Visceral Leishmaniasis in Renal Transplant Recipients: Report of 2 Cases.

Visceral leishmaniasis is a disease caused by the protozoan Leishmania and is transmitted by Lutzomyia longipalpis (sand fly). It is an endemic parasitic infection in numerous areas around the Mediterranean basin. Though immunocompetent patients may not develop the disease, in transplant recipients the use of corticoids and intensified immunosuppressants to prevent graft rejection may accelerate the disease, causing severe damage to the liver, spleen, and hematopoietic system. We report 2 cases of visceral leishmaniasis with an atypical presentation in transplant recipients. The first patient, who had a kidney transplant, was treated successfully with liposomal amphotericin B, and the second patient, a combined kidney-pancreas transplant recipient, suffered a relapse 3 years after treatment. Visceral leishmaniasis should be considered in the differential diagnosis of pancytopenia or unexplained fever occurring after organ transplantation in patients living in endemic areas or returning from endemic countries.

Likely Recurrence of C3 Glomerulonephritis in Kidney Transplantation: An Entity to Bear in Mind: Case Report.

BACKGROUND: C3 glomerulonephritis (C3GN) is an unusual entity that is caused by dysregulation and hyperactivity of the alternative complement pathway. Renal biopsy immunofluorescence study shows C3 deposits with absence of immunoglobulins and markers of the classical complement pathway. More than 50% of cases develop end-stage renal disease. Less well-known is the course of C3GN after kidney transplantation. CASE REPORT: We present the case of a 60-year-old woman with chronic kidney disease secondary to chronic glomerulonephritis of unknown origin who received a kidney transplant. Two years later, she presented worsening renal function with non-nephrotic proteinuria and microhematuria. Complement testing revealed low serum levels of C3. Kidney biopsy showed alterations compatible with C3GN that we interpreted as a relapse of the underlying disease.

Impact of blood amylase peak over vascular graft thrombosis in pancreas transplantation.

BACKGROUND: Vascular graft thrombosis (VGT) is still the achuilles heel in pancreas transplantation (PT); it is the main cause of nonimmunologic graft loss. Early diagnosis is essential to avoid transplantectomy. The aim of our study was to analyze the peak amylase during the first 3 days after PT as risk factor for VGT. METHODS: This retrospective study included 58 pancreas transplants in 55 patients from January 2007 to November 2011. They underwent an anticoagulation protocol based on unfractionated heparin and low-molecular-weight heparin. The technique consisted of enteric drainage and systemic venous drainage. The primary endpoint was VGT with consideration of multiple relevant variables. The maximum amylase level was determined during the first 3 days after transplantation. A receiver operating characteristic analysis was performed to establish a cutoff point as (mean plus one standard deviation; 745 mg/dL), calculating the sensitivity, specificity, and predictive values. RESULTS: Recipient characteristics were 71% males with an overall mean age of 39 years (range, 23-55) and body mass index 24 (range, 19-36). The donor sex was similar. Mean donor age was 32 years with occurrences of hypotension in 9%, cerebrovascular brain death in 46%. Mean ischemia time was 10 hours and 45 minutes. Mean blood amylase peak was 395 mg/dL. Seven VGT cases were diagnosed during the postoperative period including six with complete thrombosis requring transplantectomy. Bivariate analysis showed the group of subjects with amylase levels above 745 mg/dL to display on eight-fold greater risk for VGT (odds ratio = 8.6; P = .032). The area under the curve of blood amylase peak during the first 3 days to detect VGT was 0.630 (95% confidence interval 0.41-0.84). CONCLUSIONS: A blood amylase peak above 745 mg/dL in the first 3 days after transplantation was associated with risk for VGT.

Creatinine clearance and proteinuria as early markers of kidney graft survival.

