https://www.kidney-international.org/article/S0085-2538(15)58302-6/pdf

The impact of hepatitis C virus infection on renal allograft recipients

Urinary tract infection (UTI) is common in renal transplant recipients. Frequency of UTIs depend on many factors such as age, female gender, kidney function, co-morbidity, type and amount of immunosuppression, urological instrumentation and/or the follow-up period (short term or long term) after kidney transplantation. UTI may worsen graft and patient survival. A significant proportion of renal transplant recipients with UTIs may develop acute pyelonephritis (APN), which is an independent risk factor for deterioration of graft function. Renal transplant recipients with UTIs are often clinically asymptomatic as a consequence of immunosuppression. UTI, however, may progress to APN (particularly in the early post-transplant period), bacteraemia and the full blown picture of urosepsis. Strategies for long term prophylaxis and antimicrobial treatment of UTI in renal transplant recipients are discussed.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2362.2008.02014.x

Urinary tract infection in renal transplant recipients

https://www.ajkd.org/article/0272-6386(95)90617-7/pdf

Hepatitis C virus : the nephrologist's view

https://www.ajkd.org/article/S0272-6386(01)02061-3/pdf

Hepatitis C virus infection and renal transplantation

Hepatitis C virus (HCV) is the predominant cause of posttransplant non-A, non-B hepatitis among renal allograft recipients. Prior studies evaluating the impact of HCV in kidney transplantation have been retrospective in design and based largely on changes in serum transaminases. We studied a group of HCV-infected end-stage renal disease patients prospectively with pretransplant liver biopsies and close virologic and biochemical follow-up posttransplant. Fourteen patients have been followed a mean of 11.6 +/- 5.6 months posttransplant (range, 5-21 months). Six had changes of chronic hepatitis on pretransplant liver biopsy while 8 showed only mild histologic abnormalities. Circulating viral titers increased several-fold over baseline levels during posttransplant follow-up. Viral replication was particularly enhanced immediately following a course of antilymphocyte therapy. Although all patients showed a 2-3 fold increase in alanine aminotransferase (ALT) following transplantation, there were no association noted between pretransplant liver histology, the use of FK506 and/or cyclosporine-based immunosuppression, and the magnitude of ALT change posttransplant. The only clinical outcome found to differ significantly was a higher incidence of cytomegalovirus infection among patients with chronic hepatitis. All patients are alive with functioning grafts. There have been no episodes of fulmiinant or subfulminant liver failure. We conclude that HCV-infected patients can be safely transplanted with excellent short-term follow-up. Continued monitoring with sequential liver biopsies will be needed to define the long-term course of HCV infection in an immuno-suppressed population.

A prospective study of hepatitis C virus infection in renal allograft recipients.

Hepatitis C antibody in renal transplant patients.

Incidence of urinary tract infections and vesicorenal reflux: a comparison between conventional and antirefluxive technique of ureter implantation.

High incidence of significant bacteriuria in kidney graft recipients with triple therapy.

Is determination of PP 65 useful for early diagnosis of cytomegalovirus infection in renal transplantation

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Hepatitis C antibody in renal transplant patients.

Incidence of urinary tract infections and vesicorenal reflux: a comparison between conventional and antirefluxive technique of ureter implantation.

High incidence of significant bacteriuria in kidney graft recipients with triple therapy.

Is determination of PP 65 useful for early diagnosis of cytomegalovirus infection in renal transplantation