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Nephrology 2 > Glomerulonephropathies > Flashcards

Glomerulonephropathies Flashcards

1
Q

List the 6 glomerulonephropathies

A
  • nephritic syndrome
  • post strep glomerulonephritis
  • IgA nephropathy
  • Henoch-Schonlein Purpura
  • Rapidly progressive glomerulonephritis
  • Interstitial nephritis
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2
Q

What is the difference between Nephritic and Nephrotic?

A
  • *Nephritic**:
  • positive for RBC*
  • red cell or mixed cellular casts*
  • variable degrees of proteinuria
  • *Nephrotic**
  • proteinuria greater than 3.5g/day
  • lipiduria
  • fatty casts
  • edema
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3
Q

Nephritic Causes

A
  • Postinfectious glomerulonephritis
  • IgA nephropathy
  • Henoch-Schonlein purpura (aka IgA Vasculitis)
  • Mesangial Proliferative Glomerulonephritis
  • Lupus Nephritis
  • Rapidly Progressive(crescentic) glomerulonephritis
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4
Q

Nephrotic Causes

A
  • systemic… Diabetic nephropathy, amyloidosis, systemic lupus
  • minimal change dz (children)
  • focal segmental glomerulosclerosis
  • membranous nephropathy
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5
Q

What are the two types of Nephritic Dz, describe each and give an example.

A

Focal nephritic: -inflammatory lesions in less than 1/2 of glomeruli

-UA shows RBC, occasional RBC casts, mild proteinuria

Example: IgA Nephropathy

  • *Diffuse Nephritic**:
  • Affects greater than 1/2 of glomeruli
  • UA similar to focal but with more proteinuria
  • edema, HTN, renal insufficiency

Example: Post Strep Glomerulonephritis

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6
Q

Nephrotic Dz Patterns, describe and give an example.

A

Affects many glomeruli

Without obvious inflammation or immune complexes

edema, hyperlipidemia, hypoalbuminemia

Ex. Diabetic neuropathy

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7
Q

Post Streptococcal Glomerularnephritis

  • primarily affects what age group?
  • when does this develop?
  • does abx treatment prevent glomerular dz?
A
  • primarily affects children between 5-12yrs
  • develops 1-3wks post strep throat infection or 3-6wks post skin infection w/ group A beta-hemolytic strep
  • Abx tx does not always prevent glomerular dz
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8
Q

Post strep Glomerulonephritis

  • pathophys
  • Can viral illness and parasitic infections be associated with glomerulonephritis?
A

Pathophys: caused by glomerular immune complex dz induced by group A beta hemolytic strep.

Glomerular immune complex dz triggers complement activation and inflammation.
*immune complex irritates glomerular vessel leading to inflammation and narrowing of capillary lumen

-you bet they can!!

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9
Q

Clinical Signs and Sx of Post strep glomerulonephritis

A
  • often asymptomatic
  • microscopic hematuria….gross hematuria
  • proteinuria (can reach nephrotic range)
  • Edema
  • HTN
  • Increased SCr
  • Variable decline in GFR
  • Hypocomplementemia (C3, C4)
  • acute renal failure and need for dialysis is uncommon.
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10
Q

Posts strep glomerulonephritis

-serology

A

Serology: looking for elevated titers of abys to extracellular strep products.

  • Streptozyme test measures 5 streptoccocal abys:
    1. Antistreptolysin (ASO)**
    2. Anti-hyaluronidase
    3. Anti-streptokinase
    4. Anti-nicotinamide-adenine dinucleotidase
    5. Anti-DNAse B abys

-*Is positive in 95% of pts d/t pharyngitis and about 80% of those with skin infections.

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11
Q

Biopsy is not typically performed in PSGN pts to confirm diagnosis since hx of recent strep infection is very specific, but biopsy can be performed if ?

A
  • other glomerular disorders are being considered b/t they deviate from natural course of PSGN
  • presents late without a clear history of prior strep infection.
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12
Q

PSGN:
-persistently low C3 levels beyond 6wks are suggestive of a dx of what type of glomerulonephritis?

-Recurrent episodes of hematuria are suggestive of what type of glomerulonephropathy?

A

membranoproliferative

recurrent episodes of hematuria are suggestive of IgA nephropathy and are Rare in PSGN.

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13
Q

Post strep glomerularnephritis Tx & Prognosis

A

Treatment:

-Treat the volume overload

–sodium and water restriction

–Lasix (volume and HTN)

–Those with acute renal failure, dialysis may be required.

Prognosis:

  • complete recovery, resolution begins within first 2 wks
  • smaller subset of pts have late renal complications (HTN, increased proteinuria, renal insufficiency)
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14
Q

IgA Nephropathy

  • aka
  • most common in who?
  • primarily affects what age group?
A

aka: Bergers Dz

Most common in Asians and Caucasians, Males

primarily affects ages 15-35

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15
Q

WHat is the most common cause of acute nephritis worldwide?

What is the most common lesion to cause primary glomerulonephritis in the developed world?

What is the most common cause of vasculitis in children?

A
  1. Post strep glomerulonephritis
  2. IgA Nephropathy
  3. Henoch Scholein Purpura
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16
Q

Etiology? Pathophysiology of IgA nephropathy

A

Etiology: unknown

Pathophysiology:

-dysregulated synthesis and metabolism of IgA resulting in IgA immune complexes that favor mesangial deposition.

