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• W2616623071 abstract "Individualizing predonation risks and inherent risks of donation redefine high- and low-risk living kidney donor candidates. See the article from Muzaale et al on page 1823. Individualizing predonation risks and inherent risks of donation redefine high- and low-risk living kidney donor candidates. See the article from Muzaale et al on page 1823. In the current issue of AJT, a study by Muzaale et al contributes to a new paradigm for selecting living kidney donors (1Muzaale A Althoff K Sperati CJ et al.Risk of end stage renal disease in HIV-positive potential live kidney donors.Am J Transplant. 2017; (doi: 10.1111/ajt.14235.)Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar). Even though human immunodeficiency virus (HIV) infection causes end-stage renal disease (ESRD), selected HIV-positive individuals are shown to have 9-year ESRD risks comparable to those who smoke cigarettes, which is not a contraindication to donation (2Grams ME Sang Y Levey AS et al.Kidney-failure risk projection for the living kidney-donor candidate.N Engl J Med. 2016; 374: 411-421Crossref PubMed Scopus (256) Google Scholar). The authors argue, plausibly, that these individuals should be allowed to donate to HIV-positive recipients; however, certain other ESRD risk factors such as hypertension and nephrolithiasis are contraindications to donation. Although its exclusion criteria may be somewhat arbitrary, many have believed that this “old” paradigm resulted in no increase in ESRD risk after living kidney donation (3Reese PP Caplan AL Kesselheim AS et al.Creating a medical, ethical, and legal framework for complex living kidney donors.Clin J Am Soc Nephrol. 2006; 1: 628-633Crossref Scopus (56) Google Scholar,4Cozzi E Biancone L López-Fraga M et al.Long-term outcome of living kidney donation: Position paper of the European committee on organ transplantation council of Europe.Transplantation. 2016; 100: 270-271Crossref PubMed Scopus (10) Google Scholar). Two recent studies have promulgated a very different paradigm. Muzaale et al, in an 8-year study in JAMA, found postdonation rates of ESRD that were eight times those of well-matched nondonor controls (5Muzaale AD Massie AB Wang MC et al.Risk of end-stage renal disease following live kidney donation.JAMA. 2014; 311: 579-586Crossref PubMed Scopus (668) Google Scholar). This surprising eightfold risk of donation was attributed to lower postnephrectomy GFRs, which caused new postdonation kidney diseases to reach ESRD more quickly in donors (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar). Grams et al found a wide spectrum of predonation risks in potentially acceptable donor candidates (2Grams ME Sang Y Levey AS et al.Kidney-failure risk projection for the living kidney-donor candidate.N Engl J Med. 2016; 374: 411-421Crossref PubMed Scopus (256) Google Scholar). Over a 6.4-year interval, risk was increased by hypertension and low-grade proteinuria, with lesser effects of obesity and smoking. Both studies found that “normal” demographic factors of black race, young age, and low-normal GFRs increased ESRD risk several fold, often more than medical abnormalities. The latter two factors could markedly increase the race-related risks of HIV candidates, which would then be increased eightfold more by donation. Muzaale et al, however, said that current selection practices produced lifetime postdonation ESRD risks of <1%. For young well-selected donors, Grams et al predicted predonation lifetime risks that were ≈25% of those in unselected individuals. These familiar low risk estimates raised little alarm and promoted acceptance of the new paradigm (4Cozzi E Biancone L López-Fraga M et al.Long-term outcome of living kidney donation: Position paper of the European committee on organ transplantation council of Europe.Transplantation. 2016; 100: 270-271Crossref PubMed Scopus (10) Google Scholar) but must be respectfully challenged. In the United States, unselected young adults have a 3.5% lifetime ESRD risk but low initial rates that approximate those of Muzaale and colleagues’ medically normal controls. With age, more and more kidney diseases begin, usually taking decades to reach ESRD. GFR also decreases normally with age, causing late-onset kidney diseases to reach ESRD sooner. Type 2 diabetes increases by age 30 years and takes 20–30 years to reach ESRD, accounting for half of the yearly US total (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar,7Steiner R Ix JH Rifkin DE et al.Estimating risks of de novo kidney diseases after living kidney donation.Am J Transplant. 