Background Transplantation of nonrenal organs is often complicated by chronic renal disease with multifactorial causes. We conducted a population-based cohort analysis to evaluate the incidence of chronic renal failure, risk factors for it, and the associated hazard of death in recipients of nonrenal transplants. Methods Pretransplantation and post-transplantation clinical variables and data from a registry of patients with end-stage renal disease (ESRD) were linked in order to estimate the cumulative incidence of chronic renal failure (defined as a glomerular filtration rate of 29 ml per minute per 1.73 m2 of body-surface area or less or the development of ESRD) and the associated risk of death among 69,321 persons who received nonrenal transplants in the United States between 1990 and 2000. Results During a median follow-up of 36 months, chronic renal failure developed in 11,426 patients (16.5 percent). Of these patients, 3297 (28.9 percent) required maintenance dialysis or renal transplantation. The five-year risk of chronic renal failure varied according to the type of organ transplanted - from 6.9 percent among recipients of heart-lung transplants to 21.3 percent among recipients of intestine transplants. Multivariate analysis indicated that an increased risk of chronic renal failure was associated with increasing age (relative risk per 10-year increment, 1.36; P Conclusions The five-year risk of chronic renal failure after transplantation of a nonrenal organ ranges from 7 to 21 percent, depending on the type of organ transplanted. The occurrence of chronic renal failure among patients with a nonrenal transplant is associated with an increase by a factor of more than four in the risk of death.

/pdf/chronic-renal-failure-after-transplantation-of-a-nonrenal-28y19xje8d.pdf

Chronic renal failure after transplantation of a nonrenal organ.

The complex nature of critical illness often necessitates the use of multiple therapeutic agents, many of which may individually or in combination have the potential to cause renal injury. The use of nephrotoxic drugs has been implicated as a causative factor in up to 25% of all cases of severe acute renal failure in critically ill patients. Acute tubular necrosis is the most common form of renal injury from nephrotoxin exposure, although other types of renal failure may be seen. Given that this is a preventable cause of a potentially devastating complication, a comprehensive strategy should be used to avoid nephrotoxicity in critically ill patients including: accurate estimation of pre-existing renal function using serum creatinine-based glomerular filtration rates, avoidance of nephrotoxins if possible, ongoing monitoring of renal function, and immediate discontinuation of suspected nephrotoxins in the event of renal dysfunction.

/pdf/an-overview-of-drug-induced-acute-kidney-injury-1xw8aiggeg.pdf

An overview of drug-induced acute kidney injury.

https://deepblue.lib.umich.edu/bitstream/handle/2027.42/72899/j.1600-6143.2006.01271.x.pdf;sequence=1

Pediatric transplantation in the United States, 1995-2004.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-6143.2006.01248.x

Kidney disease after heart and lung transplantation

Background Pediatric heart transplantation is entering its third decade, allowing for the first time an analysis of a large group of true long-term survivors, specifically children who have survived ≥10 years post-transplantation. Methods Fifty-two patients ≤18 years, who had undergone heart transplantation at Stanford between August 1974 and June 1993 and survived ≥10 years, were retrospectively reviewed. Results Forty (77%) patients are currently alive. Thirteen survived >15 years and 5 >20 years (the longest being 26 years). Actuarial survival was 79.4% at 14 years and 53.1% at 20 years. Cardiomyopathy was the reason for transplantation in 71% and congenital heart disease (CHD) in 29%. At last evaluation, 71% were on a cyclosporine-based regimen and 23% a tacrolimus-based regimen; 33% were steroid-free. Twenty-seven percent were totally free from treatable rejection, 44% developed serious infections, 69% were receiving anti-hypertensives, and 8% required renal transplantation. Neoplasms occurred in 23%, graft coronary artery disease (CAD) in 31%, and 15% required re-transplantation. Of the 12 deaths, CAD was the most common cause ( n = 4), followed by non-specific late graft failure ( n = 3), infection ( n = 2), rejection ( n = 1), non-lymphoid cancer ( n = 1) and lymphoid cancer ( n = 1). Physical rehabilitation and return to normal lifestyle has been nearly 100%. Conclusions Heart transplantation in pediatric patients is compatible with true long-term survival with a growing cohort of children approaching their second and third decades. The gradual constant-phase decrease in survival noted in earlier studies appears to be continuing. Rejection and infection are low but persistent risks after the first years. Graft CAD and non-specific late graft dysfunction are the leading causes of death after 10 years. Rehabilitation is excellent.

Ten- and 20-year Survivors of Pediatric Orthotopic Heart Transplantation

https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1600-6143.2002.20811.x

Long-term comparison of tacrolimus- and cyclosporine-induced nephrotoxicity in pediatric heart-transplant recipients.

Aims Atrial fibrillation (AF) ablation is associated with increased circulating markers of inflammation. Innate immune or inflammation pathways up-regulate mononuclear cell responses and may increase the risk for recurrent arrhythmia. Chemokines and serine protease coagulation pathways both activate innate immune responses. Here, we measured inflammatory markers in peripheral blood samples from patients after cryoballoon and/or radiofrequency pulmonary vein isolation and assessed the capacity for the inhibition of chemokine and serine protease pathways to block cell activation. Methods Markers of inflammation were measured in 55 patients immediately before and one day after AF ablation. Peripheral blood mononuclear cells (PBMCs) isolated from 19 patients were further tested for responsiveness to two anti-inflammatory proteins ex vivo using fluorescence assays and RT-qPCR analysis of gene expression. Results White blood cells (WBC), C-reactive protein, fibrinogen and troponin T levels were significantly elevated after ablation. PBMCs isolated from the circulating blood had increased activation with Phorbol 12-myristate 13-acetate. Cell activation, as measured by membrane fluidity, was blunted after treatment with a broad-spectrum chemokine modulating protein, M-T7, which interferes with chemokine/glycosaminoglycan (GAG) interactions, but not by Serp-1, a serine protease inhibitor (serpin) that targets both thrombotic and thrombolytic pathway proteases. Differential gene expression changes in the apoptotic pathway were identified with M-T7 and Serp-1. Conclusions Patients undergoing AF ablation have significantly increased inflammatory markers. Inhibition of chemokine signaling, but not serine proteases, reduced the activation of monocytes isolated from patients, in vitro. Targeting chemokines have the potential to reduce post-ablation activation of circulating leukocytes.

Atrial Fibrillation Ablation Increases Inflammation-Chemokine Modulation Suppresses Activation of Leukocytes Isolated after Ablation.

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Long-term comparison of tacrolimus- and cyclosporine-induced nephrotoxicity in pediatric heart-transplant recipients.

Atrial Fibrillation Ablation Increases Inflammation-Chemokine Modulation Suppresses Activation of Leukocytes Isolated after Ablation.