Nephrotic Syndrome

Sign and Symptoms
1. Proteinuria – because problems with the glomerulus membrane.
2. Hypoproteinemia (hypoalbuminemia) – because lost in the urine.
3. Hyperlipidemia, hypercholesterolemia – due to increased lipoprotein synthesis to try to compensate for the loss of plasma albumin to maintain the plasma oncotic pressure. Also because there’s a decrease in clearance of triglyceride-rich lipoproteins due to inhibition of lipoprotein lipase and triglyceride lipase.
4. Oedema – because decrease in plasma oncotic pressure causing an extravasation of plasma water into the interstitial space. Noticeable in the face in the morning and predominately in lower extremities later in the day.
5. Facial swelling – due to the oedema (noticeable in the morning).
6. Swollen abdomen – accumulation of fluid in the abdominal cavity (ascites).
7. Shortness of breath – fluid accumulation in the space around the lungs (pleural effusion).
8. Foamy appearance of the urine – due to presence of protein in the urine.
9. Weight gain from fluid retention.
Others:
Poor appetite
High blood pressure
Susceptible to infections
Hypertension, hematuria and azotemia (rare)
Thromboembolism

Causes and Risk Factors
1. Minimal change disease
- idiopathic, but can occur due to drug use (NSAIDs) and hematologic malignancies (Hodgkin
lymphoma)
- edema and proteinuria but renal function normal
- more common in children age 2-6
2. Membranous Nephropathy
- deposition of immune complexes on the GBM causing GBM thickening (inflammation?)
- idiopathic but can be due to infection (Hepatitis B), drugs (gold, penicillamine, NSAIDs),
autoimmune (SLE), cancer
- more common after the age 40
3. Focal Segmental Glomerulosclerosis
- scattered (segmental) mesangial sclerosis in some but not all glomeruli.
- usually idiopathic, but can be caused by heroin use, HIV infection, obesity or nephron loss
(reflux nephropathy, subtotal nephrectomy), genetic causes
*http://www.cdc.gov/genomics/hugenet/reviews/NPH2.htm*
4. Diabetes mellitus (diabetic nephropathy)
- hyperglycaemia causes glycosylation of glomerular protein which is responsible for the
vascular endothelial damage, causing the GBM to become thickened.
- positive nodular deposits (mucopolysaccharides, fibrils and collagen) appear in the
mesangial space, at the periphery of the glomerulus, pushing the capillaries
- arteriosclerosis of the afferent and efferent arterioles
- walls of the vessels become abnormally thick but weak (bleed, leak protein, slow flow of
blood)
- occurs in long-standing diabetic patients
5. Systemic lupus erythematosus
- similar to membranous nephropathy
6. Renal amyloidosis (insoluble protein fibers are deposited in tissues and organs, making them
more rigid)
7. Infection (Hepatitis B & C)
8. Drug exposure (Gold, NSAIDs, penicillamine, heroin taken intravenously)
9. Malignancy (lymphoma, leukaemia)
10. Hereditary disorders
11. Immune disorders