Cytomegalovirus-Induced Tubulointerstitial Nephritis in a Renal Allograft Treated by Foscarnet Therapy

Wong, K.M.; Chan, Yiu Han; Chan, Siu Kwong; Mak, Chun; Chau, Kwong Wing; Li, Chun Sang

doi:10.1159/000013592

Cited by 10 publications

(2 citation statements)

References 12 publications

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“…Indicators of allograft dysfunction, such as coding for transplant failure or rejection, performance of percutaneous kidney biopsy and hemodialysis frequently co-occurred with CMV disease coding, possibly reflecting a bi-directional relationship between CMV and kidney failure (27). CMV can cause nephritis (3;28), trigger upregulation of alloantigens thereby promoting allograft rejection (27), or cause gastrointestinal tract disease resulting in emesis and/or diarrhea and subsequent dehydration and acute tubular necrosis (16;18;26). Conversely, kidney failure can cause decreased clearance of immunosuppressive medications, or prompt the administration of anti-lymphocyte antibodies or high-dose steroids if acute allograft rejection is proven or suspected, thereby increasing the net state of immunosuppression and promoting CMV disease (15;27;29;30).…”

Section: Discussionmentioning

confidence: 99%

Delayed-Onset Cytomegalovirus Disease Coded During Hospital Readmission After Kidney Transplantation

et al. 2014

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Background Use of prophylactic anti-CMV therapy for 3 to 6 months after kidney transplantation can result in delayed-onset CMV disease. We hypothesized that delayed-onset CMV disease (occurring ≥ 100 days post-transplant) occurs more commonly than early-onset CMV disease, and that it is associated with death. Methods We assembled a retrospective cohort of 15,848 adult kidney transplant recipients using 2004 to 2010 administrative data from the California and Florida Healthcare Cost and Utilization Project State Inpatient Databases. We identified demographic data, comorbidities, CMV disease coded during readmission and inpatient death. We used multivariate Cox proportional hazards modeling to determine risk factors for delayed-onset CMV disease and inpatient death. Results Delayed-onset CMV disease was identified in 4.0% and early-onset CMV disease was identified in 1.2% of the kidney transplant recipients. Risk factors for delayed-onset CMV disease included previous transplant failure or rejection (HR 1.4) and residence in the lowest-income ZIP codes (HR 1.2). Inpatient death was associated with CMV disease occurring 101–365 days post-transplant (HR 1.5), CMV disease occurring > 365 days post-transplant (HR 2.1), increasing age (by decade: HR 1.5), non-white race (HR 1.2), residence in the lowest-income ZIP codes (HR 1.2), transplant failure or rejection (HR 3.2), prior solid organ transplant (HR 1.7) and several comorbidities. Conclusions These data showed that delayed-onset CMV disease occurred more commonly than early-onset CMV disease, and that transplant failure or rejection is a risk factor for delayed-onset CMV disease. Further research should be done to determine if delayed-onset CMV disease is independently associated with death.

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Section: Discussionmentioning

confidence: 99%

Delayed-Onset Cytomegalovirus Disease Coded During Hospital Readmission After Kidney Transplantation

et al. 2014

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“…However, knowledge of the pathology of renal allograft loss, rejection and nephropathy in CMV continues to evolve. Descriptions of the renal allograft in CMV disease have usually highlighted a tubulointerstitial nephritis with the tubules containing nuclear and cytoplasmic inclusions (3–6). However, Richardson et al.…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus‐Induced Glomerular Vasculopathy in Renal Allografts: A Report of Two Cases

Onuigbo

Haririan

Ramos

et al. 2002

American Journal of Transplantation

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Cytomegalovirus (CMV) remains a major viral pathogen complicating renal transplantation. Tubulointerstitial nephritis is the commonly acknowledged and wellcharacterized pathologic feature of renal allograft CMV disease. There is controversy about whether there is a distinct entity as a CMV glomerulopathy in the absence of tubulointerstitial disease. We describe two patients with renal allograft dysfunction who displayed distinct features of CMV glomerular vasculopathy, in the absence of overt viral cytopathic changes involving the tubules.

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Cytomegalovirus Infection

2016

Diagnostic Pathology: Kidney Diseases

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Background. Cytomegalovirus (CMV) infection during fetal life causes severe symptoms and is associated with prolonged viral excretion. Previous studies reported low CD4 + T-cell responses to CMV infection in early life, contrasting with large responses of effector CD8 + T cells. The mechanisms underlying the defective CD4 + T-cell responses and the possible dissociation with CD8 + T-cell responses have not been clarified. Methods. The magnitude and the quality of the fetal CD8 + and CD4 + T-cell responses to CMV infection were compared to those of adults with primary or chronic infection. Results. In utero CMV infection induced oligoclonal expansions of fetal CD4 + and CD8 + T lymphocytes expressing a T-helper type 1 or Tc1 effector phenotype similar to that of adult CMV-specific cells. However, the effector cytokine responses and the polyfunctionality of newborn CD4 + and CD8 + T cells were markedly lower than those of adult cells. This reduced functionality was associated with a higher expression of the programmed death 1 inhibitory receptor, and blockade of this receptor increased newborn T-cell responses. Conclusions. Functional exhaustion limits effector CD4 + and CD8 + T-lymphocyte responses to CMV during fetal life.

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Cytomegalovirus-Induced Tubulointerstitial Nephritis in a Renal Allograft Treated by Foscarnet Therapy

Cited by 10 publications

References 12 publications

Delayed-Onset Cytomegalovirus Disease Coded During Hospital Readmission After Kidney Transplantation

Delayed-Onset Cytomegalovirus Disease Coded During Hospital Readmission After Kidney Transplantation

Cytomegalovirus‐Induced Glomerular Vasculopathy in Renal Allografts: A Report of Two Cases

Cytomegalovirus Infection

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