2014; 14: 538-544Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). These factors make lifetime ESRD accrue exponentially (Figure 1) but unpredictably for a given medically normal young individual. Yet Muzaale and colleagues’ eightfold relative risk and 1% absolute postdonation lifetime risk require the impossible exclusion of 96% of 25-year-old candidates who will develop ESRD (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar), but only 10% of their lifetime ESRD will occur in the next 20 years (7Steiner R Ix JH Rifkin DE et al.Estimating risks of de novo kidney diseases after living kidney donation.Am J Transplant. 2014; 14: 538-544Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). As in past studies by others, the low ESRD rates of Muzaale et al came from the early postdonation “honeymoon period,” before they increased exponentially (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar). The study design of Grams et al required large losses of GFR over short intervals, favoring diseases that were already under way at entry. These diseases caused proteinuria and hypertension that “predicted” ESRD, but over longer intervals, the converse is not true. Normal blood pressures and urinalyses at age 25 years do not predict the absence diabetes or bladder outlet obstruction in later life. Moreover, the studies of Grams et al and Muzaale et al were too short to allow classic development of diabetic ESRD, which represents fully half of lifetime donor risk (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar,7Steiner R Ix JH Rifkin DE et al.Estimating risks of de novo kidney diseases after living kidney donation.Am J Transplant. 2014; 14: 538-544Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). This is similar to excluding cancer from a study that attempts to predict mortality. Importantly, not until 25 years after donation does post donation diabetes cause an eightfold increase in ESRD (8Anjum S Muzaale AD Massie AB et al.Patterns of end-stage renal disease caused by diabetes, hypertension, and glomerulonephritis in live kidney donors.Am J Transplant. 2016; 16: 3540-3547Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar), mirroring the early exponential increase shown in Figure 1. The current study does not rule out similar late exponential increases in ESRD rates from HIV infection. Ethical donor selection nevertheless requires long term risk estimates, and new paradigm “demographic” concepts can structure a different approach. For example, if medical selection (improbably) halved the 7.5% lifetime ESRD risk of unselected young blacks, and donation increased it only fourfold, their risk would be 15%. For non-blacks, it would be 5%. However, GFR-related risk is also GFR-related safety. Young candidates with the lowest GFRs will have ESRD risks that are well above these group averages, but long term risk will reciprocally diminish to well below the group average as predonation GFR increases. In middle age, the standard requirement for a minimum GFR of 80 ml/min already deselects the highest risk, lowest third of the normal range. Furthermore, middle-aged candidates who will develop lifetime ESRD will often have slowly progressive kidney diseases and be identifiable. These factors make medically normal older candidates very low risk (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar,7Steiner R Ix JH Rifkin DE et al.Estimating risks of de novo kidney diseases after living kidney donation.Am J Transplant. 2014; 14: 538-544Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). Such considerations can contribute to a uniform risk standard that better excludes certain candidates who are young or black or who have low-normal GFRs and allows others with medical abnormalities that the old paradigm forbids (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar,7Steiner R Ix JH Rifkin DE et al.Estimating risks of de novo kidney diseases after living kidney donation.Am J Transplant. 2014; 14: 538-544Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). Thresholds may be somewhat arbitrary, but so are those in the old paradigm. Although some clarification is needed (6Steiner R Moving closer to understanding the risks of living kidney donation.Clin Transplant. 2016; 30: 10-16Crossref PubMed Scopus (19) Google Scholar), we must incorporate this very different paradigm into the selection of living kidney donors. The author of this manuscript has no conflicts of interest to disclose as described by the American Journal of Transplantation." @default.
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• W2616623071 title "A Very Different Paradigm for Living Kidney Donor Risk" @default.
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