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Narrative Pathophysiology of Nephrotic Syndrome

Nephrotic syndrome is caused by increased permeability of the glomerular capillary wall, leading to massive protein loss in the urine and low albumin levels in the blood. In minimal change disease, T-cell dysfunction may alter cytokines and cause loss of glycoproteins in the capillary wall. In focal segmental glomerulosclerosis, mutations in podocyte proteins or plasma factors from lymphocytes may increase permeability. Edema forms from low oncotic pressure due to low albumin, activating systems like renin-angiotensin-aldosterone that retain sodium and water. Lipid levels rise due to increased hepatic protein synthesis and reduced lipid breakdown related to low lipoprotein lipase.

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35 views1 page

Narrative Pathophysiology of Nephrotic Syndrome

Nephrotic syndrome is caused by increased permeability of the glomerular capillary wall, leading to massive protein loss in the urine and low albumin levels in the blood. In minimal change disease, T-cell dysfunction may alter cytokines and cause loss of glycoproteins in the capillary wall. In focal segmental glomerulosclerosis, mutations in podocyte proteins or plasma factors from lymphocytes may increase permeability. Edema forms from low oncotic pressure due to low albumin, activating systems like renin-angiotensin-aldosterone that retain sodium and water. Lipid levels rise due to increased hepatic protein synthesis and reduced lipid breakdown related to low lipoprotein lipase.

Uploaded by

NicaMariannePaña
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as EHTML, PDF, TXT or read online on Scribd
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Narrative Pathophysiology of Nephrotic Syndrome The underlying abnormality in nephrotic syndrome is an increase in permeability of the glomerular capillary wall,

which leads to massive proteinuria and hypoalbuminemia. The cause of the increased permeability is not well understood. In minimal change disease it is possible that T-cell dysfunction leads to alteration of cytokines, which causes a loss of negatively charged glycoproteins within the glomerular capillary wall. In focal segmental glomerulosclerosis, a plasma factor, perhaps produced by lymphocytes, may be responsible for the increase in capillary wall permeability. Alternately, mutations in podocyte proteins (podocin, -actinin 4) are associated with focal segmental glomerulosclerosis. Steroid-resistant nephrotic syndrome is associated with mutations in NPHS2 (podocin) and WT1 genes. Although the mechanism of edema formation in nephrotic syndrome is incompletely understood, it seems likely that, in most instances, massive urinary protein loss leads to hypoalbuminemia, which causes a decrease in the plasma oncotic pressure and transudation of fluid from the intravascular compartment to the interstitial space. The reduction in intravascular volume decreases renal perfusion pressure, activating the reninangiotensin-aldosterone system, which stimulates tubular reabsorption of sodium. The reduced intravascular volume also stimulates the release of antidiuretic hormone, which enhances the reabsorption of water in the collecting duct. This theory does not apply to all patients with nephrotic syndrome because some patients actually have increased intravascular volume with diminished plasma levels of renin and aldosterone. Therefore, other factors, including a primary renal avidity for sodium and water, may be involved in the formation of edema in some patients with nephrotic syndrome. In the nephrotic state, serum lipid levels (cholesterol, triglycerides) are elevated for two reasons. Hypoalbuminemia stimulates generalized hepatic protein synthesis, including synthesis of lipoproteins. In addition, lipid catabolism is diminished, as a result of reduced plasma levels of lipoprotein lipase, related to increased urinary losses of this enzyme.

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