University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

393

Pages:

2
Author:

Mariam A. A.

Nephrotic and Nephritic Syndrome Notes The Nephrotic Syndrome • • • • • A clinical complex that includes: - Massive proteinuria, with daily protein loss in the urine of 3.5 g or more in adults - Hypoalbuminemia, with plasma albumin levels less than 3 g/dL - Generalized edema, the most obvious clinical manifestation. - Hyperlipidaemia and lipuria There is a derangement of capillary walls of the glomeruli that results in increase permeability to plasma proteins - This allows proteins to escape. The relative frequencies of the several causes of the nephrotic syndrome vary according to age - For example, in people ages from 1 to 7 years old the nephrotic syndrome is almost always caused by a lesion primary to the kidney - In adults it is often due to renal manifestations of a systemic disease - The most common systemic causes of the nephrotic syndrome in adults are diabetes, amyloidosis, and systemic lupus erythematosus. The most important primary glomerular lesions that characteristically lead to the nephrotic syndrome are focal and segmental glomerulosclerosis and minimal change disease - The latter is more important in children the former in adults. - Two other primary lesions membranous nephropathy and membranoproliferative glomerulonephritis, also commonly produce the nephrotic syndrome Minimal change disease - Relatively benign disorder and the most common causes of nephrotic syndrome in children - Characteristically, the glomeruli have a normal appearance by light microscopy but show diffuse effacement of podocyte foot processes when viewed with the electron microscope. - Although it can occur at any age, but the most common age is 1 to 7. - The pathogenesis of proteinuria in minimal-change disease remains to be elucidated. On the basis of some experimental studies, the proteinuria has been attributed to a circulating, possibly T cell–derived, factor that causes podocyte damage and effacement of foot processes. Neither the nature of such a putative factor nor a causal role of T cells, however, is established in the human disease.