Renal Vascular Acute Kidney Injury

Renal vascular acute kidney injury is acute loss of kidney function caused by occlusion or severe compromise of renal arterial or venous circulation, or by atheroembolism to small renal vessels. It is under diagnosed because it mimics other causes and requires imaging to confirm. It is an emergency when the kidney is salvageable, since warm ischaemia causes irreversible loss within 60 to 90 minutes of complete occlusion, though collateral flow can preserve function for up to 24 hours.

Categories:

• Renal artery thrombosis or embolism: cardioembolism (atrial fibrillation, infective endocarditis, left ventricular thrombus, prosthetic valve, myxoma), in situ thrombosis (atheroma, fibromuscular dysplasia, vasculitis, hypercoagulability), aortic or renal artery dissection, trauma, iatrogenic injury during angiography or surgery
• Renal artery stenosis: bilateral, or in a solitary kidney, with ACE inhibitor or angiotensin receptor blocker exposure, or acute "flash" occlusion
• Renal vein thrombosis: nephrotic syndrome (particularly membranous), malignancy (renal cell carcinoma), dehydration in infants, pregnancy, hypercoagulable states, trauma
• Atheroembolic disease: cholesterol crystal showering after arterial catheterisation, vascular surgery, anticoagulation or thrombolysis
• Aortic dissection or abdominal aortic aneurysm involving the renal arteries

Bilateral occlusion or occlusion of a solitary kidney causes anuric acute kidney injury; unilateral occlusion may be silent in the presence of a normal contralateral kidney.

• Sudden flank or abdominal pain, nausea, vomiting, fever
• Haematuria, new or worsening hypertension, oliguria or anuria
• Elevated LDH (often above 2 times the upper limit), leucocytosis, raised aspartate aminotransferase
• Source of emboli: irregular pulse, murmurs, peripheral embolic signs
• Renal vein thrombosis: flank pain, haematuria, increase in proteinuria, enlarged kidney; pulmonary embolism may coexist
• Atheroembolism: livedo reticularis, blue toes, eosinophilia, low complement, gradual stepwise creatinine decline over weeks after an arterial procedure
• Flash pulmonary oedema and creatinine rise after starting an ACE inhibitor in bilateral stenosis

Red flags: anuria, new severe hypertension, evidence of aortic dissection (tearing pain, pulse deficit), peripheral emboli, atrial fibrillation without anticoagulation, nephrotic syndrome with flank pain.

• Creatinine, urea, electrolytes, LDH, full blood count, eosinophils, complement, urinalysis (haematuria, mild proteinuria), cardiac enzymes
• ECG and echocardiography (transoesophageal if endocarditis or atrial thrombus is suspected)
• CT angiography with arterial and venous phases: wedge shaped perfusion defects, absent enhancement, filling defects in the renal vein; use despite contrast risk when diagnosis alters management
• Doppler ultrasound: absent or diminished flow, tardus parvus waveform; renal vein thrombus; peak systolic velocity above 200 cm/s suggests stenosis
• Magnetic resonance angiography without gadolinium contrast (time-of-flight) when contrast is contraindicated
• Renal scintigraphy: absent perfusion
• Thrombophilia screen, antiphospholipid antibodies, blood cultures when relevant
• Atheroembolism: biopsy showing cholesterol clefts in arcuate and interlobular arteries

Differentials: pyelonephritis, ureteric colic, acute tubular injury, aortic dissection, interstitial nephritis, thrombotic microangiopathy.

Renal artery occlusion

• Immediate unfractionated heparin 80 units/kg intravenous bolus, then 18 units/kg/h, adjusting to an activated partial thromboplastin time of 1.5 to 2.5 times control.
• Endovascular treatment for salvageable kidneys, preferably within 3 hours of onset but up to 24 hours when collateral flow is present or the kidney is solitary or both are affected: catheter directed thrombolysis (alteplase 0.5 to 1 mg/h locally), aspiration thrombectomy, or angioplasty with stenting for dissection or stenosis.
• Open surgical thrombectomy or bypass when endovascular treatment fails.
• Long term anticoagulation for cardioembolic sources: apixaban 5 mg twice daily (2.5 mg twice daily if two of age 80 or over, weight 60 kg or less, creatinine 133 micromol/L or more) or warfarin with INR 2 to 3.
• Treat the source: antibiotics for endocarditis, left ventricular thrombus anticoagulation.

Renal vein thrombosis

• Anticoagulation: enoxaparin 1 mg/kg every 12 hours (once daily at 1 mg/kg when eGFR is below 30), then warfarin with INR 2 to 3 or a direct oral anticoagulant, continued for at least 6 months and for as long as nephrotic syndrome or the predisposing state persists.
• Thrombolysis or thrombectomy only for bilateral thrombosis with acute kidney injury or threatened life.

Bilateral renal artery stenosis with acute kidney injury

• Stop ACE inhibitor or angiotensin receptor blocker; manage blood pressure with calcium channel blocker (amlodipine 5 to 10 mg daily) or beta blocker; revascularise with angioplasty and stenting for flash pulmonary oedema, refractory hypertension or progressive renal failure.

Atheroembolic disease

• Supportive: blood pressure control, avoid further arterial manipulation, withdraw anticoagulants if safe.
• Atorvastatin 40 to 80 mg daily; aspirin 75 mg daily for vascular disease.
• Corticosteroids (prednisolone 0.5 to 1 mg/kg daily) are used by some in severe disease with eosinophilia but evidence is limited.
• Dialysis for uraemic complications; a substantial proportion need long term renal replacement.

Monitoring. Creatinine, LDH and blood pressure daily; repeat imaging at 3 months; echocardiography for emboli source.

Refer urgently to vascular surgery or interventional radiology and nephrology for any renal artery occlusion.