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What is the general problem of Nephrotic Syndrome and what is its hallmark?

The general problem is that something messed up the integrity of the podocytes of the GBM that messes up proper filtration. Hallmark is proteinuria greater than 3.5 mg per day.


What are 8 general features patients with Nephrotic Syndrome will present with clinically?

1. Massive Proteinuria
2. Generalized edema (pronounced, moreso than nephritic syndrome)
3. Hypogammaglobunemia --> more prone to infections.
4. Hypoalbuminemia, most abundant protein in the blood is albumin.
5. Hypercoagulable state due to loss of Anti Thrombrin 3 which makes you pro-coagulable. Also loss of anti-plasmin to a lesser degree.
6. Hyperlipidemia, hypercholestorelimia, lipiduria --> all perhaps due to the liver trying to compensate for the colloid pressure in the blood.
7. Salt and water retention leading to HTN.
8. Oval fat bodies and/or free fat in the urine.


What environmental agents are common culprits of nephrotic syndrome?

Staph and Pneumococcal infections.


What is a complication of patients with Membranous nephropathy?

Renal vein thrombosis due to hypercoagulable state.


What are 5 causes of Nephrotic Syndrome?

1. Membranous Nephropathy
2. Minimal Change diseases
3. Focal Segmental Glomerulosclerosis
4. Membranoproliferative Glmoerulonephritis
5. Secondary MPGN


What is the difference between highly selective proteinuria and poorly selective?

Highly selective will only allow low mw proteins like albumin and transferrin. Poorly selective will allow bigger molecules to be filtered like globulins in addition to the smaller ones.


What causes the soft and pitting generalized edema in nephrotic syndrome? What are the more severe complications of this generalized edema?

Heavy loss of albumin which messes up the colloid pressure in the blood. Pleural effussions and ascites


What can be assumed if proteinuria is poorly selective?

Damage to the glomerular capillary walls are fairly extensive.


Why do we have HTN in nephrotic syndrome?

Hypovolumeia is sensed, which triggers the RAS (renin aldosterone system) --> salt and water retention --> HTN.


Why is there increased lipoprotein synthesis in the liver?

Perhaps to counteract the loss of oncotic pressure in the blood. However these lipids leak across the filtration barrier leading to lipiduria.