Massive proteinuria greater than 3.5g per day is the hallmark sign of nephrotic syndrome disease processes. Massive proteinuria is caused by derangement in the glomerular capillary walls that result in increased permeability to plasma proteins.
Edema is swelling of the face, lower extremities, and hands due to loss of oncotic pressure within the blood because of lost protein.
Increased risk of infection can result due to decreased immunoglobulin levels due to protein losses in the urine.
Patients with nephrotic syndrome are hypercoagulable, making them more prone to developing a thromboembolism. This occurs from proteinuria, where patients lose protein C and protein S in the urine, along with antithrombin. Futhermore, because albumin is lost in the urine, there is decreased binding of plasminogen to fibrin, which leads to impaired fibrinolysis. Albumin losses also lead to increased availability of thromboxane A2 (which is normally bound to albumin), causing platelets to aggregate.
Hyperlipidemia is also an important component, thought to be caused by increased synthesis of lipoproteins in the liver.
Fatty casts are groups of lipid-rich epithelial cells, formed due to elevated lipid levels, which are trapped in the kidney and are seen on microscopic urinalysis.
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