Pathological influence of obesity on renal structural changes in chronic kidney disease

Access this Article

Search this Article

Author(s)

    • KATO Shigeko
    • Department of Pathology, Nagasaki University Graduate School of Biomedical Sciences
    • NAZNEEN Arifa
    • Department of Pathology, Nagasaki University Graduate School of Biomedical Sciences
    • NAKASHIMA Yumiko
    • Department of Pathology, Nagasaki University Graduate School of Biomedical Sciences
    • NISHINO Tomoya
    • Second Department of Internal Medicine, Nagasaki University School of Medicine and Dentistry
    • FURUSU Akira
    • Second Department of Internal Medicine, Nagasaki University School of Medicine and Dentistry
    • YORIOKA Noriaki
    • Department of Advanced Nephrology, Graduate School of Biomedical Sciences, Hiroshima University
    • TAGUCHI Takashi
    • Department of Pathology, Nagasaki University Graduate School of Biomedical Sciences

Abstract

BACKGROUND: Role of obesity in renal pathological and structural changes remains poorly investigated, and this study was designed to examine the pathological effects of obesity on renal structural components in patients with chronic kidney diseases (CKD). METHODS: The study subjects were obese (body mass index, BMI > or = 25 kg/m2) patients with nonglomerulonephritis (non-GN, n = 26), IgA nephropathy (IgAN, n = 19), benign nephrosclerosis (BNS, n = 15), and thin basement membrane disease (TMD, n = 6), and 65 nonobese controls (n = 20, 20, 10, and 15, respectively). Patients were evaluated for glomerular lesions (mesangial proliferation and focal segmental/global glomerulosclerosis), glomerular size, and thickness of glomerular basement membrane (GBM). RESULTS: Urinary protein was higher in obese non-GN, IgAN, and BNS groups than in the respective controls. Focal segmental glomerulosclerosis (FSGS) lesions were noted in all obesity groups. The glomeruli were larger in size in obese than in nonobese patients of the non-GN and IgAN groups. The glomeruli of nonobese TMD and BNS patients were significantly larger in size than those of nonobese non-GN patients. GBM were thicker in obese than in nonobese patients irrespective of types of glomerular diseases, but only significantly so in non-GN and BNS groups. CONCLUSION: In non-GN, IgAN, and BNS, obesity worsens proteinuria and is associated with structural changes such as glomerulomegaly and GBM thickening, similar to changes observed in obesity-related nephropathy. Obesity seems to worsen the renopathological state in CKD.

Journal

  • Clinical and experimental nephrology

    Clinical and experimental nephrology 13(4), 332-340, 2009-08-01

    Springer Japan

References:  24

Cited by:  1

Codes

  • NII Article ID (NAID)
    10025586697
  • NII NACSIS-CAT ID (NCID)
    AA11126935
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    13421751
  • Data Source
    CJP  CJPref  IR 
Page Top