17
Q

IgA nephropathy Presentation (3 ways)

A
  1. )Gross hematuria that may be recurrent*
    - flank pain
    - fever
    * 50%*
  2. )Microscopic hematuria…eventually gross hematuria
    - mild proteinuria
    * 30%*
  3. )Nephrotic Syndrome (proteinuria, lipiduria, fatty casts)
    - edema
    - renal insufficiency
    - HTN
    - Hematuria
    * 10%*
18
Q

IgA nephropathy Diagnosis

A

-Urinalysis

  • confirmation is by kidney bx:
  • -prominent IgA deposits in the mesangium and along glomerular capillary walls

–C3 and IgG are also deposited

–mesangial IgA deposition may be seen with cirrhosis, celiac dz, and HIV infection

19
Q

Treatment of IgA nephropathy

Prognosis

A

Treatment:
Blood pressure control: ACEI/ARB

Severe or progressive Dz tx:
-corticosteroids/immunosuppressants

Prognosis:
-most pts enter sustained clinical remission

-some may have persistent low-grade hematuria &/or proteinuria

-slow progression ot ESRD in 50% 
signs this will happen... 
--elevated SCr
--HTN 
--persistent protein excretion about 1000mg/day
20
Q

Henoch-Scholein Purpura
-aka

  • pathophys
  • cause
  • most common in what age group?
A

Aka: IgA vasculitis

Patho: systemic vasculitis characterized by tissue deposition of IgA immune complexes

Cause: unknown, immune-mediated vasculitis

-3-15years

21
Q

Tetrad of clinical manifestations for HSP/IgA Vasculitis

A
  1. palpable purpura (typically over LE and feet) w/o thrombocytopenia or coagulopathy
  2. arthritis/arthralgias
  3. abdominal pain
  4. renal dz/failure
    - other manifestations may be mild asymptomatic hematuria, proteinuria, nephrotic syndrome and even renal failure.
22
Q

HSP Nephritis:

  • how does this differ from IgA Glomerulonephritis?
  • Dx
  • prognosis
  • Tx
A
  • has identical histological findings, but HSP has IgA immune complex deposition vasculitis systemically.
  • Dx: confirmed by kidney bx, but this is reserved fro when dx is uncertain or severe renal involvement.
  • Prognosis:
  • recurrence is common

-minority develop persistent renal manifestations of end-stage renal dz

Tx:

  • supportive; glucocorticosteroids
  • for those who develop ESRD dialysis and renal transplant can be performed.
23
Q

Rapidly Progressive Glomerulonephritis:

-characterized by?

A
  • Characterized by rapid progression to end stage renal failure in days, weeks, months.
  • Will see crescent formation on bx
24
Q

Crescent formation pathophysiology

A

formation is in response to severe injury to glomerular capillary wall. initially begins as active inflammation of capillary wall resulting in movement of plasma products including fibrinogen into bowmans space w/ subsequent fibrin formation, the influx of Mfs and Tcells release proinflamm cytokines. Fibrocellular and fibrous crescents develop.

25
Q

What are the types of Rapidly progressive Glomerulonephritis? What is each one?

A

1.Anti-glomerular basement membrane (Goodpastures syndrome)

–aby dz of lungs and glomerulus caused by anti-GRM abys.

2.Immune Complex RPGN

–deposition of immune complexes in the glomeruli

–may be IgA nephropathy, post-infectious glomerulonephropathies, and lupus nephritis

3.Pauci-immune RPGN: a necrotizing glomerulonephritis and vasculitis

–ANCA positive

–systemic sx of vasculitis

26
Q

Presentation of Rapidly Progressive Glomerulonephritis

A

Insidious onset:

  • fatigue
  • edema

More Acute onset:

  • macroscopic hematuria
  • oliguria
  • edema
  • renal insufficiency

GBM type:

  • pulm hemorrhage, hemoptysis
  • pulmonary infiltrates
  • dyspnea
27
Q

RPGN evaluation

A
  • urinalysis**** will show:
  • -hemturia
  • -red cell casts
  • -proteinuria
  • high BUN and Creatinine
  • renal bx
  • serologic assays to determine type and cause (ANCA = Pauci, anti-GBM = goodpastures, antinuclear aby = immune complex)
28
Q

RPGN Tx

A

Empiric therapy w/ severe dz while awaiting bx results:
-pulse methylpredisolone

-oral or IV cyclophosphamide
(immunosuppression/chemo)

  • sometimes plasmapheresis
  • send to nephrologist
  • when Crescent found on bx they have ESRD and will not respond to immunosuppressive therapy.
29
Q

Interstitial Nephritis

  • pathophysiology
  • etiologies
A

Patho: renal lesion that causes a decline in creatinine clearance and is characterized by inflamm infiltrate in the kidney interstitium w/ edema and possible tubular cell damage.

Etiologies:
-**mainly **caused from drug rxns (PCN, Sulfa, NSAIDS)

-may be cause from other sources such as infectious dz (strep, CMV, histoplasmosos, Rocky Mtn Spttd fever) or autoimmune dz (Lupus, sjogrens, sarcoid, cryoglobulinemia)

30
Q

Presentation of Interstitial Nephritis

  • Urinalysis findings
  • tx
  • prognosis
A

Presentation:

  • fever (80%)
  • Rash
  • arthralgias
  • peripheral blood esoinophilia (80%)
  • oliguria
  • azotemia

Urinalysis:

  • RBC (95%)
  • White cells and white cell casts
  • proteinuria commonly found in NSAID related interstitial nephritis

Tx:

  • supportive
  • removal of inciting agent**

if renal failure persisits:
-short course of corticosteroids; high dose methylprednisolone or prednisone 1-2wks then taper

Prognosis:

  • good prognosis
  • rarely progresses to ESRD
  • recovery usually over weeks to months.
31
Q

What is the best initial test to working up discolored urine?

when do we admit pts with GN?

What must be guaranteed with pts who have GN?

A

Urinalysis

HTN, edema, or renal dysfunction

must guarantee a follow up appt!

Nephrology 2 (7 decks)

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