Acute kidney injury after complex incisional hernia repair in kidney transplant recipients

Abstract

Incisional hernia after abdominal organ transplantation is affecting between 1.7% and 23% of transplant recipients. The majority of the reports on hernia repair in post-transplant setting are focused on surgical techniques and complications and not on the effect on this procedure on kidney graft function. In the nontransplant setting acute kidney injury (AKI) may lead to chronic kidney disease and even death, but it's epidemiology in kidney transplantation, outside the peritransplant period, has not been well characterized. The aim of this study was to examine the incidence and consequences of, unrelated to acute rejection, AKI in kidney transplant recipients undergoing complex hernia repair. We have conducted a retrospective review of all herniorrhaphies done in our center for complex (very large, recurrent or deemed inoperable, because of loss of domain) incisional hernias. AKI was defined by KDIGO/RIFLE criteria of acute kidney injury. 14 procedures were identified in 14 individuals (9 male (64%),5 female (36%); mean age 54.8 yrs. (range 40-70) performed at a median 2.5 years (range 1-12) after kidney transplantation. All operations were done with component separation technique and completed successfully. AKI was detected in 2 patients (14.3%) presenting immediately after herniorrhaphy with oligo-anuria (urine output of 0.2 mL/kg/h × 12 hr. and 0.4 mL/kg/h × 12 hr.) and nearly two fold elevation of serum creatinine (from 0.6 mg/ld. to 1.15 mg/ld. and from 1.5 mg/ld. to 3.0 mg/ld.). Despite elevated abdominal pressure of ≤ 20 mm Hg, decompression laparotomy was being withheld. The management included withdrawal of intravenous cyclosporine and hydration. No renal replacement therapy was instituted. One patient required mechanical ventilation because of severe acidosis. In both patients, over the ensuing 48 hours, the urine output increased gradually, serum creatinine decreased to baseline levels, immunosuppression with calcineurin inhibitors (CNI) has been resumed and the patients were discharged after 11 and 22 days of in-hospital stay. In our opinion, the precipitating factor of AKI in this series was acute decrease in kidney blood perfusion caused by combination of surgical procedure related increase in intraabdominal pressure and arteriolar vasospasm induced by intravenous cyclosporine (blood levels 120-125 ng/dL). Despite good renal function, kidney transplant recipients remain at high risk for AKI from a variety of causes, including a combination of prerenal and renal hypoperfusion. We conclude, that AKI can arise with significant frequency (14%) after complex hernia repair in the late post-transplantation period and recommend to raise the index of suspicion of transplant physicians and general surgeons alike toward this occurrence.