The objective of this study was to analyze factors that are involved in the progression of renal allograft damage in the first 6 mo after transplantation. Donor and 6-mo protocol biopsies of 83 patients who received a renal transplant were classified using the Chronic Allograft Damage Index (CADI). Histologic changes were compared and correlated to clinical parameters at transplantation, at 6 mo, and annually over 2 yr. All CADI components increased significantly in the 6-mo posttransplantation period, except chronic vascular changes and the percentage of glomerulosclerosis. Total cholesterol and LDL- cholesterol at the time of biopsy correlated positively with mesangial matrix increase, and HDL cholesterol correlated negatively with vascular intima increase. High BP at biopsy was associated with tubular atrophy. Diastolic BP at biopsy correlated with 6-mo CADI (CADI-6). Patients with diastolic BP > or =85 mmHg at biopsy had a higher difference between CADI score in protocol biopsies and CADI score in donor biopsies (DeltaCADI) and higher creatinine at 1 and 2 yr. CADI in donor biopsies (CADI-0) >1 was more frequently found in older (odds ratio [OR], 1.07; 95% confidence interval [CI], 1.01 to 1.14) and nontraumatic dead donors (OR, 3.89; 95% CI, 1.13 to 13.33). CADI-6 >3 was more frequently found in those with CADI-0 >1 (OR, 3.82; 95% CI, 1.19 to 12.21), older donors (OR, 1.05; 95% CI, 1.01 to 1.10), and number of AB mismatches (OR, 2.36; 95% CI, 1.09 to 5.10). CADI-0, CADI-6, and DeltaCADI correlated significantly with serum creatinine at hospital discharge, at 6 mo, and at 2 yr. DeltaCADI was affected by initial percentage of glomerulosclerosis (OR, 1.10; 95% CI, 1.02 to 1.19) and creatinine at hospital discharge (OR, 1.01; 95% CI, 1.00 to 1.02). Donor-related as well as nonimmunologic factors, such as hypertension and dyslipidemia, are associated with increased risk for renal allograft damage progression.
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http://dx.doi.org/10.1681/ASN.2004060475 | DOI Listing |
Artif Organs
January 2025
Department of Surgery, Albany Medical College, Albany, New York, USA.
Background: Patients with end-stage renal disease often face prolonged waiting times for kidney transplants. Historically, the use of marginal kidneys was limited due to suboptimal preservation methods. Normothermic machine perfusion (NMP) preserves physiological activity during the preservation process, potentially improving graft function and viability, expanding the use of marginal kidneys.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
NIHR Great Ormond Street Hospital Biomedical Research Centre, University College London Great Ormond Street Institute of Child Health, London, UK.
Acute kidney injury (AKI) in paediatric kidney transplant recipients is common. Infection including urinary tract infection (UTI) and rejection are the most common causes in children. Surgical complications often cause AKI early post-transplant, whereas BK polyomavirus nephropathy rarely occurs in the first month post-transplant.
View Article and Find Full Text PDFIndian J Nephrol
June 2024
Departmet of Nephrology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.
Case Rep Transplant
January 2025
Comprehensive Transplant Center, Department of Surgery, Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Kidney allograft torsion (KAT) is a rare but critical complication of kidney transplantation that can lead to graft loss due to acute ischemia. This report presents a case of KAT resulting in graft loss 9 months following intraperitoneal simultaneous pancreas and kidney (SPK) transplant and reviews previous reports to identify potential high-risk features. A 38-year-old female with end-stage renal disease secondary to Type 1 diabetes mellitus underwent an intraperitoneal enteric drained SPK transplant.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Kidney Disease Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
METTL3, a key enzyme in N6-methyladenosine (m6A) modification, plays a crucial role in the progression of renal fibrosis, particularly in chronic active renal allograft rejection (CAR). This study explored the mechanisms by which METTL3 promotes renal allograft fibrosis, focusing on its role in the macrophage-to-myofibroblast transition (MMT). Using a comprehensive experimental approach, including TGF-β1-induced MMT cell models, METTL3 conditional knockout (METTL3 KO) mice, and renal biopsy samples from patients with CAR, the study investigates the involvement of METTL3/Smad3 axis in driving MMT and renal fibrosis during the episodes of CAR.
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