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Nephrology > nephrotic syndrome > Flashcards

nephrotic syndrome Flashcards

1
Q

Major features of nephrotic syndrome?

A
  • 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
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2
Q

Major features of nephritic syndrome?

A
  • 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

  • RED CELL CASTS
  • oliguria
  • azotemia
  • HTN
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3
Q

Incidence of nephrotic syndrome?

A
  • children: 2:100,000 new cases/year
    primarily: MCD
  • adults: 3:100,000 new cases/year, variety of etiologies
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4
Q

Etiologies of nephrotic syndrome?

A
  • adults: Systemic diseases such as DM, amyloidosis, HIV, and SLE
  • NSAIDs
  • MCD
  • SFG
  • membranous nephropathy

children: minimal change disease predominant cause

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5
Q

Pathophys of nephrotic syndrome?

A
  • 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
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6
Q

What proteins are lost in the urine?

A
  • 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
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7
Q

Cause of hypoalbinemia?

A
  • 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
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8
Q

Increase in lipids etiology? Risks?

A
  • 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)
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9
Q

Occurrence of MCD?

A
  • 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
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10
Q

Etiologies of MCD?

A
  • 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
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11
Q

Tx for MCD in children? SE of this med?

A
  • respond well to steroids
  • SEs: short term - insomnia, GI upset, HTN, psychosis, blood sugar increase
    long term - immunosuppression, ulcers, cataracts, adrenal axis suppression
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12
Q

What is FSGS?

A
  • 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
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13
Q

What are secondary causes of FSGS?

A
  • HIV
  • obesity
  • lupus
  • diabetes
  • chemicals that harm kidneys
  • meds
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14
Q

What is membranous nephropathy? How is it characterized?

A
  • 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
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15
Q

Secondary causes of membranous nephropathy?

A
  • Hep B antigenemia and also Hep C
  • autoimmune diseases such as lupus
  • cancer
  • drugs such as gold, captopril and NSAIDs
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16
Q

Complications of Nephrotic syndrome?

A
  • edema
  • hypovolemia
  • HTN
  • acute renal failure
  • protein malnutrition
  • thromboembolism
  • infection: losing immunoglobulins
  • deficiency of Vit D and hypocalcemia
  • increased risk for development of atheroscerosis
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17
Q

Dx of nephrotic syndrome?

A
  • 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)
    Syphilis
    Hep B and C serology’s
    measurement of cryoglobulins
    antistrep abs (cross over with PSGN)
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18
Q

What are the CIs to renal bx?

A
  • 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
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19
Q

Tx of proteinuria?

A
  • 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
20
Q

Tx of edema?

A
  • dietary Na+ restriction
  • loop diuretics
  • edema should be reversed slowly to prevent acute hypovolemia
21
Q

Tx of hyperlipidemia?

A
  • lipid abnorm reverse with resolution of disease

- statins are used initially

22
Q

Tx of hypercoagulability?

A
  • not presently recommended to anticoagulate proph
23
Q

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

A

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

24
Q

What are the systemic causes of nephrotic disease?

A 
amyloidosis
diabetic nephropathy
HIV assoc nephropathy
SLE
Hep C
Multiple myeloma
sickle cell disease
TB 
gout
25
Q

What is amyloidosis?

A
  • 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
26
Q

Primary and secondary amyloidosis?

A
  • primary:
    deposition of light chain Ig - AL
    deposition of heavy chain Ig - AH
  • secondary: primarily autoimmune disorders, some cancers
27
Q

Tx of amyloidosis?

A
  • 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
28
Q

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

A
  • Diabetic nephropathy (4000 cases a year)
29
Q

Diabetic nephropathy etiology?

A
  • 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
30
Q

What should initial screening of diabetics always include?

A
  • 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
31
Q

RFs of diabetic nephropathy?

A
  • genetic susceptibility
  • age
  • BP
  • GFR
  • race: higher in Blacks and NAs
  • glycemic control
  • obesity
  • smoking
32
Q

significance of protein in urine in spot collection?

A
  • normal: less than 30
  • microalbuminuria: 30-299
  • macroalbuminuria: greater than 299 (should show up on std dipstick test)
33
Q

Pathophy os diabetic nephropathy?

A
  • intraglom HTN and ischemic injury result in glomerulosclerosis
  • hyperglycemia can induce directly mesangial expansion and damage in part by glycation of matrix of proteins
  • circulating advanced glycation end products
  • prod of cytokines, inflammation, and endothelial growth factors
34
Q

What signs point to a different causative agent of albumineria other than diabetic nephropathy?

