Nephrotic syndrome (NS) is characterized by hypoalbuminemia, severe proteinuria, and peripheral edema, frequently in conjunction with hyperlipidemia. Individuals usually show symptoms of weariness and swelling, but no signs of serious liver damage or cardiac failure. With characteristic medical symptoms and evidence of hypoalbuminemia and severe proteinuria, NS can be diagnosed. The majority of NS episodes are classified as unexplained or primary; the most prevalent histopathological subgroups of primary NS in people are focal segmental glomerulosclerosis and membraneous nephropathy. Thrombosis of the veins with high cholesterol levels is a significant NS risk. Acute renal damage and infection are further possible side effects. The pathobiochemistry of NS involves alterations in genes that affect the selectivity of the kidneys and abnormalities in proteins related to podocytes. Understanding the molecular mechanisms that influence these processes is crucial to developing specific and targeted therapeutic approaches. The need for invasive renal biopsies throughout the diagnosis process may be lessened by the development of non-invasive nephrotic syndrome biomarkers, such as microRNAs. Corticosteroids are frequently used as the initial line of defense in NS treatment. However, some individuals need other treatments since a resistant type of NS also exists. The use of calcineurin inhibitors, mycophenolate mofetil, and rituximab is mentioned in the text, along with current research to identify safer and more efficient therapeutic choices. The complicated kidney condition NS has several underlying causes and symptoms. For the diagnosis of this ailment as well as the creation of focused therapies, an understanding of the pathophysiology and the identification of possible biomarkers are essential.
Keywords: deficiency; kidney; nephrotic syndrome; proteinuria; steroid sensitive.
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