Predictors of Chronic Kidney Disease in Long-Term Survivors of Lung and Heart-Lung Transplantation

Canales, Mary K.; Youssef, Patrick; Spong, Richard; Ishani, Areef; Savik, Kay; Hertz, M.; Ibrahim, Hassan N.

doi:10.1111/j.1600-6143.2006.01458.x

Cited by 58 publications

(41 citation statements)

References 44 publications

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“…8,9,12 Recipients between 25 and 35 years old had a 1.6-fold increase in risk compared with recipients between 18 and 25 years old. In a previous study, increased risk with age was believed to be due to a greater burden of atherosclerotic vascular disease.…”

Section: Discussionmentioning

confidence: 99%

“…[6][7][8] In the overall lung transplant population, the cumulative incidence of posttransplant renal dysfunction has been reported to range between 4% and 35%, depending on how renal dysfunction is defi ned and the severity of renal dysfunction. 1,[9][10][11][12] Renal dysfunction complicates posttransplant management, as it usually prompts a reduction in the dosing of immunosuppressive medications or, if severe enough, necessitates a change in the immunosuppressive regimen. 7 It can also progress to require dialysis and/or kidney transplantation.…”

Section: Cohort Selectionmentioning

confidence: 99%

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Risk of Post-Lung Transplant Renal Dysfunction in Adults With Cystic Fibrosis

Quon

Mayer-Hamblett

Aitken

et al. 2012

Chest

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Cystic fi brosis (CF) is the third most common indication for lung transplantation worldwide and, alongside COPD, is the most common indication for bilateral lung transplantation. 1 Lung transplant survival has improved signifi cantly over the past 2 decades, and currently 50% of CF lung transplant recipients can expect to live . 7 years. 1 Improved post-lung transplant survival has been largely attributed to increased 1-year survival due to advances in surgical technique and postoperative care and improvements in immunosuppressive regimens leading to reduced rates of acute rejection. 1,2 As a result of improved post-lung transplant survival, CF lung transplant recipients can expect to experience multiple medical complications over time related to transplant. 3 Renal dysfunction is a wellrecognized complication of nonrenal organ transplantation. [4][5][6] Although its cause is often multifactorial,

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Section: Discussionmentioning

confidence: 99%

Section: Cohort Selectionmentioning

confidence: 99%

Risk of Post-Lung Transplant Renal Dysfunction in Adults With Cystic Fibrosis

Quon

Mayer-Hamblett

Aitken

et al. 2012

Chest

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“…In most LTx recipients renal function deteriorates progressively, often resulting in CKD (1). Progression from CKD to end-stage renal disease (ESRD) currently develops in between 3% and 10% of LTx recipients (2)(3)(4).…”

Section: Introductionmentioning

confidence: 99%

Former Smoking Is a Risk Factor for Chronic Kidney Disease After Lung Transplantation

Hellemons¹,

Agarwal²,

Bij³

et al. 2011

American Journal of Transplantation

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Chronic kidney disease (CKD) is a common complication after lung transplantation (LTx).Smoking is a risk factor for many diseases, including CKD. Smoking cessation for >6 months is required for LTx enlistment. However, the impact of smoking history on CKD development after LTx remains unclear. We investigated the effect of former smoking on CKD and mortality after LTx. CKD was based on glomerular filtration rate (GFR) ( 125 I-iothalamate measurements). GFR was measured before and repeatedly after LTx. One hundred thirty-four patients never smoked and 192 patients previously smoked for a median of 17.5 pack years. At 5 years after LTx, overall cumulative incidences of CKD-III, CKD-IV and death were 68.5%, 16.3% and 34.6%, respectively. Compared to never smokers, former smokers had a higher risk for CKD-III (hazard ratio [

