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RENAL II - Path and Phys Exam 1 > Robbins Chapter 20 - The Kidney - Part 2 > Flashcards

Robbins Chapter 20 - The Kidney - Part 2 Flashcards

1
Q

Destruction of glomeruli/reduction of GFR to 30-50%

A

ESRD progresses at a steady rate

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2
Q

2 major characteristics of progressive renal damage

A

Principal injury- Focal segmental glomerulosclerosis

Accompaning injury - Tubulointerstitial fibrosis

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3
Q

FSGS

A

Progressive fibrosis after injury
Increased proteinuria and impaired function
Initiated by adaptive change: compensatory hypertrophy of healthy areas of kidney

Reduction in renal mass -> HTN and hypertophy -> Epithelial damage -> proteinuria -> mesangial proliferation and macrophage infiltration -> accumulate ECM -> sclerosis
(vicious cycle)

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4
Q

Interrupting glomerulosclerosis process

A

Renin-angiotensin inhibitors

reduce HTN and inhibit compensatory mechanisms

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5
Q

Tubulointerstitial fibrosis

A

Tubular damage and interstitial inflammation

Better correlation in decline of renal function

Ischemia downstream, surrounding inflammation, or loss of peritubular capillary network

Proteinuria can directly injure and activate tubular cells

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6
Q

Nephritic syndrome

A

Inflammation of glomeruli

**Hematuria, red cell casts in urine, azotemia, oliguria, mild to moderate HTN
Proteinuria and edema are common but not as severe

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7
Q

Acute proliferative glomerulonephritis/ Postinfectious Glomerulonephritis

A

Diffuse proliferation of glomerular cells
Influx of leukocytes
Typically cause by immune complexes

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8
Q

Poststreptococcal Glomerulonephritis

A

1-4 weeks post group A strep infection with certain M proteins (12, 4 and 1)
Usually children age 6-10
Immune complexes formed in situ

Elevated antibody titers, decreased serum complement, granular immune deposits

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9
Q

SpeB

A

Principle antigenic determinant for poststrep GN

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10
Q

Poststrep GN Morphology

A

Enlarged, hypercellular glomeruli
IgG, C3 and IgM deposits in mesangium and GBM - focal and sparse
Subepithelial humps
Subendothelial deposits early on

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11
Q

Poststrep GN Clinical course

A

Young child with malaise, fever, nausea, oliguria, hematuria (coke colored urine) 1-2 weeks after sore throat

Mild proteinuria, periorbital edema, mild HTN
Adult more atypical with sudden HTN, edema and BUN

95% children recover with minimal therapy
60% adults recover quickly
Small numbers progress to rapid progressive GN

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12
Q

Nonstrep Acute GN

A

Similar course with staph, pneumonia, meningococcemia, hep B, hep C, HIV, varicella, mono, malaria, toxo

Staph differs by sometimes creating IgA deposits

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13
Q

Rapid progressive GN

A 
No specific etiology
Rapid loss of function
Severe oliguria and nephritic signs
Death in weeks to months
Crescents in most glomeruli
**Immunologically mediated - 3 types
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14
Q

Type 1 - anti GBM

A

Linear immune deposits in GBM

Antibodies to portion of collagen IV alpha3 chain

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15
Q

Goodpasture syndrome

A 
Antibodies cross react
Pulmonary hemorrhage (recurrent hemoptysis) with renal failure
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16
Q

HLA-DRB1

A

Associated with type 1 (autoimmunity)

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17
Q

Type 2 - immune complex deposition

A

Complication of any immune complex nephritides

Postinfectious, SLE, IgA nephropathy, and Henoch-Schonlein purpura

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18
Q

Type 3 - Pauci-immune

A

Lack of detectable anti-GBM or immune complexes
Circulating antineutrophil cytoplasmia antibodies
May be associated with Wegener granulomatosis but usually idiopathic
**Manifestation of small vessel vasculitis or polyangiitis limited to peritubular capillaries

19
Q

Wegener granulomatosis

A

Granulomatosis with polyangiitis

Inflammation of blood vessels restricting blood flow to certain organs

20
Q

RPGN morphology

A

Distinctive crescents with prominent fibrin strands

May show ruptures in GBM - allows leukocytes and coagulation material through

21
Q

RPGN clinical course

A

Hematuria with blood cell casts, moderate proteinuria, variable HTN and edema
Serum analysis can be helpful (antiGBM, antinuclear, ANCAs)
Culminates in oliguria
Serum exchange may help some early on as well as steroid treatment
Many patients require chronic dialysis

