Abstract
Kidney function declines with age in the majority of the population. Although very few older people progress to end stage, the consequences of doing so are burdensome for the patient and very expensive for the society. Although some of the observed decline is likely due to changes in the vasculature, much is associated with the development of age-associated glomerulosclerosis. This article will review the well-established structural and functional changes in the glomerulus with age. The role of calorie restriction in modifying age-related pathology will be discussed. The importance of the podocyte as a critical cell in the aging process is considered using animal models and human biopsy material. Newer data on changes in gene expression driven by nuclear factor kappa beta (NFkB) and possible changes in biology in the glomerulus are discussed. The relationship between pathways involved in aging and the decline in kidney function is reviewed. There is speculation on the significance of these changes in relation to normal and pathological aging.
Highlights
Kidney function declines with age in the majority of the population
The basement membrane is lined by epithelial cells, known as podocytes
The key cell involved in glomerulosclerosis is the podocyte, a highly differentiated neuron-like epithelial cell with limited capacity for cell division and replacement [13,14,15,16,17,18]
Summary
Kidney function declines with age in the majority of the population. very few older people progress to end stage, the consequences of doing so are burdensome for the patient and very expensive for the society. Using Fischer 344 rats that are fed different diets, it is possible to look at how high-calorie intake might interact with age-associated glomerulosclerosis (Figure 2). Work on Fischer 344 rats had shown that calorie restriction prevents the development of age-associated glomerulosclerosis [34].
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