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“…Moreover, the fibrogenic potential of tacrolimus also appears to be lower (210), although these results could not be confirmed in a more recent study (135). In nonrenal solid organ transplantation, there are singleand multicenter studies as well as registry analyses demonstrating the benefit of tacrolimus over cyclosporine with regard to renal function (24, [211][212][213][214], although other studies did not observe this benefit of tacrolimus over cyclosporine (215).…”

Section: Comparison Between Cyclosporine and Tacrolimusmentioning

confidence: 99%

Calcineurin Inhibitor Nephrotoxicity

Naesens

Kuypers²,

Sarwal³

2009

Clinical Journal of the American Society of Nephrology

1,266

1,000

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The use of the calcineurin inhibitors cyclosporine and tacrolimus led to major advances in the field of transplantation, with excellent short-term outcome. However, the chronic nephrotoxicity of these drugs is the Achilles' heel of current immunosuppressive regimens. In this review, the authors summarize the clinical features and histologic appearance of both acute and chronic calcineurin inhibitor nephrotoxicity in renal and nonrenal transplantation, together with the pitfalls in its diagnosis. The authors also review the available literature on the physiologic and molecular mechanisms underlying acute and chronic calcineurin inhibitor nephrotoxicity, and demonstrate that its development is related to both reversible alterations and irreversible damage to all compartments of the kidneys, including glomeruli, arterioles, and tubulo-interstitium. The main question-whether nephrotoxicity is secondary to the actions of cyclosporine and tacrolimus on the calcineurin-NFAT pathway-remains largely unanswered. The authors critically review the current evidence relating systemic blood levels of cyclosporine and tacrolimus to calcineurin inhibitor nephrotoxicity, and summarize the data suggesting that local exposure to cyclosporine or tacrolimus could be more important than systemic exposure. Finally, other local susceptibility factors for calcineurin inhibitor nephrotoxicity are reviewed, including variability in P-glycoprotein and CYP3A4/5 expression or activity, older kidney age, salt depletion, the use of nonsteroidal anti-inflammatory drugs, and genetic polymorphisms in genes like TGF-␤ and ACE. Better insight into the mechanisms underlying calcineurin inhibitor nephrotoxicity might pave the way toward more targeted therapy or prevention of calcineurin inhibitor nephrotoxicity.Clin J Am Soc Nephrol 4: 481-508, 2009. doi: 10.2215/CJN.04800908 T he introduction of the calcineurin inhibitor (CNI) cyclosporine in human kidney transplantation in the late 1970s revolutionized transplantation medicine, and made transplantation a preferable therapeutic intervention for end-stage renal diseases (1,2). In 1984, the potent immunosuppressive properties of another CNI, tacrolimus, were discovered, and tacrolimus was used successfully in human liver, kidney, and heart allograft recipients (3,4). Currently, 94% of kidney transplant recipients are discharged after transplantation with a CNI-based immunosuppressive regimen (5).The immunosuppressive properties of cyclosporine and tacrolimus result from inhibition of calcineurin, a calcium-and calmodulin-dependent phosphatase (protein phosphatase 3 [PPP3C], formerly PP2B). Intracellularly, these completely different molecules bind to cyclophylin and FKBP12 for cyclosporine and tacrolimus, respectively (6 -9). The competitive binding of cyclosporine-cyclophylin and tacrolimus-FKBP12 complexes to calcineurin inhibits phosphatase activity of calcineurin. This inhibition then suppresses the transcription of IL-2 via inhibition of the dephosphorylation and impaired translocation of the nucl...

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Predictors of Chronic Kidney Disease in Long-Term Survivors of Lung and Heart-Lung Transplantation

Cited by 58 publications

References 44 publications

Risk of Post-Lung Transplant Renal Dysfunction in Adults With Cystic Fibrosis

Risk of Post-Lung Transplant Renal Dysfunction in Adults With Cystic Fibrosis

Former Smoking Is a Risk Factor for Chronic Kidney Disease After Lung Transplantation

Calcineurin Inhibitor Nephrotoxicity

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