The Role of Obesity and Its Bioclinical Correlates in the Progression of Chronic Kidney Disease

Laura Chalmers, Frederick J. Kaskel, Oluwatoyin Bamgbola

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.

Original languageEnglish (US)
Pages (from-to)352-364
Number of pages13
JournalAdvances in Chronic Kidney Disease
Volume13
Issue number4
DOIs
StatePublished - Oct 2006

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Chronic Renal Insufficiency
Obesity
Hypertension
Kidney
Adipocytes
Fibrosis
Maternal Deprivation
Fetal Proteins
Morbidity
Azotemia
Fatty Acid Synthases
Angiotensinogen
Hyperhomocysteinemia
Lipolysis
Plasminogen Activator Inhibitor 1
Sympathetic Nervous System
Incidence
Hyperinsulinism
Kidney Diseases
Leptin

Keywords

  • chronic kidney disease
  • insulin resistance
  • metabolic syndrome
  • Obesity

ASJC Scopus subject areas

  • Nephrology

Cite this

The Role of Obesity and Its Bioclinical Correlates in the Progression of Chronic Kidney Disease. / Chalmers, Laura; Kaskel, Frederick J.; Bamgbola, Oluwatoyin.

In: Advances in Chronic Kidney Disease, Vol. 13, No. 4, 10.2006, p. 352-364.

Research output: Contribution to journalArticle

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