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 in the blood due to lost protein.
Increased risk of infection can result due to decreased immunoglobulin levels, a critically important protein susceptible to loss in the urine.
Patients with nephrotic syndrome are hypercoagulable, making them more prone to developing a thromboembolism. This occurs from proteinuria and loss of anticoagulant proteins like antithrombin III and plasminogen. Pro-coagulation is additionally increased as clotting factors I, VII, VIII and X increase as a result. Furthermore, because albumin is lost in the urine, there is decreased binding of plasminogen to fibrin leading to impaired fibrinolysis. Albumin losses increase the availability of thromboxane A2 ( normally bound to albumin, but now moving freely in the serum), leading to platelet aggregation.
Hyperlipidemia is thought to be caused by increased synthesis of lipoproteins in the liver.
Fatty casts are groups of lipid-rich epithelial cells in the kidney, formed due to elevated lipid levels and are seen on microscopic urinalysis.
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