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What lab value determines proteinuria?
>300 mg per 24 hours is abnl
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What is glomeular proteinuria?
leakage of plasma proteins through an altered glomerular filtration barrier
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What is tubular proteinuria?
- Failure of reabsorption of lower molecular weight plasma protein
- never exceeds 2 grams per 24 hours
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What is overflow proteinuria?
- Results from filtration of proteins, that are present in excess in the circulation
- suspected with multiple myeloma or other lymphoproliferative disorders
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What is hypoalbuminemia?
<3 grams/d:
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What are the features of nephrotic syndrome?
- PHPHLH
- Proteinuria
- Hypoalbuminemia
- Peripheral edema
- Hyperlipidemia
- Lipiduria
- Hypercoaguability
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What is the primary factor of nephrotic syndrome?
proteinuria as a result of altered permeability of the glomerular filtration barrier for protein, namely GBM
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What is the best way to determine nephrotic syndrome?
Renal bx
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What causes HL in nephrotic syndrome?
- Increased hepatic lipoprotein synthesis
- Decreased oncotic pressure
- Increased urinary loss of regulatory proteins
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What causes hypercoaguability in nephrotic syndrome?
- Increased urinary loss of antithrombin III
- altered levels of activity of proteins C and S, hyperfibrinoginemia, and platelet aggregability
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What are clinical findings in nephrotic syndrome?
- Edema (starts peripheral, then mirrors CHF)
- Protein malnutrition
- Iron resistant microcytic hypochromic anemia
- Hypocalcemia (secondary to losses of urinary vit D binding)
- Increased susceptibility to infections due to losses and inability to maintain globulins
- Thrombosis
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How do you tx proteinuria in nephrotic syndrome?
- ACEs and ARBs: give trial, monitor K, if not about 5.2, continue
- They are renal protective
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How do you tx edema in nephrotic syndrome?
What are you cautious about?
- Salt restriction and loop diuretics
- Losing >1kg/day (2.2lbs) can cause prerenal azotemia causing person to have fluid restriction
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How do you tx HL with nephrotic syndrome?
Aggressive statins, monitor LFTs
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How do you tx hypercoaguability with nephrotic syndrome?
- Everyone needs to be on aspirin
- Everyone with thrombosis needs to be on Coumadin for at least 6mo
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What does MCD show on light microscopy?
Glomerular size and architecture are nl
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What is a poor prognosis with MCD?
presence of mesangial hypercellularity or spare deposits of C2 and IgM
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Fusion of foot processes of visceral epithelial cells
MCD
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What causes MCD?
- Idiopathic m/c,
- URI, immunizations, atopy, rifampin, NSAIDs, interferon
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What do MCD lab studies show?
All nl
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How do you tx MCD?
- Steroids: continue several weeks after proteinuria has resolved, at least 8 weeks (adults 20-24weeks)
- Alkylating agents (cyclophosphamide or chlorambucil) if continue to relapse
- Cyclosporine (last resort): usually lifetime use
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Sclerosis with hyalinosis involving portions of fewer than 50% of glomeruli on tissue section
FSGS
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What does FSGS light microscopy show?
FSglomerulonephritis with entrapment of amorphous hyaline material, most commonly at areas of juxtamedullary glomeruli
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What causes FSGS?
Unknown, most likely immunologic, >50% of nephrons must be loss
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How do you tx FSGS?
- Steroids
- Renal transplant (recurrence 50%)
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What are poor prognostic indicators of FSGS?
- HAHA:
- HTN
- abnl renal function
- heavy proteinuria
- African American
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What is the leading cause of idiopathic nephrotic syndrome in adults?
Membranous nephropathy
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What are secondary causes of Membranous nephropathy?
Hepatitis, syphilis, SLE, RA, sarcoidosis
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Diffuse thickening of GBM without inflammation or proliferation
Membranous nephropathy
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How do you tx Membranous nephropathy?
- Salt restriction, strict BP control, ACEi
- Transplantation successful
- Steroids not effective (no evidence of inflammation)
- Cyclophosphamide, clorambucil, and cyclosporine decrease amount of proteinuria but do NOT decresae time to ESRD
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What is membranoproliferative glomerulonephritis?
Thickening of GBM with proliferative changes seen on light microscopy
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Presence of subendothelial and mesangial deposits on electron microscopy
membranoproliferative glomerulonephritis Type 1
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C3, IgG, IgM
membranoproliferative glomerulonephritis Type 1
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What are clinical features of membranoproliferative glomerulonephritis Type 1?
Heavy proteinuria, active urinary sediment, nl or mildly impaired GFR
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What conditions is membranoproliferative glomerulonephritis associated with?
Hepatitis, HIV, leukemia
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How do you tx membranoproliferative glomerulonephritis type 1?
There is none known
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Presence of electron dense deposits within GBM and other renal basement membranes
Type 2 membranoproliferative glomerulonephritis
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What are clinical features of Type 2 membranoproliferative glomerulonephritis?
Proteinuria and nephrotic syndrome or hematuria
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What is the most common autoantibody in Type 2 membranoproliferative glomerulonephritis?
IgG
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How do you tx membranoproliferative glomerulonephritis Type 2?
none
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How effective is transplantation with membranoproliferative glomerulonephritis?
Often has recurrence
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Extracellular deposition of fibrous protein in site throughout the body
Amyloidosis
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Glomeruli are filled with amorphous deposits that stain positive with congo red and show green birefringence
amyloidosis
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How do you tx amyloidosis?
- Alkylating agents (melphalan) and predinose to reduce proteinuria and improve renal function
- Melphalen and stem cell transplants can induce remission in 80% but have 45% mortality rate
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How bad is the prognosis with primary amyloidosis?
It can lead to ESRD on avg of 2-3 years
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