Adipose tissue as risk factor for kidney disease

Abstract

Obesity remains the leading risk factor for increased risk of acute kidney diseases and increased risk for progression to chronic kidney disease. Accumulation of excess adipose tissue in various body compartments is an underpinning characteristic of obesity. In the human body, adipose tissue in the body is mainly stored as subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). Adipose tissue is biologically active and may interact with metabolic processes. Excess adipose tissue accumulation may be pathogenic through adverse endocrinologic or immunologic activity, and metabolic changes affect kidney function by decreasing the glomerular filtration rate (eGFR). Estimation of GFR is mainly based on serum biomarkers such as serum creatinine and or cystatin C. Adipocytes release cystatin C in a time-dependent manner and are not associated with serum creatinine. Pathophysiological mechanisms linking adipose tissue and cystatin C in humans remain unknown, and potential crosstalk mechanisms related to adipose tissue and kidney diseases remain scarce. In the clinical context, assessment of kidney function is based on the eGFR calculation based on serum biomarkers measurement, and whether other inflammatory parameters may help to explore the pathophysiological link or mechanism between adipose tissue and kidney function through biomarkers exploration remains unknown. This chapter aims to provide further insights into the mechanisms that link adipose tissue and kidney crosstalk by exploring kidney function biomarkers.