Acute renal ischemia caused by in-stent thrombosis is a common scenario, especially after complex endovascular treatments. Covid-19 is a disease characterized by an elevated risk of thrombosis. These associations can lead to rapid loss of renal function end renal failure with the need for dialysis.

An 88-years-old male patient presented to the emergency room with epigastric and left lumbar pain, anuria, fever, and dyspnea from about 24 hours. The vitals were a body temperature of 38°C, blood pressure of 210/100 mmHg, heart rate of 110 bpm, respiratory rate of 25 bpm, oxygen saturation of 92%; the lung auscultation revealed rhonchi and diminished pulmonary murmur and signs of cardiac overload. He had a history of hypertension, ischemic cardiopathy, and chronic renal disease stage III with just the left kidney functioning. He had a previous abdominal aortic repair with endoprosthesis and triple chimney into the superior mesenteric artery and both renals. The right renal stent underwent thrombosis without an immediate diagnosis and treatment. The laboratory test yielded a potassium 5.0 mEq/L, serum creatinine of 2.16 mg/dl, and lactate dehydrogenase (LDH) 195 U/L, with a baseline estimated glomerular filtration rate of 13.6ml/min/1.70m2. After 9-hours, creatinine and LDH were 3.02 mg/d and 409 U/L. After 20 hours, the levels were 5.67 mg/d and 1141 U/L. At the 12 h control, the pattern continued until reaching a creatinine of 8 mg/dl. At the screening with PCR for Sars-Cov2, the patient resulted positive. He started hemodynamic stabilization and dialysis. A Chest Rx yielded signs of pulmonary edema; an Ecocolor-Doppler was negative for an obstructive urological disease; After a Computed Tomography Angiography (CTA) he was diagnosed with acute thrombosis of the left renal stent with minimal contrast flow.

In local anesthesia through percutaneous left brachial access, a McNamara catheter was placed in the left renal artery and started an infusion with 100.000 UI of urokinase per hour for 24 hours. Considering the ischemia time and the solitary renal function, after 24 hours of urokinase the vascular team decided to place a stent-in-stent placement. We performed thromboaspiration with an AXS Catalyst 6 Fr catheter (Stryker Neurovascular, Mountain View, CA, USA). The fresh thrombus intra-stent was "pushed" into a terminal vessel to free the collaterals and avoid a major percentage of renal parenchymal loss, then a B-graft 7x37 mm and a distal overlapped 5x37 mm (Peripheral Stent Graft System, Bentley Innomed, Hechingen, Germany) were placed. The final angiography showed patency of the stents, an inferior polar renal artery, and slow flow to the rest of the accessory vascularity. Immediately after the patient underwent urgent dialysis. At the 48-hours control, the serum creatinine levels dropped to 2,3 mg/dl, and the LDH to 2500 U/L. The patient was discharged with his basal renal function (1,8 mg/dl) in the absence of ulterior dialysis treatments.

Complex endovascular treatments present a high risk of stent thrombosis, the risk is even higher if the treatment is associated to Covid-19. There is a lack of concrete evidence about the timing for medical and surgical treatments for patients with in-stent acute renal occlusion. We suggest attempting renal revascularization because endovascular options with thromboaspiration and intraarterial thrombolysis offers a safe method to restore the renal function and save the remaining renal parenchyma. In our case, despite the prolonged ischemia and the >50% of parenchyma loss on the CTA, we exemplify the potential benefits of revascularization options. If clinical suspicion is present, we suggest the use of DUS and CTA with the minimum threshold and an aggressive treatment. We hope this case helps to obtain a definitive protocol for diagnosis and treatment.