Kidney is one of the tissues affected by age that involves cellular and structural changes inside the kidney and notably implicates with comorbidity, related to cardiovascular disease aging. Aging kidney causes the elderly susceptible to clinical deterioration from ordinary stimulation that younger individual can compensate, including acute renal injury, volume depletion or overload, sodium and potassium level disorders, and toxic reaction against kidney excreted drugs. As one of the organs with the fastest aging rate, kidney shows several age-related decline in both structural and functional with 30% of the glomerulus are damaged and represent diffuse glomerular sclerosis by age 75 and explain why the prevalence of chronic kidney disease (CKD) and end-stage renal disease are very common in the elderly. The cross-sectional population-based study by The National Health and Nutrition Examination Survey supports the theory of age-related decline in kidney function, although some other subjects did not have an absolute decline in kidney function. The underlying molecular mechanisms could be the target of future therapeutic strategies. Aging is a natural biological process characterized by a gradual decline in cellular function as well as progressive structural change of organ systems. In aging kidney, there are interactions of genetic factors, environmental changes, and cellular dysfunction that lead to the typical structural and functional changes. One of the most popular theory of aging is the theory of free radicals or oxidative stress based on the fact that cells are under chronic oxidative stress due to an imbalance between pro oxidants and antioxidants. Reactive oxygen species are oxygen-derived oxidizing compounds that are highly reactive, consisting of free radicals and non-radicals. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) refer to both reactive radicals and non-radical derivatives of oxygen and nitrogen. Reactive oxygen and nitrogen species (RONS) are produced by all aerobic cells and play an important role in aging as well as age-related diseases. Lipid peroxidation is a process of oxidative degradation of lipids that process by which free radicals bind to lipid electrons in the cell membrane resulting in direct cell damage. Lipid peroxidation can cause cellular damage in several ways such as impairing the integrity of the plasma membrane and subcellular organelles by peroxidation, “chain reaction” of ROS production, and activation of phospholipase A2 (PLA2) caused by lipid peroxidation. Fatty acids and other PLA2 metabolites (such as lysophospholipids) are known to damage cell membranes. In the development of kidney damage, the process of lipid peroxidation plays an important role. This is presumably due to the large number of long-chain polyunsaturated fatty acids (PUFAs) in the lipid composition of the kidneys and there are substantial evidence to suggest that ROS is involved in the ischemic, toxic, and immunologically mediated pathogenesis of renal injury, but the cellular mechanisms that result in cell injury and death are still being studied.
Part of the book: Accenting Lipid Peroxidation