10. Ma LJ, Fogo AB: Model of robust induction of glomerulosclerosis in mice: Importance of genetic background. Kidney Int 64: 350 –355, 2003 11. Brosius FC 3rd, Alpers CE, Bottinger EP, Breyer MD, Coffman TM, Gurley SB, Harris RC, Kakoki M, Kretzler M, Leiter EH, Levi M, McIndoe RA, Sharma K, Smithies O, Susztak K, Takahashi N, Takahashi T: Mouse models of diabetic nephropathy. J Am Soc Nephrol 20: 2503– 2512, 2009 12. Laouari D, Burtin M, Phelep A, Martino C, Pillebout E, Montagutelli X, Friedlander G, Terzi F: TGF- mediates genetic susceptibility to chronic kidney disease. J Am Soc Nephrol 22: 333–341, 2011 13. Terzi F, Burtin M, Hekmati M, Federici P, Grimber G, Briand P, Fried- lander G: Targeted expression of a dominant-negative EGF-R in the kidney reduces tubulo-interstitial lesions after renal injury. J Clin Invest 106: 225–234, 2000 14. Lautrette A, Li S, Alili R, Sunnarborg SW, Burtin M, Lee DC, Friedlander G, Terzi F: Angiotensin II and EGF receptor cross-talk in chronic kidney diseases: A new therapeutic approach. Nat Med 11: 867– 874, 2005 15. Osterholm AM, He B, Pitkaniemi J, Albinsson L, Berg T, Sarti C, Tuomilehto J, Tryggvason K: Genome-wide scan for type 1 diabetic nephropathy in the Finnish population reveals suggestive linkage to a single locus on chromosome 3q. Kidney Int 71: 140 –145, 2007 16. Rogus JJ, Poznik GD, Pezzolesi MG, Smiles AM, Dunn J, Walker W, Wanic K, Moczulski D, Canani L, Araki S, Makita Y, Warram JH, Krolewski AS: High-density single nucleotide polymorphism genome- wide linkage scan for susceptibility genes for diabetic nephropathy in type 1 diabetes: discordant sibpair approach. Diabetes 57: 2519 – 2526, 2008 17. Pillebout E, Weitzman JB, Burtin M, Martino C, Federici P, Yaniv M, Friedlander G, Terzi F: JunD protects against chronic kidney disease by regulating paracrine mitogens. J Clin Invest 112: 843– 852, 2003 18. Harris RC, Chung E, Coffey RJ: EGF receptor ligands. Exp Cell Res 284: 2–13, 2003 See related article, “TGF- Mediates Genetic Susceptibility to Chronic Kidney Disease,” on pages 327–335. Atrial Fibrillation in Dialysis Patients: A Neglected Comorbidity Mohamed G. Atta Johns Hopkins School of Medicine, Baltimore, Maryland J Am Soc Nephrol 22: 203–205, 2011. doi: 10.1681/ASN.2010121250 Atrial fibrillation is the most common and potentially dif- ficult to treat cardiac arrhythmia encountered in clinical practice. It is classified according to its temporal pattern as paroxysmal (self-limiting), persistent (amenable to cardio- version), or permanent. 1 Although the frequency of each type depends on the population studied, it is estimated that paroxysmal fibrillation accounts for 35% to 66% of all cases of atrial fibrillation. 2–4 The prevalence of this disorder in- creases with age, rising above 5% in people older than 65 years of age. 5 Independent risk factors for fibrillation, from long-term fol- low-up data of the Framingham study, include male sex, hyper- tension, diabetes, heart failure, and valvular heart disease. 6 Be- cause of its high prevalence, hypertension accounts for most cases of fibrillation in the population compared with all other risk fac- tors. Among chronic kidney disease patients starting dialysis, 36% have heart failure, and an additional 7% develop heart failure while receiving dialysis. 7 Consequently, it is not unexpected that those patients on renal replacement therapy are at a particularly increased risk for the development of atrial fibrillation compared with the general population. The prevalence of atrial fibrillation in dialysis patients is also driven by the changing age distribution of this population. Thirty years ago, approximately 27% of new end-stage kidney disease patients in the United States who began chronic renal replacement therapy were 65 years of age. In 2005, the total number of patients who started renal replacement therapy in the United States was 106,912, of which 52,434 (49%) were 65 years of age. 8 Although the incidence rates between 2000 and 2005 have been relatively stable for most age groups (changing 3.0%), the incidence rate has grown 10% from 1570 to 1725 per million for patients 75 years of age. In the general population, atrial fibrillation may affect lon- gevity because it is associated with approximately doubling all-cause and cardiovascular mortality rates. 9,10 Mortality, as expected in this setting, is driven by cerebrovascular events, progressive ventricular dysfunction, and increased coronary mortality. In addition, age-adjusted incidence of stroke in the Framingham study after 34 years of follow-up was nearly five- fold higher when nonrheumatic atrial fibrillation was present compared with those without atrial fibrillation. 11 The mechanism that triggers most atrial premature beats that initiate frequent paroxysms of fibrillation originates in the pulmonary veins, which has generated interest in ablative ther- apy of this region in selected patients. 12 Despite its important clinical relevance and potential effect on morbidity and mor- tality, there have been very limited data studying this comor- bidity in dialysis patients in the United States and only a few worldwide published reports in this population. 13–16 In this issue, Winkelmayer et al. examine the epidemiology (including prevalence, risk factors, and mortality) of atrial fi- brillation in patients on maintenance dialysis in the United States over a period of 15 years (1992 to 2006) using the U.S. Renal Data System annual cohorts. The overall prevalence of atrial fibrillation in this patient population exceeded 10% in 2006. In older patients, the prevalence was 13.2% in patients aged 65 to 75 years, 19.2% in those aged 75 to 85 years, and 22.5% in those 85 years of age. More importantly, atrial fi- brillation was associated with considerable excess mortality in Published online ahead of print. Publication date available at www.jasn.org. Correspondence: Dr. Mohamed G Atta, Johns Hopkins School of Medicine, 1830 East Monument Street, Suite 416, Baltimore, Maryland 21205. Phone: 410-955-5268; Fax: 410-955-0485; E-mail: matta1@jhmi.edu Copyright © 2011 by the American Society of Nephrology EDITORIALS www.jasn.org J Am Soc Nephrol 22: 197–206, 2011 Editorials 203