Glomerular Diseases Flashcards

1
Q

Function of kidney

A
  • barrier: size and charge
  • Filters 120-180L/day of plasma water
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2
Q

inflammation of the capillaries

A

GN (Glomerular Nephritis)

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3
Q

Attract ____ to the tuft and react with antigens/epitopes to produce more cytokines and proteases causing damage

A
  • neutrophils,
  • Macs
  • T cells
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4
Q

Persistent GN that worsens renal function is always accompanied by

A
  • interstitial nephritis,
  • renal fibrosis
  • tubular atrophy
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5
Q

Best histo correlate of GN

A

TIN

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6
Q
  • Asymptomatic, +3-5 RBCs/hpf in a spun first voided urine
  • Gross - rare except in IgA nephropathy and sickle cell disease
  • R/O atomic lesions esp in men; ddx - BPH, IN, papilary necrosis, stones, cysts, vascular
A

Hematuria

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7
Q

Sustained: more than 1-2 gm/24 hours
- Seen in some inflammatory glomerular disease

A
  • Proteinuria
  • pyuria
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8
Q
  • 1-2 gm/day proteinuria,
  • hematuria with RBC casts,
  • pyuria,
  • HPN,
  • edema,
  • decreasedGFR
A

ACUTE NEPHRITIC

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9
Q

RPGN + lung hemorrhage (GPS, ANCA, LN, cryoglobulinemia)

A

PULMONARY-RENAL

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10
Q
  • heavy proteinuria,
  • HPN,
  • high chole,
  • hypo alb,
  • edema/anasarca,
  • mxic hematuria
A

NEPHROTIC SYNDROME

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11
Q

abnormal or injured BM due to autoimmune response + mxic hematuria, mild
to heavy proteinuria + HPN, variable increase in crea

A

BASEMENT MEMBRANE

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12
Q

vascular injury producing hematuria and moderate proteinuria

A

GLOMERULAR-VASCULAR

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13
Q

Done in selected patients, clinically stable, adequate blood clotting parameters and willing and able to receive treatment

A

ULTRASOUND GUIDED BIOPSY

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14
Q

LIGHT MX
- Hand and E:
- PAS:
- Jones methenamine silver stain:
- Congo red:
- Masson’s trichrome:

A
  • Hand and E: cellularity and architecture
  • PAS: CHO moieties
  • Jones methenamine silver stain: enhance BM structure
  • Congo red: amyloid deposits
  • Masson’s trichrome: collagen deposits, degree of glomerulosclerosis and interstitial fibrosis
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15
Q
  • prototype for acute endocapillary proliferative GN
  • Developed countries: elderly M>F; 2-14 y.o.
  • Skin and throat infections with M type streptococci
    + Skin 2-6 weeks after impetigo
    + Pharyngitis 1-3 weeks after infection
A

POST STREP GN

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16
Q

Renal bx of POST STREP GN:

A

-hypocellularity (mesangial and endothelial cells),
- PMN infiltrates,
- granular sub endothelial
deposits (IgG, IgM, C3, C4, C5-9),
- sub epithelial deposits (“humps”)

17
Q

Labs of POST STREP GN:

  • nephrotic protenuria
  • 1st week (90%): CH50 and C3
  • RF (30-40%), cryoglobulins and CiCs ANCA against myeloperoxidase
  • Confirmatory:
    + strep culture,
    + ASOT,
    + antiDNAase and antihyaluronidase
A

Labs of POST STREP GN:

  • nephrotic protenuria (20% of adults)
  • 1st week (90%): low CH50 and C3
  • (+) RF (30-40%), cryoglobulins and CiCs (60-70%) ANCA against myeloperoxidase (10%)
  • Confirmatory: (+) strep culture, increased ASOT, + antiDNAase and antihyaluronidase
18
Q

POST STREP GN
° treatment

A
  • control HPN, edema, dialysis
  • Anti strep antibiotic treatment for ALL PATIENTS AND COHABITANTS
  • NO role for immunotherapy even with crescents
19
Q

