Abstract
Chronic kidney disease is a global public health concern. Diabetes, hypertension, and obesity are major contributors to the global burden of the ease and are important traditional risk factors.
Common obesity is a typical civilization disease with chronic metabolic changes. The adipose tissue is the largest endocrine organ in the body, and in its overgrowth there is a gradual but extensive cardiometabolic change due to insulin resistance, proinflammatory status and endothelial dysfunction with irreversible central dysregulation of energetic homeostasis.
The cardiovascular and renal effects of common obesity may have their origins in childhood overweight. The early life nutrition has life-long effects on the susceptibility of an individual to develop obesity, diabetes, cardiovascular disease and chronic kidney disease.
Although the mechanisms of renals due to early life nutritional programming remain largely unknown, experimental and clinical studies suggest the burdening role of early life obesity in longstanding cardiovascular and renal diseases. The kidney can be programmed by a number of intrauterine and neonatal insults.
Low birth weight is one of the most identifiable markers of a suboptimal prenatal environment, and the important intrarenal factors sensitive to programming events include decreased nephron number and altered control of the renin-angiotensin-aldosteron system. High birth weight and exposure to maternal diabetes or obesity can enhance the risk for developing chronic kidney disease in later life.