INTRODUCTION: In patients who receive a kidney transplant from expanded criteria donors (ECDs), few studies are available concerning the relation between the clinical characteristics, pretransplant biopsies, and graft outcomes. AIM: To identify early clinical markers predicting worse graft survival in recipients of kidneys from ECDs. MATERIALS AND METHODS: Between 1999 and 2006, we performed a prospective, observational study in 180 recipients of kidney grafts from ECDs that had undergone a preoperative biopsy to evaluate viability. The patients received immunosuppression with basiliximab, late introduction of tacrolimus, mycophenolate mofetil, and steroids. Data were gathered on demographic and posttransplantation clinical characteristics at 1, 3, 6, and 9 months, including estimates of proteinuria and of the glomerular filtration rate using the Modification of Diet in Renal Disease (MDRD) formula. RESULTS: The mean age of the donors was 63.54 years and of the recipients, 58.38 years. A creatinine clearance below the median (40 mL/min, interquartile range 32-50 mL/min) in the first posttransplant year was significantly associated with worse death-censored graft survival (log-rank 14.22, P<.0001). A proteinuria value above the median (100 mg/24 h, interquartile range 40-275 mg/24 h) at 1 year posttransplant significantly reduced the death-censored graft survival (log-rank 14.3, P<.0001). Multivariate Cox analysis showed that a creatinine clearance<40 mL/min in the first year (hazards ratio [HR] 5.7, 95% Confidence Interval [CI] 1.62-20.37; P=.007) and proteinuria at 1 year greater tan 100 mg/24 h (HR 8.3, 95% CI 2.15-32.06; P=.002) were independent risk factors for death-censored graft loss after adjusting for donor age and acute rejection episodes. CONCLUSIONS: Limited renal function and/or low proteinuria at 1 year posttransplant were associated with worse kidney graft survival among recipients of kidneys from ECDS.

[Induction treatment by combining immunoglobulins, plasmapheresis and rituximab in hypersensitive patients receiving cadaveric renal allograft]. / Tratamiento de inducción combinando inmunoglobulinas, plasmaféresis y rituximab en pacientes hipersensibilizados que reciben trasplante renal de cadáver.

In our Universitary Hospital of Canarias we iniciated in May 2008 a induction therapy protocol for sensitized patients receiving cadaveric renal graft using intravenous immunoglobulins, plasmapheresis and rituximab plus immunosuppression with prednisone, tacrolimus and mycophenolate mofetil. We present the results of four patients. Everyone had anti-HLA antibodies rate (PRA by CDC) more than 75%, were on a waiting list during 4 to 17 years and follow-up time was 10-14 months after transplantation. Patient and graft survival in this period was 100%. Only one patient suffered a humoral acute rejection and another one cellular rejection, in both cases reversible with treatment. During the first year, no evidence of de novo donor-specific antibodies was detected. All patients had significantly reduced the CD19+ cells percentage after infusion of rituximab. Neurological symptoms suggestive of progressive multifocal leukoencephalopathy or serious viral infections after transplantation have not been observed. Additionally, no immediate side effects were observed after administration of medication. In summary, induction therapy by combining immunoglobulin, plasmapheresis and rituximab in hypersensitive patients allows the realization of deceased kidney transplantation with good results in the short and medium-term without serious side effects. It remains to know whether this success will continue in the long term.

[A study using nondecalcified bone biopsy of the incidence and presentation forms of renal osteodystrophy]. / Estudio con biopsia ósea sin descalcificar de la incidencia y formas de presentación de la osteodistrofia renal.

BACKGROUND: Renal osteodystrophy (ROD) is a common complication of chronic renal failure. Fibrous osteitis and, to a lesser extent, osteomalacia are the predominant lesions. The aim of the present study was to evaluate the prevalence of the different forms of ROD. METHODS: Nondecalcified bone biopsies were evaluated in 100 patients with end-stage renal disease (57 in pre-dialysis and 43 on hemodialysis) in whom biochemical (calcium, phosphorus, alkaline phosphatase, parathyroid hormone) and histomorphometric studies were carried out. Bone biopsies were classified in four histological groups: mild, fibrous osteitis (FO), osteomalacia (OM) and mixed type (FO + OM). RESULTS: 96% of patients had histological findings of ROD with the following distribution: 41% mild; 30% FO; 14% OM; and 11% mixed. The most advanced types of ROD were seen in interstitial renal diseases. Pre-dialysis OM was associated with metabolic acidosis, a low phosphocalcic product and relative hypophosphoremia. Chronic aluminium poisoning was uncommon (7%) and was basically associated with OM. No instance of aluminium poisoning with osteodystrophy and bone fractures was seen. CONCLUSIONS: The most severe histological forms of OM were found in hemodialysis patients with persistent hypophosphoremia and associated with osteosclerosis.