P0510INFLAMMATORY BOWEL DISEASE IN KIDNEY TRANSPLANTATION:CASE REPORT

Abstract

Abstract Introduction Kidney transplantation has become the treatment of choice for chronic end-stage renal disease because it improves not only the quality of life of patients but also their survival rate. However, several complications can be observed in transplant patients such as immune rejection, infections and recurrence of initial nephropathy etc. Case summary A 21-year-old man diagnosed with chronic end-stage renal failure 5 years ago with a renal biopsy showing an aspect of proliferative glomerulonephritis. The study of the alternate complementary path show a C3 low level, C4 and CH50 normal level, H factor and I factor was normal too. The patient presented purpuric skin lesions with a biopsy of granular deposits of C3. We started extra renal purification by peritoneal dialysis and the patient had, one year later, a kidney transplant from his mother. Ten month later, we have notice a progressive renal function decline with an aspect of proliferative membranous glomerulonephritis with deposits predominant of c3 in graft biopsy. The diagnosis of the recurrence of the initial nephropathy was made but the treatment was delayed by the onset of cutaneous leishmaniosis. Few months later the patient was presented with diarrhea lasting more than a month, which led us to do a colonoscopy, which objectified an aspect of chronic inflammatory bowel disease evoking earlier a Crohn's disease. Therefore, we stopped tacrolimus and put the patient on full dose corticosteroid therapy and azathioprine without having a remission, and appearance of skin lesions at the elbow and pelvis evoking pyoderma gangrenosum in skin biopsy. In addition, the patient has presented an ischemic retinal damage probably related to a deregulation of the alternate complement pathway. Discussion The complement system is not only a host defense system against microbes, but also a surveillance system that contributes to maintain tissue homeostasis and tissue repair. However, uncontrolled complement activation can induce tissue damage, and inappropriate activation is involved in the pathogenesis of various conditions like autoimmune diseases, sepsis and transplant and extensive inflammation and tissue damage. The impairment of alternative path can explain the extra-renal manifestation of this patient especially the appearance of inflammatory bowel disease witch can be explained by impaired local immune defense in the gut. Conclusion Immune system abnormalities can occur after kidney transplantation this leads to the appearance of several inflammatory abnormalities such as chronic inflammatory bowel disease which may in our case be due to an abnormality of the alternate pathway of the complement.