Being Overweight Is Related to Faster Decline in Annual Glomerular Filtration Rate in Kidney Transplant.

Few studies have examined the relationship between non-immunological factors and glomerular filtration rate (GFR) decline in kidney transplant. Correcting these factors in native kidneys slows the progression of chronic kidney disease. The aim of this study was to analyze the association between the control of non-immunological factors and the annual decline of GFR. METHODS: A single-center, retrospective study was performed. We included 128 patients who received kidney transplants between 2000 and 2015, with at least 1-year post-transplant follow-up. Clinical records were reviewed. GFR was estimated by CKD-EPI. Three groups were defined according to the annual change in eGFR (ΔGFR 2016-1015): non-progressors (> -1 mL/min/1.73 m2), slow progressors (> -1 and < -5 mL/min/1.73 m2), and fast progressors (< -5 mL/min/1.73 m2). Percentage of achievement of KDIGO target was also analyzed. RESULTS: The mean GFR was 62.5 mL/min/1.73 m2. Glomerulonephritis was the most common cause of kidney failure (36%). When the fast progressor group was compared with the non-progressor group, they differed significantly in age-patients were younger (40 ± 12.3 vs 45 ± 13.1 years)-post-transplant body mass index (27.4 ± 5.6 vs 25.2 x ± 5.9 kg/m2), and serum uric acid, which was significantly higher (6.4 ± 1.7 vs 5.5 ± 1.58 mg/dL). There were no differences between the groups with regard to blood pressure, dyslipidemia, proteinuria, or venous bicarbonate. Target systolic blood pressure was achieved by 45% of patients. Biopsy-proven acute rejection was higher in the fast progression group, although this was not statistically significant (13 [24.5%] vs 8 [13.1%]). CONCLUSIONS: High body mass index was associated with a faster decline in glomerular filtration rate in this study. Target blood pressure <140/90 mm Hg was achieved in less than 50% of cases.

Acute Antibody-Mediated Rejection in Kidney Transplant Based on the 2013 Banff Criteria: Single-Center Experience in Uruguay.

BACKGROUND: Acute antibody-mediated rejection (AMR) diagnosis criteria have changed in recent consensus of Banff, with current evidence of C4d-negative AMR. Our objective was to evaluate incidence of AMR in renal transplantation according to Banff 2013 criteria and to examine the histological features and outcome. METHODS: This retrospective study involved all kidney transplants with histological diagnosis of acute rejection (AR) at our center between 2000 and 2014. All the biopsies with AR were re-assessed by a nephro-pathologist and classified by use of the Banff 2013 criteria. RESULTS: Of 205 kidney transplants, biopsy-proven AR was diagnosed in 25 cases (12%). Re-assessing them according to Banff 2013 criteria, AMR was diagnosed in 17 (8.3%) and represented 68% of the confirmed rejections. AMR diagnosis was performed on day 23 ± 26, with median of 11 days. From the 17 cases, 7 had concomitant T-cell-mediated rejection. All cases presented endothelial edema and acute tubular necrosis. Glomerulitis was found in 12 cases and capillaritis in 14. In 3, associated thrombotic micro-angiopathy (TMA) was found. Intimal and transmural arteritis was evidenced in 5 and 1 patient. In 2, transplant glomerulopathy was present. Seven of the 10 biopsies with C4d staining in the peri-tubular capillaries were positive. Twelve cases received plasmapheresis, 6 received gamma-globulin, and 6 received rituximab. After administration of anti-AMR therapy, 16 cases recovered renal function, reaching a serum creatinine level of 1.5 ± 0.6 mg %. Graft survival at 1 year was lower in the AMR group versus patients without AMR (81.9% vs 98.9%, log-rank test, P < .001). Risk factors for AMR were re-transplant (30% vs 7%, P = .02), HLA-DR mismatch (1.06 ± 0.65 vs 0.7 ± 0.6, P = .03), panel-reactive antibody (28% ± 33 vs 6.2 ± 13, P = .00), and delayed graft function (82% vs 30%, P = .00). CONCLUSIONS: Adapting the new Banff 2013 criteria increased the sensitivity of the diagnosis of ARM. Regarding our data, despite an adequate response to the therapy, it resulted in a worse graft survival by the first year of renal transplant.