OBJECTIVE.: To analyze the risk factors for new-onset diabetes mellitus (NODM) in liver transplant recipients using the Organ Procurement and Transplant Network/United Network for Organ Sharing database. METHODS.: Among 20,172 primary liver recipients (age > or =18 years) transplanted between July 2004 and December 2008 in Organ Procurement and Transplant Network/United Network for Organ Sharing databases, 15,463 recipients without pretransplant diabetes were identified. Risk factors for NODM were examined using multivariate Cox regression analysis. RESULTS.: NODM was reported in 26.4% of recipients (median follow-up, 685 days). Independent predictors of NODM development included recipient age (> or = 50 vs. <50 years, hazard ratio [HR]=1.241), African American race (HR=1.147), body mass index (> or = 25 vs. <25, HR=1.186), hepatitis C (HR=1.155), recipient cirrhosis history (HR=1.107), donor age (> or = 60 vs. <60 year, HR=1.152), diabetic donor (HR=1.151), tacrolimus (tacrolimus vs. cyclosporine, HR=1.236), and steroid at discharge (HR=1.594). Living donor transplant (HR=0.628) and induction therapy (HR=0.816) were associated with a decreased risk of NODM. CONCLUSION.: The incidence of NODM was 26.4% in liver recipients with a median follow-up time of 685 days. Identified risk factors for NODM in liver transplantation were similar to that in kidney transplantation. Some of the identified factors are potentially modifiable, including obesity and the choice of immunosuppressive regimens.
NODM is common and occurs in more than a quarter of heart recipients during the median follow-up period of 2 years. Risk factors for NODM after heart transplant are similar to those reported in other solid organ transplants. Some of these factors, such as BMI and immunosuppressive regimen, are potentially modifiable.
The objectives of this study are to examine the incidence of new-onset diabetes mellitus after transplant (NODAT) and to identify its risk factors in adult lung transplant recipients using the Organ Procurement and Transplant Network/United Network of Organ Sharing database. Between July 2004 and December 2007, a total of 3540 adults (≥18 yr old) received their first single- or double-lung transplant alone and had at least one follow-up report of post-transplant diabetic status. Among these, 2991 recipients were identified as not having diabetes mellitus (DM) pre-transplant. Risk factors for NODAT were examined. DM was newly reported in 33.4% of the 2991 recipients over the median follow-up time of 670 d. Significant independent risk factors for the development of NODAT included male gender (HR = 1.15), recipient age ≥50 (1.46), African American (1.39), higher body mass index (1.51 for ≥30 vs. 18-25), cystic fibrosis (3.30), and tacrolimus use at discharge (1.67). NODAT occurred in a third of adult lung transplant recipients during the median follow-up period. Some of the risk factors for NODAT after lung transplant are similar to those reported in other solid-organ transplants. Cystic fibrosis is a strong risk factor for development of NODAT after lung transplant.
COVID‐19 has been associated with acute kidney injury and published reports of native kidney biopsies have reported diverse pathologies. Case series directed specifically to kidney allograft biopsy findings in the setting of COVID‐19 are lacking. We evaluated 18 kidney transplant recipients who were infected with SARS‐CoV‐2 and underwent allograft biopsy. Patients had a median age of 55 years, six were female, and five were Black. Fifteen patients developed COVID‐19 pneumonia, of which five required mechanical ventilation. Notably, five of 11 (45%) biopsies obtained within 1 month of positive SARS‐CoV‐2 PCR showed acute rejection (four with arteritis, three of which were not associated with reduced immunosuppression). The remaining six biopsies revealed podocytopathy (
n
= 2, collapsing glomerulopathy and lupus podocytopathy), acute tubular injury (
n
= 2), infarction (
n
= 1), and transplant glomerulopathy (
n
= 1). Biopsies performed >1 month after positive SARS‐CoV‐2 PCR revealed collapsing glomerulopathy (
n
= 1), acute tubular injury (
n
= 1), and nonspecific histologic findings (
n
= 5). No direct viral infection of the kidney allograft was detected by immunohistochemistry,
in situ
hybridization, or electron microscopy. On follow‐up, two patients died and most patients showed persistent allograft dysfunction. In conclusion, we demonstrate diverse causes of kidney allograft dysfunction after COVID‐19, the most common being acute rejection with arteritis.
CMV mismatch (D+/R-) was no longer a risk factor for acute rejection in kidney recipients who received antiviral prophylaxis but was still an independent risk factor for death-censored graft failure, all-cause mortality, and viral infection-related mortality.
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