Pathophysiology of acute kidney injury on a molecular level: A brief review

Abstract

Acute Kidney Injury (AKI) is a clinical condition with various etiologies. It is also known as acute renal failure, which is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days in patients. It causes an increase of waste products in blood and makes it hard for the patient kidneys to keep the right balance of fluid in the body. It can also affect other vital organs such as the brain, heart, and lungs. AKI is common in patients who are in the hospital, in intensive care units, and especially in older adults. It results in increased accumulation of a nitrogenous surplus in blood and a reduction in urine volume. The pathophysiology of various types of AKI is different. The earlier we can identify the causes the more effective treatment can be administered. This review attempts to identify changes on a molecular level during different stages of the disease and further discussed understanding the pathophysiology of AKI to find important molecules involved in various metabolic pathways, various phases and types of AKI, and the effect of drugs on kidneys and cellular level changes. This review article would help to design new drugs and the consequences of their metabolites to avoid Acute Kidney Injury.

Keywords

• acute kidney injury
• aki pathogenesis
• molecular entities