Background End-stage renal disease disproportionately affects black persons, but it is unknown when in the course of chronic kidney disease racial differences arise. Understanding the natural history of racial differences in kidney disease may help guide efforts to reduce disparities. Methods We compared white/black differences in the risk of end-stage renal disease and death by level of estimated glomerular filtration rate (eGFR) at baseline in a national sample of 2,015,891 veterans between 2001 to 2005. Results Rates of end-stage renal disease among black patients exceeded those among white patients at all levels of baseline eGFR. The adjusted hazard ratios (HR) for end-stage renal disease associated with black versus white race for patients with an eGFR ≥90, 60-89, 45-59, 30-44, 15-29, and <15 mL/min/1.73m2, respectively were 2.14 (95% confidence interval [CI], 1.72-2.65), 2.30 (95% CI, 2.02-2.61), 3.08 (95% CI, 2.74-3.46), 2.47 (95% CI, 2.26-2.70), 1.86 (95% CI, 1.75-1.98), and 1.23 (95% CI, 1.12- 1.34). We observed a similar pattern for mortality, with equal or higher rates of death among black persons at all levels of eGFR. The highest risk of mortality associated with black race was also observed among those with an eGFR 45-59 mL/min/1.73m2 (HR 1.32, 95% CI, 1.27-1.36). Conclusion Racial differences in the risk of end-stage renal disease appear early in the course of kidney disease and are not explained by a survival advantage among blacks. Efforts to identify and slow progression of chronic kidney disease at earlier stages may be needed to reduce racial disparities.

BackgroundHealthy People 2020 aim to reduce fatal atherosclerotic cardiovascular disease (ASCVD) by 20%, which translates into 310 000 fewer events annually assuming proportional reduction in fatal and nonfatal ASCVD. We estimated preventable ASCVD events by implementing the American College of Cardiology/American Heart Association (ACC/AHA) 2013 Cholesterol Guideline in all statin‐eligible adults. Absolute risk reduction (ARR) and number needed‐to‐treat (NNT) were calculated.Methods and ResultsNational Health and Nutrition Examination Survey data for 2007–2012 were analyzed for adults aged 21 to 79 years and extrapolated to the US population. Literature‐guided assumptions were used including (1) low‐density lipoprotein cholesterol falls 33% with moderate‐intensity statins and 51% with high‐intensity statins; (2) for each 39 mg/dL decline in low‐density lipoprotein cholesterol, 10‐year ASCVD 10 risk would fall 21% when ASCVD 10 risk was ≥20% and 33% when ASCVD 10 risk was <20%; and (3) either all statin‐eligible untreated adults or all with ASCVD 10 risk ≥7.5% would receive statins. Of 175.9 million adults aged 21 to 79 years not taking statins, 44.8 million (25.5%) were statin eligible. Treating all statin‐eligible adults would prevent an estimated 243 589 ASCVD events annually (ARR 5.4%, 10‐year NNT 18). Treating all statin‐eligible adults with ASCVD 10 risk ≥7.5% reduces the number treated to 32.2 million (28.2% fewer), whereas ASCVD events prevented annually fall only 10.5% to 217 974 (6.8% ARR, NNT 15).ConclusionsImplementing the ACC/AHA 2013 Cholesterol Guideline in all untreated, statin‐eligible adults could achieve ≈78% of the Healthy People 2020 ASCVD prevention goal. Most of the benefit is attained by individuals with 10‐year ASCVD risk ≥7.5%.

Herlitz junctional epidermolysis bullosa is an autosomal recessive disorder characterized by generalized blistering at the lamina lucida of the cutaneous basement membrane. The monoclonal antibody GB3 has been used as a diagnostic probe because of its lack of reactivity in patient skin. The antigen recognized by GB3 has been identified as laminin-5, a glycoprotein consisting of three subunits (alpha 3, beta 3 and gamma 2). To identify the laminin-5 protein chain that contains the epitope recognized by GB3 and to determine if chain assembly is required for antibody recognition, we expressed a gamma 2 protein constructed from a full-length gamma 2 cDNA. Radioimmunoprecipitation of the culture medium from 293 cells revealed that both GB3 and anti-gamma 2 polyclonal antibodies were capable of directly precipitating recombinant gamma 2 without coprecipitation of other proteins. In immunodepletion experiments, each antibody removed most of the protein that was reactive with the other antibody. The epitope recognized by GB3 is present only when the complex is in the native conformation because GB3 reacted only with the non-reduced laminin-5, but not the reduced laminin-5 in immunoblots. Moreover, because GB3 reacted with laminin-5 of SCC25 cells (gamma 2 in the heterotrimer) but not recombinant gamma 2 in 293 cells (gamma 2 alone) during indirect immunofluorescence staining, this epitope may be dependent upon a less stable conformation of gamma 2. We conclude that GB3 recognizes the gamma 2 chain of laminin-5 and that the epitope is entirely contained in the native form of the gamma 2 chain.

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