Revascularization of a single-kidney occluded stent for renal salvage complicated by guide wire distal artery perforation and reperfusion injury

Background The complexity of the case, including the rarefied simultaneous occurrence of complications—iatrogenic, as well as reperfusion injury, invite reporting and publication. Case presentation A 39-year-old woman with a single-functioning left kidney, previous left renal artery stenting (RAS), and known hypercoagulopathy was hospitalized for flash pulmonary edema, elevated serum creatinine (9.7 mg/dl), and refractory hypertension. She was subsequently referred to our center [2] for endovascular treatment of acute renal ischemia (AKI) due to RAS occlusion. Periprocedural complications of guide-wire arterial perforation and reperfusion injury resulted in life-threatening hemorrhage. Conclusions Following more than 48 h of hypoperfusion of the left kidney, revascularization of the thrombosed RAS was successfully attempted with selective, trans-catheter thrombolysis, and balloon angioplasty. Ultra-selective, nephron-sparing coil embolization was successfully performed. The patient’s creatinine level decreased to 2.8 mg/dl at 12 days and to 1.5 mg/dl at 3 months. After 1 year of follow-up, the stent remains patent, and the patient is asymptomatic with stable renal function.

Dual role of protease activated receptor 4 in acute kidney injury: contributing to renal injury and inflammation, while maintaining the renal filtration barrier upon acute renal ischemia reperfusion injury

Ischemia reperfusion (I/R) injury triggers the activation of coagulation and inflammation processes involved in the pathophysiology of acute kidney injury (AKI). Coagulation proteases upregulated upon renal I/R injury activate protease activated receptors (PARs), which form an important molecular link between inflammation and coagulation. PAR4 is the major thrombin receptor on mouse platelets, and the only PAR that is expressed on both human and murine platelets. In addition, PAR4 is expressed on other cells including podocytes. We here sought to determine the contribution of PAR4 in the host response to renal I/R injury. Hence, we subjected PAR4 knockout and wild-type mice to renal I/R injury. PAR4 knockout mice exhibited an increased tolerance to renal tubular necrosis and showed a decreased neutrophil influx in response to renal I/R, independent from platelet PAR4. On the other hand, PAR4 deficiency resulted in albumin cast formation in peritubular capillaries and showed a tendency towards albuminuria. Transmission Electron Microscopy revealed an increase in podocyte foot process effacement. Our findings suggest that PAR4 contributes to renal injury likely through facilitating neutrophil migration, independent from platelet PAR4. In addition, PAR4 fulfils an important function in the maintenance of podocyte integrity following renal I/R insult. Subsequently, loss of PAR4 results in albuminuria.