22
Q

Nephrotic syndrome

A

Derangement in glomerular capillary walls resulting in increased permeability to plasma proteins

Massive proteinuria (greater than 3.5 gm)
Hypoalbuminemia (less than 3 gm)
General edema
Hyperlipidemia and lipiduria

Vulnerable to infection - loss of immunoglobulins
Thrombotic/thromboembolic complications - loss of anticoagulants -> renal vein thrombosis

23
Q

Generalized edema

A

Decreased colloid osmotic pressure or increased hydrostatic pressure (increased sodium and water retention)

24
Q

Highly selective proteinuria

A

Mostly low weight proteins (albumin)

25
Q

Poorly selective proteinuria

A

Variety of protein loss, low and high weight

26
Q

Most frequent cause of nephrotic syndrome in under 17 in NA

A

Lesion primary to the kidney

27
Q

Most frequent cause of nephrotic syndrome in adults in NA

A

Systemic disease

28
Q

Most frequent systemic cause of nephrotic syndrome

A

Diabetes, amyloidosis, SLE

29
Q

Most frequent primary lesions causing nephrotic syndrome

A

Minimal-change disease (children), membranous glomerulopathy (adults) and focal segmental glomerulosclerosis

30
Q

Less common cause of nephrotic syndrome

A

Proliferative glomerulonephritides: MPGN and IgA nephropathy

31
Q

Membranous Nephropathy

A

Diffuse thickening of glomerular capillary wall due to deposits of Ig on subepithelial side
75% primary
25% secondary/systemic problem

32
Q

Systemic causes of membranous nephropathy

A

Drugs (penicilamine, captopril, gold, NSAIDS)
Malignant tumors (lung, colon, melanoma)
SLE (10-15%)
Infections (hep B, hep C, syphilis, schistosomiasis, malaria)
Other autoimmune

33
Q

Membranous Nephropathy Pathogenesis

A

Chronic immune complex mediated
Secondary - known antigens
Primary - idopathic, linked to HLA-DQA1, usually antibodies to renal autoantigen (phospholipase A receptor)

C5b-C9 MAC makes capillary leaky

34
Q

Membranous Nephropathy Morphology

A

Diffuse thickening of glomerular capillary wall on subepithelial side
Segmental sclerosis may eventually occur

35
Q

Membranous Nephropathy clinical course

A

Usually insidious onset of nephrotic syndrome
Proteinuria nonselective
Does not respond well to corticosteroids
Progressive sclerosis leads to increased creatinine and BUN and HTN
10% renal failure, 40% chronic disease
Recurs in 40% who receive transplant for ESRD

36
Q

Minimal change disease

A

Relatively benign
Diffuse effacement of foot processes, glomerulus appears normal, no deposits, lipoprotein reabsorption
Peak incidence between age 2 and 6
Some form of immune dysfunction - angiopoietin-like-4

37
Q

Minimal change disease clinical course

A

Massive proteinuria, renal function remains ok without hematuria and HTN
Drastically respond to corticosteroids although it may recur and individual may become steroid dependent

38
Q

Minimal change disease associated with

A 
Hodgkin lymphoma in adults as well as other lymphomas and leukemias
NSAID therapy (acute interstitial nephritis)
39
Q

Most common cause of nephrotic syndrome in adults in US

A

Focal Segmental Glomerulosclerosis

40
Q

Focal Segmental Glomerulosclerosis

A

Sclerosis of some glomeruli and only portion (segment) of capillary tuft is involved

Higher incidence of hematuria, reduced GFR and HTN
Proteinuria more nonselective
Poor response to corticosteroids
50% develop ESRD

41
Q

Types of FSGS

A 
Primary - idiopathic
In association - HIV, heroin use, sickle-cell, obesity
Secondary event - scarring
Adaptive response to loss of tissue
May be inherited
42
Q

Idiopathic FSGS

A

10% nephrotic syndrome in children

35% nephrotic syndrome in adults

43
Q

FSGS Pathogenesis

A

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RENAL II - Path and Phys Exam 1 (3 decks)

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