First, it is uncertain whether the GD on a renal biopsy specimen represents the total nephron number of the whole kidney. Therefore, the finding of a low GD observed in the patients with GH may not necessarily reflect a low number of glomeruli. Accurately determining the origin of the low GD in the biopsy specimens of those with GH requires further
investigations. Second, there is a possibility that some of the 34 patients might have had FGS without nephrotic syndrome or benign nephrosclerosis, because these two LY2835219 mw diseases could not be completely excluded merely on the basis of the morphological findings. However, the possibility of the presence of FGS patients would be considerably Selleck GDC 0449 low, since only four patients (12 %) had segmentally sclerosed glomeruli in this study. Some patients with benign nephrosclerosis Selleckchem BMN 673 may also have been enrolled in this study, since most of the patients with GH had arteriolar hyalinosis. Nevertheless, it was meaningful that the subpopulation of patients with
benign nephrosclerosis could be identified by the characteristics of low GD with GH on the biopsy specimens, if such cases had been included in our study. In summary, among the 34 proteinuric CKD patients without known glomerular diseases, those with GH had significantly lower GD compared to those without GH. The BMI and GD values were identified as significant factors that correlated with the mean GV. The values for the mean GV were significantly higher in the overweight and obese groups than in the non-obese group, and the values for the GD were significantly lower in
the obese group than in the non-obese group. Thus, we could identify a subgroup of patients who were characterized as having a high Cediranib (AZD2171) BMI and GV and a low GD, among the proteinuric CKD patients without known glomerular diseases. Acknowledgments We are grateful to Ms. Tomoko Hayakawa for her valuable technical assistance. Conflict of interest The authors declare that no conflict of interest exists. Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. References 1. Coresh J, Astor B, Greene T, Eknoyan G, Levey A. Prevalence of chronic kidney disease and decreased kidney function in the adult US population: Third National Health and Nutrition Examination Survey. Am J Kidney Dis. 2003;41:1–12.PubMedCrossRef 2. Eknoyan G, Lameire N, Barsoum R. The burden of kidney disease: improving global outcome. Kidney Int. 2004;66:2681–3.CrossRef 3. Coresh J, Selvin E, Stevens LA, Manzi J, Kusek JW, Eggers P, et al. Prevalence of chronic kidney disease in the United States. JAMA. 2007;298:2038–47.PubMedCrossRef 4. de Jong PE, van der Velde M, Gansevoort RT, Zoccali C. Screening for chronic kidney disease: where does Europe go? Clin J Am Soc Nephrol.