letter to the editor
Table 1 | Baseline data after coarsened exact matching
Age, years Male gender, % Current smoking, % Systolic BP, mmHg BMI, kg/m2
Kidney donors n ¼ 1901
Controls n ¼ 31,575
46.0±11.5 41.9 44.2 123.6±10.0 24.1±2.8
45.7±11.8 41.9 45.5 122.5±10.3 24.1±2.7
Abbreviations: BMI, body mass index; BP, blood pressure.
We appreciate Drs Moody and Townend3 for their interest in our article2 and for raising some insightful comments in their letter, ‘The importance of selecting controls in kidney donor outcome studies’. We are aware of the differences in mean age between kidney donors and controls. Accordingly, all Cox regression analyses were adjusted to account for this. Coarsened exact matching was performed to create adjusted survival curves that could be compared. However, we did not include baseline data after coarsened exact matching in our paper. Please find these data in Table 1. Mean age at death is susceptible to differences in baseline age and follow-up time, and has no relation to the actual number of deaths in each group. Survival curves are more informative. Any possible impact on our results from differences in estimated glomerular filtration rate owing to the differences in age at baseline would be handled by adjusting for age in the survival analyses. We have not considered the possibility of age-adjusting renal function in the control group, as donors underwent a thorough evaluation and creatinine values were not available for the control group. 1. 2. 3.
Clancy M, Geddes C. Acceptable mortality after living kidney donation. Kidney Int 2014; 85: 1240–1241. Mjen G, Hallan S, Hartman et al. Long-term risks for kidney donors. Kidney Int 2014; doi:10.1038/ki.2013.460. (e-pub ahead of print). Moody W, Townend J. The importance of selecting controls in kidney donor outcome studies. Kidney Int 2014; 85: 1240.
viruria compared with those without JC viruria. In a cohort of 282 renal transplant recipients (80% white, 239 JC negative and 43 JC positive), we found that isolated JC viruria, without JC or BK viremia, was associated with protection from acute renal allograft rejection (13.8% for JC vs. 2.3% for JC þ , P ¼ 0.04). Kaplan–Meier analysis for acute rejection–free survival was also favorable for JC þ compared with that for JC (log-rank P ¼ 0.05) recipients. There was no difference for death-censored graft survival (P ¼ 0.6) or patient survival (P ¼ 0.1). JC þ recipients tended to be less likely to be coinfected with BK virus (7% for JC þ vs. 14.2% for JC , P ¼ 0.2). Divers et al.,1 and an accompanying editorial by Kopp2 speculate that JC virus may protect against other polyomaviruses that are associated with kidney disease or it may alter cellular function rendering the kidney less susceptible to damage. Our findings support their speculations for the protective role of isolated JC viruria and expand the implications to the kidney transplant population in addition to the African-American population. 1.
Divers J, Nunez M, High K et al. JC polyoma virus interacts with APOL1 in African Americans with nondiabetic nephropathy. Kidney Int 2013; 84: 1207–1213. Kopp JB. JC viruria and kidney disease in APOL1 risk genotype individuals: is this a clue to a geneenvironment interaction? Kidney Int 2013; 84: 1069–1072.
Ana P. Rossi1, Kelsey L. Anderson1 and Daniel C. Brennan1 1 Section of Transplant Nephrology, Washington University School of Medicine in St Louis, Barnes-Jewish Hospital, St Louis, Missouri, USA Correspondence: Daniel C. Brennan, Washington University School of Medicine in St Louis, Transplant Nephrology, Barnes-Jewish Hospital, Campus Box 8126, 660 S. Euclid Avenue, St Louis, Missouri 63110, USA. E-mail: [email protected]
Kidney International (2014) 85, 1242; doi:10.1038/ki.2014.38
Geir Mjen1, Stein Hallan2 and Hallvard Holdaas3 1
Department of Medicine, Oslo University Hospital, Oslo, Norway; Department of Nephrology, St Olav University Hospital, Trondheim, Norway and 3Department of Transplant Medicine, Oslo University Hospital, Oslo, Norway Correspondence: Geir Mjen, Department of Medicine, Oslo University Hospital, Kirkeveien Oslo, Oslo 0027, Norway. E-mail: [email protected]
Kidney International (2014) 85, 1241–1242; doi:10.1038/ki.2014.37
JC polyoma virus and kidney disease To the Editor: In a recent article, Divers et al.1 describe the interaction between apolipoprotein L1 (APOL1) genotypes and JC viruria, and their relationship with nondiabetic nephropathy in African Americans. The authors found that in African Americans with two APOL1 risk alleles, the prevalence of kidney disease was lower for those with JC 1242
The Authors Reply: We appreciate the novel observation by Brennan and colleagues1 that shedding of urinary tract JC polyomavirus (JCV) associates with reduced rates of acute renal allograft rejection. Bacterial urinary tract infections trigger acute rejection and non-JC viral infections may do the same. This finding further supports the protective effects of urinary tract JCV on chronic kidney disease (CKD) and APOL1 gene–JCV interactions reducing risk of nondiabetic nephropathy.2,3 These diverse clinical scenarios suggest that JCV exhibits a commensal relationship with urothelial and kidney cells. JC viruria is not likely indicative of true infection, but colonization. This is akin to protective gastrointestinal (GI) tract bacteria that inhibit the growth of pathologic strains. As such, asymptomatic urinary tract JCV shedding could reflect health. In the absence of JCV, pathologic viruses may infect urothelial cells, ascend to and infect kidney cells, and cause chronic renal dysfunction or acute rejection. All studies support that a single urothelial viral strain inhibits the growth of others.1–3 Relative to the GI Kidney International (2014) 85, 1238–1244