ABSTRACT
Malaria has protean clinical manifestations and renal complications, particularly acute renal failure that could be life threatening. To evaluate the incidence, clinical profile, out-come and predictors of mortality in patients with malarial acute renal failure, we retrospectively studied the last two years records of malaria induced acute renal failure in patients with peripheral smear positive for malarial parasites. One hundred (10.4%) (63 males, 37 females) malaria induced acute renal failure amongst 958 cases of acute renal failure were evaluated. Plasmodium (P). falciparum was reported in 85%, P. vivax in 2%, and both in 13% patients. The mean serum creatinine was 9.2 ± 4.2 mg%, and oligo/anuria was present in 82%; 78% of the patients required hemodialysis. Sixty four percent of the patients recovered completely, 10% incompletely, and 5% developed chronic kidney failure; mortality occurred in 21% of the patients. Low hemoglobin, oligo/anuria on admission, hyperbilirubinemia, cerebral malaria, disseminated intravascular coa-gulation, and high serum creatinine were the main predictors of mortality. We conclude that malaria is associated with acute renal failure, which occurs most commonly in plasmodium falciparum infected patients. Early diagnosis and prompt dialysis with supportive management can reduce morality and enhance recovery of renal function.
Subject(s)
Acute Kidney Injury/parasitology , Malaria, Falciparum/complications , Malaria, Vivax/complications , Acute Kidney Injury/diagnosis , Acute Kidney Injury/mortality , Acute Kidney Injury/therapy , Adult , Biomarkers/blood , Biopsy , Creatinine/blood , Female , Hemoglobins/metabolism , Humans , Incidence , India , Kidney Failure, Chronic/mortality , Kidney Failure, Chronic/parasitology , Kidney Failure, Chronic/therapy , Malaria, Falciparum/mortality , Malaria, Falciparum/therapy , Malaria, Vivax/mortality , Malaria, Vivax/therapy , Male , Middle Aged , Renal Dialysis , Retrospective Studies , Time Factors , Treatment Outcome , Young AdultABSTRACT
Collapsing glomerulopathy (CG), characterized histologically by segmental/global glomerular capillary collapse, podocyte hypertrophy and hypercellularity and tubulo-interstitial injury; is characterized clinically by massive proteinuria and rapid progressive renal failure. CG is known to recur in renal allograft and rarely de novo. We report de novo CG 3 years post-transplant in a patient who received renal allograft from haplo-identical type donor.
Subject(s)
Kidney Cortex Necrosis/pathology , Kidney Failure, Chronic/surgery , Kidney Transplantation/pathology , Adult , Complement C4b/analysis , Epithelial Cells/pathology , Humans , Hyperplasia , Hypertension/complications , Kidney Failure, Chronic/etiology , Kidney Tubules/pathology , Male , Peptide Fragments/analysis , Reoperation , Waiting ListsABSTRACT
BACKGROUND: Hemolytic uremic syndrome (HUS)/thrombotic microangiopathy (TMA) (tissue-limited HUS) is a well-recognized serious complication of renal transplantation, affecting 3% to 14% patients who are administered calcineurin inhibitor-based immunosuppression. We performed a retrospective study to examine the incidence, etiology, course, and outcome of HUS/TMA in our experience. PATIENTS AND METHODS: This retrospective study of 1540 renal allograft biopsies performed between January 2000 and October 2007 was performed to assess the incidence of HUS/TMA. Institute Transplant Registry records were reviewed for clinical history, laboratory findings, medications, and outcome. The offending drug was substituted in all subjects and plasmapheresis was added as an adjuvant until recovery of allograft function. RESULTS: TMA was observed in 17 (1.1%) biopsies. Two of 17 patients experienced recurrent HUS; 15 were drug-induced (12 with cyclosporine, three with Sirolimus); 10 were TMA; and five HUS. Nine patients developed HUS/TMA within 3 months of transplantation with eight developing it within 1 year posttransplantation. Graft function recovered in 12, while five did not recover. The HUS group showed 60% recovery compared with 80% among the TMA group. Two patients were lost; both displayed HCV seropositivity and one also showed anti-cardiolipin antibody. CONCLUSION: Early allograft biopsy with prompt diagnosis and management by drug substitution +/- plasmapheresis in posttransplant HUS/TMA plays an important role in allograft outcome. TMA showed better recovery than HUS.
