenteral or oral anticoagulation under local unusual-site policy.
2Quantify nephrotic syndrome, image a suspicious renal mass and review transient and persistent prothrombotic factors, distinguishing tumour thrombus because its treatment is not anticoagulation alone.
3Agree at least three to six months or longer treatment according to provoking-factor persistence and specialist guidance, with earlier imaging or intervention if renal function or clot burden worsens.

04Intervention candidateSelect salvageable renal tissueRecent main-artery occlusion, threatened solitary kidney, bilateral infarction, dissection or deterioration despite initial therapy is present.

1Review CTA with an experienced endovascular team to estimate onset, residual perfusion, collateral flow and whether substantial viable renal mass remains.
2Balance catheter thrombolysis, aspiration thrombectomy, angioplasty, stenting or surgery against bleeding, contrast, embolisation and arterial-injury risks.
3If intervention proceeds, document peri-procedural anticoagulant or antiplatelet management and intensive renal, bleeding, BP and reperfusion surveillance.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

Provides prompt anticoagulation for confirmed acute RVT or embolic or thrombotic renal infarction while the longer plan is decided.

Unfractionated or low-molecular-weight heparin

Use 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.

Offers monitored longer-term therapy when unusual-site evidence, severe renal impairment, antiphospholipid syndrome or interaction profile makes it preferable.

Vitamin K antagonist

Start 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.

May offer an oral option for some bland RVT or embolic infarction patients after the MDT accepts extrapolation from usual-site thrombosis evidence.

Direct oral anticoagulant

Use only a licensed VTE regimen selected for creatinine clearance, age, weight and interactions under specialist local guidance.

Renal-vein-specific data are limited; avoid casual substitution in severe renal failure, pregnancy, mechanical valves, high-risk antiphospholipid syndrome, active tumour thrombus or when urgent procedures and rapid reversal are likely.

Treats acute pain while vascular diagnosis and reperfusion decisions proceed, with short-course opioid rescue when necessary.

Paracetamol-based analgesia

Give paracetamol 1 g orally or intravenously up to four times daily in suitable adults, reducing for low weight or liver risk.

Avoid overdose from combination products and adjust the plan for frailty or liver disease; NSAIDs may worsen renal perfusion, bleeding and anticoagulant toxicity and are usually avoided.

May salvage viable renal tissue in selected recent main-artery occlusion, dissection or threatened total functioning renal mass.

Catheter-directed reperfusion

Thrombolysis, aspiration thrombectomy, angioplasty or stenting follows an experienced centre's anatomy-specific procedural protocol, not a standard ward dose.

Benefit declines with established infarction; intracranial or active bleeding, delayed presentation, contrast injury, access haemorrhage, distal embolisation and reperfusion damage must be weighed urgently.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute kidney injury

Extensive bilateral, solitary-kidney or transplant involvement can sharply reduce filtration and cause electrolyte, acid-base and volume emergencies.

Persistent renovascular hypertension

Ischaemic but viable renal tissue may continue renin secretion, leaving difficult hypertension after the acute pain settles.

Thrombus extension and embolism

Renal-vein clot can extend into the vena cava or embolise to the lungs, while an untreated cardiac source can cause further systemic infarction.

Renal atrophy and chronic impairment

Infarcted parenchyma heals as scar, reducing functional renal mass and increasing later CKD risk when reserve is limited.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

In the acute phase, trend pain, urine output, creatinine, potassium, haemoglobin, platelets, blood pressure and signs of bleeding or new emboli rather than relying on one post-contrast creatinine.
Review anticoagulant dose whenever kidney function, weight, interacting treatment or procedural plans change, and use anti-Xa or APTT only where the chosen protocol indicates.
For arterial infarction, arrange rhythm assessment and follow new or worsened hypertension, since renin release can persist after the acute pain resolves.
For RVT, follow serum albumin and urine protein alongside renal function; ongoing nephrosis or active cancer may prolong thrombotic risk beyond an arbitrary three-month date.
Repeat vascular imaging when symptoms, kidney function or clot extension could alter intervention or duration, not simply because a filling defect once existed.
Safety-net recurrent severe flank pain, breathlessness, haemoptysis, syncope, visible haematuria, neurological deficit and reduced urine output for urgent reassessment.
At each transition, document indication, intended minimum duration, review date, renal-dose basis, bleeding advice and which team owns the final stop-or-continue decision.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Creatinine can stay normal

A segmental infarct or even substantial unilateral loss may be masked by the other kidney, so a normal eGFR does not dismiss compatible pain and imaging clues.

LDH redirects the differential

A disproportionate LDH rise without parallel hepatocellular injury is a useful infarction clue when colic CT and urinalysis do not explain persistent pain.

The CT phase matters

A stone protocol is deliberately non-contrast; arterial occlusion and parenchymal enhancement require a different acquisition discussed explicitly with radiology.

Nephrosis is systemic thrombosis

Severe hypoalbuminaemia reflects urinary loss and altered coagulation proteins, creating pulmonary, limb and renal-vein risk rather than an isolated renal imaging problem.

Tumour thrombus is different

Enhancing extension from renal-cell carcinoma into the vein or cava requires urological-oncology planning; anticoagulation alone does not remove intravascular tumour.

Time is not the only salvage variable

Collateral perfusion, partial occlusion, dissection anatomy and total functioning renal mass modify whether late-appearing tissue may still benefit from expert intervention.

Testing can be mistimed

Acute thrombosis, heparin, warfarin and DOACs alter thrombophilia assays, so an indiscriminate acute panel can create false diagnoses and unnecessary lifelong treatment.

11Common pitfallsFrequent interpretation and management errors.

01
Accepting a negative non-contrast renal-colic CT as exclusion of renal infarction.
02
Waiting for creatinine to rise before ordering arterial imaging in unilateral disease.
03
Assuming flank pain and pyuria must be pyelonephritis despite atrial fibrillation, high LDH or a perfusion defect.
04
Treating enhancing renal-cell-carcinoma tumour thrombus as uncomplicated bland RVT.
05
Selecting and dosing a DOAC without recalculating renal function or acknowledging limited unusual-site evidence.
06
Sending a broad thrombophilia panel during acute clot and anticoagulation without haematology timing advice.
07
Stopping anticoagulation at a fixed date while severe nephrosis, malignancy or another permanent driver remains active.