Amer, Hatem

Patients with end-stage renal disease undergoing kidney transplant often have diffuse atherosclerosis and high cardiovascular morbidity and mortality rates. We analyzed the correlation of peripheral arterial disease (PAD), here quantified by an abnormal ankle–brachial index (ABI) measured within the 5 years prior to kidney transplant, with graft failure and mortality rates (primary end points) after adjusting for known cardiovascular risk factors (age, sex, smoking history, hypertension, diabetes, stroke, known coronary artery disease or heart failure, years of dialysis). Of 1055 patients in our transplant population, 819 had arterial studies within the 5 years prior to transplant. Secondary end points included myocardial infarction; cerebrovascular accident; and limb ischemia, gangrene, or amputation. Low ABI was an independent and significant predictor of organ failure (OR, 2.77 (95% CI, 1.68–4.58), p<0.001), secondary end points (HR, 1.39 (95% CI, 0.97–1.99), p<0.076), and death (HR, 1.84 (95% CI, 1.26–2.68), p=0.002). PAD was common in this population: of 819 kidney transplant recipients, 46% had PAD. Low ABI was associated with a threefold greater risk of graft failure, a twofold greater risk of death after transplant, and a threefold greater risk of secondary end points. Screening for PAD is important in this patient population because of the potential impact on long-term outcomes.

AbstractWe present a case of JC polyomavirus (JCV)‐associated nephropathy (PyVAN) in an asymptomatic deceased‐donor kidney transplant recipient. Despite the presence of viral cytopathic effect in the kidney biopsy and positive BK polyomavirus (BKV) in situ hybridization (ISH), BKV real‐time polymerase chain reaction (PCR) results of plasma and urine were negative. JCV ISH was performed and was found to be positive. JCV real‐time PCR on urine, plasma, and the kidney biopsy tissue was positive. Reduction in immunosuppression resulted in resolution of JCV viremia. This case highlights that JC‐PyVAN is a distinct clinical entity and is likely to have a better clinical outcome than BK‐PyVAN. Concurrent infection with BKV and JCV may occur, but may be difficult to confirm due to the potential for cross‐reactivity between BKV and JCV ISH stains.

Background and objectives eGFR equations have been evaluated in kidney transplant recipients with variable performance. We assessed the performance of the Modification of Diet in Renal Disease equation and the Chronic Kidney Disease Epidemiology Collaboration equations on the basis of creatinine, cystatin C, and both (eGFR creatinine-cystatin C) compared with measured GFR by iothalamate clearance and evaluated their non-GFR determinants and associations across 15 cardiovascular risk factors. Design, setting, participants, & measurements A cross-sectional cohort of 1139 kidney transplant recipients >1 year after transplant was analyzed. eGFR bias, precision, and accuracy (percentage of estimates within 30% of measured GFR) were assessed. Interaction of each cardiovascular risk factor with eGFR relative to measured GFR was determined. Results Median measured GFR was 55.0 ml/min per 1.73 m 2 . eGFR creatinine overestimated measured GFR by 3.1% (percentage of estimates within 30% of measured GFR of 80.4%), and eGFR Modification of Diet in Renal Disease underestimated measured GFR by 2.2% (percentage of estimates within 30% of measured GFR of 80.4%). eGFR cystatin C underestimated measured GFR by −13.7% (percentage of estimates within 30% of measured GFR of 77.1%), and eGFR creatinine-cystatin C underestimated measured GFR by −8.1% (percentage of estimates within 30% of measured GFR of 86.5%). Lower measured GFR associated with older age, women, obesity, longer time after transplant, lower HDL, lower hemoglobin, lower albumin, higher triglycerides, higher proteinuria, and an elevated cardiac troponin T level but did not associate with diabetes, smoking, cardiovascular events, pretransplant dialysis, or hemoglobin A1c. These risk factor associations differed for five risk factors with eGFR creatinine, six risk factors for eGFR Modification of Diet in Renal Disease, ten risk factors for eGFR cystatin C, and four risk factors for eGFR creatinine-cystatin C. Conclusions Thus, eGFR creatinine and eGFR creatinine-cystatin C are preferred over eGFR cystatin C in kidney transplant recipients because they are less biased, more accurate, and more consistently reflect the same risk factor associations seen with measured GFR.

AbstractThe majority of kidney transplant recipients die from cardiovascular events. Physical activity may be a modifiable risk factor for cardiovascular disease following transplant. The goal of our study was to examine adherence to a physical activity intervention following kidney transplant and its impact on metabolic parameters. All patients who received a kidney transplant at our center between 12/2010 and 12/2011 received usual care (n = 162), while patients transplanted between 12/2011 and 1/2013 received a 90‐day pedometer‐based physical activity intervention (n = 145). Metabolic parameters were assessed at four and 12 months post‐transplant. Baseline demographics and clinical management were similar between cohorts. Adherence to the prescription was 36.5%. Patients in the physical activity cohort had lower systolic and diastolic blood pressure four months post‐transplant compared to the usual care cohort (122 ± 18 vs. 126 ± 16 mmHg, p = 0.049 and 73 ± 10 vs. 77 ± 9, p = 0.004) and less impaired fasting glucose (20.7% vs. 30.9%, p = 0.04). Twelve‐month outcomes were not different between cohorts. Over one‐third of our cohort adhered to a pedometer‐based physical activity intervention following kidney transplant, and the intervention was associated with improved metabolic parameters. Further study of post‐transplant exercise interventions and methods to optimize long‐term adherence are needed.

AbstractBackgroundData regarding multiple myeloma (MM) that develops after kidney transplantation (KTx) are scarce. The outcomes of these patients were evaluated in a retrospective study.MethodsPatients with newly diagnosed MM after KTx were selected. Patients with a diagnosis of MM or those who received treatment for monoclonal gammopathy of renal significance (MGRS) prior to KTx were excluded.ResultsBetween 2001 and 2012, seven patients developed MM after KTx. Reasons for ESRD included ADPKD (1), C1q nephropathy (1), MPGN (2), hypertensive nephrosclerosis (2), and chronic interstitial nephritis (1). Before KTx, only four patients had monoclonal protein studies, four had monoclonal gammopathy of undermined significance (MGUS), and two of them had clonal plasma cells in bone marrow. Median follow‐up after MM was 70 months (range 19–100). Median survival was 80 months. Median time from KTx to MM was 72 months (range 3–204 months). The Kidney allograft failed in four patients due to monoclonal protein‐related renal disease. Five patients received chemotherapy: bortezomib (n = 3), lenalidomide (n = 2), melphalan (n = 1), thalidomide (n = 1), pomalidomide (n = 1), and high‐dose dexamethasone (n = 1). Three patients received ASCT.ConclusionMultiple myeloma after KTx is rare. Most patients who develop MM had MGUS prior to KTx. There is significant renal involvement in these patients. Survival is not worse when compared to MM without KTx. Further work is needed to identify the best treatment options for these patients.

AbstractMicrosporidia are opportunistic pathogens that usually cause a limited disease in the gastrointestinal tract. Occasionally, they can cause disseminated disease. In solid organ transplant recipients, disseminated disease has been reported only rarely. We describe a 68‐year‐old woman who presented with fever, cough, and acute kidney injury 6 months after kidney transplantation. Dissemination was confirmed by identification of microsporidial spores in urine and bronchoalveolar lavage fluid. Polymerase chain reaction analysis identified the species as Encephalitozoon cuniculi.