Post transplant thrombotic microangiopathy causing acute renal failure.
ABSTRACT Acute Renal Failure (ARF) in the immediate post transplant period is most commonly due to acute tubular necrosis, acute cellular rejection and calcineurin inhibitor toxicity apart from usual prerenal and post renal causes. In this report, we discuss an interesting and unusual cause of ARF due to thrombotic micro angiopathy in the immediate post transplant setting.
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ABSTRACT: Human parvovirus B19 is considered an etiologic agent of aplastic anemia in immunosuppressed patients. Mi- croscopic vasculitis, with or without renal involvement, has recently been attributed to this viral infection in immunocom- petent patients. This study describes four cases of thrombotic renal graft microangiopathy presumably secondary to B19 infection. Twelve to 50 days after transplantation, four patients presented a renal graft dysfunction with creatinine rising to 360 to 1088 mmol/L and requiring hemodialysis in three cases. Renal involvement appeared after a systemic illness character- ized by fever, fatigue and arthralgia, aplastic anemia (hemo- globin ranged from 5.3 to 7.8 g/dl), and thrombocytopenia. A thrombotic microangiopathy was observed in the renal biop- sies, and the parvovirus B19 genome was isolated by PCR from the specimens. All four patients also became IgM-posi- tive for parvovirus. Three of the four renal biopsies taken at the time of transplantation (T0) from the same patients were found positive for the B19 genome. Graft function recovered, with resolution of the aplastic anemia, within 22 to 110 d. Twenty biopsies performed as routine controls or for suspected acute rejection and nine T0 biopsies of patients with no signs of B19 infection were used. The B19 genome was found in two of 20 posttransplant biopsies and in one of nine T0 biopsies. The temporal association between aplastic anemia and the onset of thrombotic graft microangiopathy, isolation of the viral ge- nome in renal specimens, seroconversion, and endothelial tro- pism of the virus suggests that B19 could be the etiologic agent of thrombotic microangiopathy in these cases. The develop- ment of the disease after infection could depend on other detrimental cofactors, which make the patient more susceptible to microthrombi formation in the renal microvasculature. The renal graft could represent the route of B19 transmission.Journal of the American Society of Nephrology 07/2000; 11(6). · 8.99 Impact Factor
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ABSTRACT: Thrombotic microangiopathy (TMA) is a well-recognized and serious complication of renal transplantation, affecting 3% to 14% of patients administered calcineurin-inhibitor-based immunosuppression. We reviewed 1,219 biopsy reports of 742 kidney and kidney-pancreas transplants performed during 15 years at our center and found 21 biopsy-confirmed cases of TMA. On presentation, the majority (62%) had systemic TMA with manifest hemolysis and thrombocytopenia, whereas a subset had TMA localized only to the graft (38%). There were no statistically significant differences in sex, type of transplant, age, race, or type of immunosuppression. Patients with systemic TMA were more likely to be treated with plasma exchange (38% versus 13%; P < 0.05), more often required dialysis therapy (54% versus 0%; P = 0.01), and had a greater rate of graft loss (38% versus 0%; P < 0.05). No patient with the localized variant had TMA-related graft loss. Patients with localized TMA often responded to reduction, conversion, or temporary discontinuation of calcineurin-inhibitor-based immunosuppression therapy and did not routinely require plasma exchange for graft salvage. We compare our findings with the literature regarding the prognosis of TMA. Classifying patients with post-renal transplantation TMA into those with localized and systemic disease is clinically useful because each group has distinct characteristics and clinical courses.American Journal of Kidney Diseases 02/2003; 41(2):471-9. · 5.29 Impact Factor
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ABSTRACT: Analysis of the incidence, time to event, and risk factors for thrombotic microangiopathy (TMA) after renal transplantation (RT), has not been reported in a national population. This is a historical cohort study of 15,870 RT recipients in the United States Renal Data System (USRDS) with Medicare as their primary payer between January 1, 1998, and July 31, 2000, followed until December 31, 2000. Patients with Medicare claims with a diagnosis of TMA (International Classification of Diseases, 9th Revision, codes 283.11x or 446.6x) after RT were assessed by Cox regression. Among patients with end-stage renal disease owing to hemolytic uremic syndrome (HUS), 29.2% later had TMA versus 0.8% of patients with ESRD owing to other causes. The incidence of TMA in RT recipients was 5.6 episodes per 1,000 person-years (PY; 189/1,000 PY; for recurrent TMA versus 4.9/1,000 PY for de novo TMA). The risk of TMA was highest for the first 3 months after transplant. Risk factors for de novo TMA included younger recipient age, older donor age, female recipient, and initial use of sirolimus. Patient survival rate after TMA was approximately 50% at 3 years. De novo TMA is uncommon and may occur later after RT than previously reported. Risk factors for de novo TMA were also identified.American Journal of Kidney Diseases 12/2003; 42(5):1058-68. · 5.29 Impact Factor