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Flashcards in nephrotic syndrome Deck (45)
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Major features of nephrotic syndrome?

- MASSIVE PROTEINURIA (greater than 3.5 g in 24 hrs) which leads to:
HYPOALBUMINEMIA (less than 3) which leads to peripheral EDEMA because drop in oncotic pressure in vasculature so fluid leaks into surrounding tissue
- HYPERLIPIDEMIA: liver is making more proteins
- thrombotic disease
- few cells or casts in urine


Major features of nephritic syndrome?

- Lesions that cause increased cellularity w/in glomeruli, along with leukocytic infiltrate. The INFLAMMATION injures cap walls, permitting escape of RBCs into urine. This leads to decreased GFR (oliguria and azotemia). HTN result of fluid retention and increased renin released from ischemic kidneys

Key features
- oliguria
- azotemia


Incidence of nephrotic syndrome?

- children: 2:100,000 new cases/year
primarily: MCD
- adults: 3:100,000 new cases/year, variety of etiologies


Etiologies of nephrotic syndrome?

- adults: Systemic diseases such as DM, amyloidosis, HIV, and SLE
- membranous nephropathy

children: minimal change disease predominant cause


Pathophys of nephrotic syndrome?

- the glomerular cap wall: electrostatically prevents negatively charged proteins from passing through, podocyte intercellular jxns restrict the passage of proteins of certain sizes - most nephrotic diseases there is damage to GCW and this results in the loss of charge - proteins will pass through and aso damage to podocytes - allows larger proteins to pass

--massive proteinuria leads to decrease in plasma proteins which leads to fluid shift out of vasculature so decreased plasma volume, and decreased GFR so this stim increase of aldosterone secretion which will also promote edema

- pt is going to be hypovolemic


What proteins are lost in the urine?

- albumin
- clotting factors
- transferrin
- immunoglobulins (susc. to infection)
- Vit D binding protein: results in decreased levels of Vit D, this decreases calcium and then this will increase PTH


Cause of hypoalbinemia?

- partially due to loss of albumin through glomeruli
- also thought that albumin is catabolized in prox tubular cells of kidney
- low oncotic pressure stimulates hepatic lipoprotein synthesis leading to hyperlipidemia


Increase in lipids etiology? Risks?

- elevated levels of LDLs and TGs (HDL normal) due to increased hepatic synthesis and decreased peripheral metabolism
- this increases risk of CV disease
- lipiduria: OVAL FAT BODIES in the urine (fat in macrophages)


Occurrence of MCD?

- accounts for 90% of disease in children
- can occur in adults secondary to NSAIDs
- find only mild mesangial cell proliferation, no immune deposits and effacement (thinning) of epithelial cell foot processes


Etiologies of MCD?

- infections
- drugs: NSAIDs, lithium, ampicillin
- tumors: Hodgkins, leukemia
- allergies: food, bee stings, pollens
- other diseases: following allogenic stem cell for leukemia, following hematopoietic cell transplantation


Tx for MCD in children? SE of this med?

- respond well to steroids
- SEs: short term - insomnia, GI upset, HTN, psychosis, blood sugar increase
long term - immunosuppression, ulcers, cataracts, adrenal axis suppression


What is FSGS?

- most common lesion found in those with idiopathic nephrotic syndrome 35% of the time (Blacks - 50%)
- characterized by presence in SOME glomeruli of segmental areas of mesangial collapse and sclerosis - scarred tissue - have higher pressures going through rest of glomeruli
- can be primary and secondary forms


What are secondary causes of FSGS?

- obesity
- lupus
- diabetes
- chemicals that harm kidneys
- meds


What is membranous nephropathy? How is it characterized?

- most common cause of nephrotic syndrome in adults
- characterized by:
basement membrane thickening with little infiltration, deposition of immune complexes on basement membrane - allow proteins to leak through
- electron dense deposits along basement membrane
- primarily idiopathic may be due to autoabs


Secondary causes of membranous nephropathy?

- Hep B antigenemia and also Hep C
- autoimmune diseases such as lupus
- cancer
- drugs such as gold, captopril and NSAIDs


Complications of Nephrotic syndrome?

- edema
- hypovolemia
- acute renal failure
- protein malnutrition
- thromboembolism
- infection: losing immunoglobulins
- deficiency of Vit D and hypocalcemia
- increased risk for development of atheroscerosis


Dx of nephrotic syndrome?

- 24 hr urine (excreting more than 3.5 g/24 hrs)
- renal bx: for definitive dx (GOLD STD)
- More studies that may be run - if thinking secondary cause:
ANA (autoimmune)
complement (C3)
serum or urine protein electrophresis (mult myeloma, IgGs)
Hep B and C serology's
measurement of cryoglobulins
antistrep abs (cross over with PSGN)


What are the CIs to renal bx?

- uncorrectable bleeding diathesis
- small kidneys (indicate chronic irreversible disease)
- uncontrolled, severe HTN
- bilateral cystic kidneys or renal tumor
- hydronephrosis
- renal or peri-renal infection
- uncoop pt


Tx of proteinuria?

- ACEIs/ARBs: serum Cr and K+ level should be carefully monitored, these decrease the intraglomerular pressure
- protein restriction not recommended as evidence is unclear about usefulness and b/c protein losses are so heavy the pt may have malnutrition


Tx of edema?

- dietary Na+ restriction
- loop diuretics
- edema should be reversed slowly to prevent acute hypovolemia


Tx of hyperlipidemia?

- lipid abnorm reverse with resolution of disease
- statins are used initially


Tx of hypercoagulability?

- not presently recommended to anticoagulate proph


What is tx if pt develops thrombosis? DVT or PE?

lovenox then bridge with coumadin, stop lovenox when coumadin is at therapeutic levels INR: 2-3


What are the systemic causes of nephrotic disease?

diabetic nephropathy
HIV assoc nephropathy
Hep C
Multiple myeloma
sickle cell disease


What is amyloidosis?

- a group of diseases characterized by deposition of proteins (amyloid) in organs leading to their destruction and ult the death of the pt
- PP: amyloid deposition in mesangium then the capillary loops


Primary and secondary amyloidosis?

- primary:
deposition of light chain Ig - AL
deposition of heavy chain Ig - AH

- secondary: primarily autoimmune disorders, some cancers


Tx of amyloidosis?

- dialysis
- tx with mephalan than autologous hematopoietic cell transplantation (if eligible)
- remission can happen if inciting agent is removed in secondaray AA
- primary progresses to ESRD in 2-3 years, 5 year survival is less than 20% with death secondary to ESRD and heart disease


What is the most common cause of ESRD in the US?

- Diabetic nephropathy (4000 cases a year)


Diabetic nephropathy etiology?

- type 1: 20-30% will have microalbinurea after 15 years
less than 1/2 will progress to overt nephropathy
- type 2: risk is equal to that in type 1 with current therapy


What should initial screening of diabetics always include?

- urine screening for microalbuminuria
- defined as 30-300 mg/day
- special testing strips to detect microalbuminuria
- 24 hr urine collection is accepted std to confirm