Abstract

Renal Pathophysiology and Nephrotoxicity: Renal biomarkers' importance and function in the early diagnosis of acute renal damage

Author(s): Sanem Yaman

Nephrotoxicity is defined as a fast decline in kidney function brought on by the toxic effects of drugs and substances. There are several types, and some medications may have multiple negative effects on renal function. Nephrotoxic compounds are known as nephrotoxins. Nephrotoxicity is caused by a number of different factors, such as renal tubular toxicity, inflammation, glomerular injury, crystal nephropathy, and thrombotic microangiopathy. Blood urea and serum creatinine, the conventional indicators of nephrotoxicity and renal dysfunction, are viewed as being insufficiently sensitive indicators of early renal injury. Therefore, novel biomarkers that are more sensitive and highly specific and that provide information on the location of underlying renal injury were needed for the diagnosis of the early renal injuries. Blood urea and serum creatinine are less sensitive than Kidney Injury Molecule-1, Cystatin C, and neutrophil gelatinase-associated lipocalin serum levels in the diagnosis of acute kidney injury during nephrotoxicity [1].

The nephron, the kidney’s fundamental functional unit, is made up of many cell types that are arranged into the kidney. Any stimulus that causes the death of these cells has the potential to harm or even kill off the kidneys. Renal failure may have inherent or extrinsic causes. Heart disease, obesity, diabetes, sepsis, and liver and lung failure are examples of extrinsic causes. Glomerular nephritis, polycystic kidney disease, renal fibrosis, tubular cell death, and stones are a few examples of intrinsic causes. The kidney is important in regulating the toxicity of many medications, contaminants from the environment, and natural chemicals. There are a number of cancer therapies, illicit substances, antibiotics, and radiocontrast agents that are known to be nephrotoxic. Cadmium, mercury, arsenic, lead, trichloroethylene, bromate, brominated-flame retardants, diglycolic acid, and ethylene glycol are environmental contaminants that have been linked to kidney damage. Aristolochic acids and mycotoxins like ochratoxin, fumonisin B1, and citrinin are examples of naturally occurring nephrotoxicants. Mechanisms of renal failure brought on by nephrotoxicants and extrinsic factors have a number of traits. The molecular pathways regulating renal cell death share many commonalities, which is the main reason for this shared ground. The present state of the study of nephrotoxicity is outlined in this review. The emphasis is on fusing pathologically caused renal failure with our understanding of nephrotoxicity. Such methods are required to address important issues in the area, such as the development from acute kidney damage to chronic kidney disease and the diagnosis, prognosis, and treatment of both acute and chronic renal failure [2].