A
  • is occasionally due to other glomerular diseases
  • major clues suggesting nondiabetic glomerular disease:
    onset of proteinuria less than 5 years from documented onset of type 1
  • acute onset of renal disease
  • presence of active urine sediment containing red cells and cellular casts
  • signs and/or sxs of another systemic disease
  • sig reduction in GFR (greater than 30%) within 2-3 months after admin of ACEI or ARBs (Renal stenosis)
35
Q

Tx of diabetic nephropathy?

A
  • tight glycemic control
  • good BP control with ACEI or ARB (Not together)
  • sometimes Na+ restriction/addition of diuretic
  • wt loss if obese
  • cessation of smoking
  • control of hyperlipidemia
36
Q

How does HIV assoc nephropathy present? Tx?

A
  • usually presents as nephrotic syndrome in HIV pts
  • Need renal bx to confirm
  • pathology shows FSGN
  • highly active retroantiviral therapy (HAART) for prolonged course (Control HIV) - shown to slow progression
  • steroids with cyclosporine and ACEI have been used with variable success
37
Q

How does SLE present? How to monitor?

A
  • autoimmune diseae with common renal involvement (60%)
  • variety of presentations: usually nephritic type
  • need to monitor with UAs and chem panels and if + findings do renal bx
  • then tx accordingly
38
Q

WHO classification of lupus?

A
  • type 1: normal
  • type 2: mesangial proliferative
  • type 3: focal and segmental
  • type 4: diffuse proliferative
  • type 5: membranous nephropathy
39
Q

How does hep C nephrotic disease present?

A
  • 8% of all pts with ESRD
  • 3 clinicopathologiccal syndromes assocd - most common is type 1 membranoproliferative glomerulonephritis
  • hematuria, proteinuria, HTN, and anemia
  • may exhibit nephrotic syndrome
  • may have elevated serum transaminases and RF
  • hypocomplemtemia very common
40
Q

Tx indications and Tx of Hep C nephrotic disease?

A
  • main indications for tx:
    poor renal fxn, nephrotic syndrome, new or worsening HTN, fibrosis on bx, progressive disease
  • interferon may result in suppression of viremia and improvement in hepatic fxn: renal fxn rarely improves unless viral suppression occurs
  • 9 months of interferon tx
41
Q

Kidney involvement in multiple myeloma?

A
  • malignancy of plasma cells
  • renal involvement in 25% of all pts
  • myeloma kidney: presence of light chain immunoglobulins (BENCE-JONES protein) in the urine:
    cause renal toxicity, precipitates in tubules and causes tubular obstruction, and are not detected by dip sticks for protein
  • earliest tubular damage causes Fanconi’s syndrome (type II proximal renal tubular acidosis)
  • Hypercalcemia and hyperuricemia frequently seen
  • May also so plasma cell infiltration of renal parenchyma, hyperviscosity syndrome compromises renal blood flow
42
Q

Therapy for multiple myeloma renal involvement?

A
  • dx by serum electrophoresis
  • correction of hypercalcemia
  • volume repletion
  • chemo to tx underlying malignancy
  • plasmapheresis doesn’t provide any renal benefit
43
Q

Renal involvement in Sickle cell disease? Clinical manifestation? Tx?

A
  • renal dysfxn due to sickling of RBCs in renal medulla
  • congestion and stasis lead to hemorrhage, interstitial inflammation, and papillary infarcts
  • hematuria is common
  • isothenuria (urine osmolarity equal to that of the serum) is routine - pts become easily dehyrdated
  • papillary necrosis
  • primary clinical manifestation is PROTEINURIA
  • tx requires adequate hydration and control of sickle cell disease
44
Q

TB renal involvement?

A
  • classic renal manifestation of TB is the presence of microscopic pyuria with sterile urine culture - STERILE PYURIA:
    gold std - urine cultures
    do first morning, mid-stream voided specimens for 3-6 cultures
  • papillary necrosis and cavitation of renal parenchyma occur less frequently
  • renal manifestations resolve with adequate drug therapy for TB
45
Q

Kidney involvement in gout? Tx?

A
  • kidney: primary organ for excretion of uric acid
  • pts with proximal tubular dysfxn have decreased excretion of uric acid and are more prone to gouty attacks
  • deposition of crystals can occur in tubules, interstitium or urinary tract
  • disorder seen in both overproducers and underexcretors of uric acid
  • tx: avoid foods and drugs that cause hyperuricemia; bacon, sardines, liver, sweetbreads, bread, wine, diuretics, theophylline, ascoribic acid (Vit C)
  • aggressive hydration, pharamcotherapy aimed at reducing serum uric acid levels - allopurinonl, colchicine

Nephrology (15 decks)

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