Complication:
+ untreated,
+ (-) blood cultures
+ right sided endocarditis

Biopsy:
+ sub capsular hemorrhages with “flea bitten” appearance (gross)
+ focal
proliferation around a foci of necrosis with abundant mesangial, sub endothelial,
+ sub epithelial immune deposits of IgG, IgM and C3

Associated findings: embolic infarcts or septic abscesses

A

ENDOCARDITIS ASSOCIATED GN (SBE)

20
Q

SBE
- primary TX:
- prognosis:
- GN due to

A
  • primary TX: 4-6 weeks of antibiotics
  • prognosis: good renal recovery
  • GN due to persistent bacteremia
21
Q

predominant organism in Immunocompromised adults of GN due to persistent bacteremia

A

Staph

22
Q
  • deposition of ICs and C’ activation leading damage, leukocyte infiltration, activation of procoagulant factors and release of various cytokines
  • Most common clinical sign - proteinuria
  • Renal biopsy: ONLY reliable method for ID of morphologic variants
A

LUPUS NEPHRITIS

23
Q

WHO CLASSIFICATION - defines clinicopatholoic correlations, prognosticates and forms basis for treatment
recommendations

  • Class I:
  • Class Il:
    + Both I and Il -
  • Class Ill -
A

WHO CLASSIFICATION - defines clinicopatholoic correlations, prognosticates and forms basis for treatment
recommendations

  • Class I: normal histology or minimal mesangial deposits
  • Class Il: mesangial ICs with mesangial proliferation
    + Both I and Il - minimal renal manifestation with normal renal function; limited to the renal
    mesangium; excellent prognosis; NO treatment for nephritis
  • Class Ill - focal lesions with proliferation and scarring ; most varied course
    Treatment: same as class IV
24
Q
  • Global, diffuse proliferative lesions
  • Increase in anti dsDNA, low complements, hematuria, RBC casts, proteinuria (50% nephrotic range), HPN, decreased renal function(+) crescents: rapid progressive decline in renal function and worst untreated prognosis
  • remission (near normal renal function and < 330 mg/dL/day CHONuria) - with treatment excellent renal outcomes
A

Class IV

25
Q

Class IV Tx

A
  • Induction: high dose steroids + cyclophosphamide OR MMF x 2-6 months
  • maintenance: lower steroid dose + MMF OR AZA
26
Q
  • sub epithelial deposits; membranous (mixed with proliferative)
  • CHONuria (60% nephrotic), predisposed to RVT and other thrombotic complications
  • Tx same as class IV
A

Class V

27
Q
  • > 90% sclerotic, ESRD with IF
  • SLE becomes quiescent with renal failure (effect of uremia)
  • Allograft survival comparable to others
A

Class VI

28
Q
  • Lung hemorrhage + GN - GPS (pulmonary renal syndrome)
  • Target epitope: alpha 3 NC1 domain of collagen IV
  • Younger age group: explosive hemoptysis, sudden fall in Hgb, fever, dyspnea, hematuria
  • urgent kidney biopsy - confirm and prognosticate
  • (+) antiGBM and anti ANCA against MPO
  • Poor prognosis: >50% crescents, advanced fibrosis, crea 5-6 mg?dL, (+) oliguria, need foracute dialysis
  • Treatment: 8-10 or less plasmapheresis + oral prep and cyclophosphamide (maintain IS until negative titers)
A

ACUTE NEPHRITIC SYNDROME (ANTI GBM DISEASE)

29
Q
  • Episodic hematuria associated with mesangial IgA deposition
  • Male preponderance, peak 2nd and 3rd decade of life, rare familial clustering
  • distinguished from HSP by prominent systemic symptoms, younger age, (<20 y.o.), preceding infection and abdominal complaints
  • Mesangial IgA deposits
  • 2 common presentations:
    + recurrent episodes of macro hematuria during or immediately following an URTIi often accompanied by proteinuria
    + persistent asymptomatic mxic hematuria
A

ACUTE NEPHRITIC SYNDROME (IgA NEPHROPATHY)