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Renal II Cumulative Final > Renal Path 1 > Flashcards

Renal Path 1 Flashcards

1
Q

Most common cause of chronic renal failure/end stage renal disease

A

Diabetes

[second most common is HTN]

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2
Q

A daily dose of _____ may slow the decline of renal function in people with CKD

A

Folic acid

[people with CKD have a high prevalence of hyperhomocysteinemia which is associated with folate deficiency and increased risk for stroke/ASCVD]

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3
Q

More than 50% of those over 50 have ____ in the renal parenchyma

A

Cysts

[often small and asymptomatic, generally incidental findings; most common are simple cysts, but can be multilocular, may represent dysplastic kidney, polycystic disease, or a cystic tumor]

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4
Q

What is the most likely mechanism of edema present with renal disease?

A

Loss of plasma proteins (proteinuria) d/t glomerular damage —> loss of plasma oncotic pressure in vessels —> edema

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5
Q

Techniques utilized on renal biopsy include light microscopy, fluorescence microscopy, and electron microscopy

What test are these methods usually correlated with?

A

Urinalysis

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6
Q

What has the largest spike and lies closest to the positive pole in serum protein electrophoresis?

A

Albumin

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7
Q

Thin layer chromatography is used to look for what in serum?

A

Serum protein
IgG, IgA, IgM
Kappa and lambda light changes

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8
Q

4 major compartments/components of kidney used to categorize renal disease

A

Glomeruli (e.g., glomerulonephritis)

Tubules (e.g., Bence-Jones proteinuria)

Interstitium (e.g., fibrosis, inflammation, or edema)

Vessels (e.g., vasculitis, nephrosclerosis)

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9
Q

The general category of glomerular disorders is considered predominantly due to ______ disease; primary or secondary

A

Immunologic

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10
Q

What is azotemia?

A

Biochemical abnormality indicating an elevation of BUN and creatinine levels; usually related to decreased GFR

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11
Q

Azotemia is generally a result of renal disorders but may arise from 2 categories of extra-renal insults — what are they?

A

Prerenal azotemia — occurs after hypoperfusion of kidneys (hemorrhage, shock, volume depletion, and CHF) that impairs renal function in the absence of primary renal parenchymal damage

Postrenal azotemia — seen whenever urine flow is obstructed distal to calyces and renal pelvis; removal of obstruction corrects the azotemia

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12
Q

____ = azotemia + a constellation of clinical findings and biochemical abnormalities resulting from renal damage

A

Uremia

[generally a manifestation of chronic renal failure]

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13
Q

What are some clinical signs/symptoms that may be included in uremia of chronic renal failure?

A

N/V, weight loss, fatigue, anorexia

Pruritis

Polydipsia

Electrolyte abnormalities, muscle cramping

Encephalopathy

Bleeding manifestations d/t platelet dysfunction and anemia

Pericarditis

Pleuritis/pleural effusion

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14
Q

Normal GFR

A

Range from 90-120

Rule of thumb = 100 mL/min

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15
Q

Clinical manifestations of AKI

A
  1. Rapid decline in GFR
  2. Most severe forms exhibit oliguria or anuria
  3. May result from glomerular, interstitial, vascular, or acute tubular injury (most common pattern is acute tubular necrosis)
  4. Can be reversible, or progress to CKD
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16
Q

Clinical manifestations of chronic kidney disease

A

When mild, it is clinically silent

When more severe, exhibits uremia

Defined by persistently diminished GFR <60ml/min for at least 3 months from any cause, OR persistent albuminuria

CKD is generally irreversible

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17
Q

Clinical manifestations of ESRD

A
  1. GFR < 5% of normal

2. End stage of uremia

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18
Q

Major clinical manifestations of Nephrotic syndrome

A

Characterized by severe proteinuria (> 3.5g/day but may be less in children)

Hypoalbuminemia (plasma levels <3g/dL)

Severe edema

Hyperlipidemia

Lipiduria

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19
Q

Major clinical manifestations of nephritic syndrome

A

Dominated by acute onset of grossly visible hematuria

Azotemia and oliguria

Mild to moderate proteinuria

Hypertension

[proteinuria and edema are common, but not as severe as in nephrotic syndrome]

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20
Q

Clinical manifestations of rapidly progressive glomerulonephritis include signs of _____ syndrome with rapid decline in GFR; implies severe gomerular injury

A

Nephritic

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21
Q

General Pathologic responses of the glomerulus to injury

A

Hypercellularity of native cell populations, inflammatory cell infiltration, or crescent formation

Basement membrane thickening or deposits

Hyalinosis and sclerosis

[note that native cells include mesangial, endothelial, visceral epithelial (podocytes), etc.]

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22
Q

Examples of primary glomerulonephropathies

A

Acute proliferative (diffuse) glomerulonephritis

Rapidly progressive glomerulonephritis

Membranous glomerulopathy

Minimal-change disease

Focal segmental glomerulosclerosis

Membranoproliferative glomerulonephritis; dense deposit disease

IgA nephropathy

Chronic glomerulonephritis - end stage

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23
Q

Systemic diseases with glomerular involvement

A

SLE
DM

Amyloidosis
Goodpasture
Microscopic polyarteritis/angiitis
Wegener granulomatosis
Henoch-schonlein purpura
Bacterial endocarditis
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24
Q

Hereditary disorders with renal involvement

A

Alport syndrome (x-linked)

Thin Basement Membrane disease

Fabry disease

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25
Q

Diseases associated with glomerular subepithelial humps seen on microscopy

A

Acute glomerulonephritis

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26
Q

Diseases associated with epimembranous glomerular deposits on microscopy

A

Membranous nephropathy

Heymann glomerulonephritis

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27
Q

Diseases associated with subendothelial glomerular deposits seen on microscopy

A

Lupus nephritis

Membranoproliferative glomerulonephritis

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28
Q

Disease associated with mesangial deposits on microscopy

A

IgA nephropathy

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29
Q

Immune mechanisms of glomerular injury

A

Ab-mediated:
In-situ immune complex deposition—fixed, intrinsic tissue Ags (Goodpasture), or plated Ags (infectious etiology); Circulating immune complex deposition (SLE) — can be endogenous or exogenous

Cell-mediated immune injury

Activation of alternative complement

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30
Q

Descriptive patterns/distributions in categorization of glomerular disorders

A

Diffuse = involves all glomeruli

Focal = involves only subset of glomeruli

Segmental = of affected glomeruli, only portions are affected

Global = involves entire glomerulus

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31
Q

Once any renal disease, glomerular or otherwise, destroys functional nephrons and reduces the GFR to 30-50% of the normal rate, progression to end stage renal failure proceeds at a steady rate, independent of original stimulus or activity of the underlying disease.

The 2 major histologic features of such a progression are _____ and _____

A

Focal segmental glomerulosclerosis (FSGS); tubulointerstitial fibrosis

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32
Q

Most frequent clinical presentation and pathogenesis of postinfectious glomerulonephritis

A

Most frequent clinical presentation = nephritic syndrome

Pathogenesis = immune complex mediated; circulating or plated antigen

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33
Q

Glomerular pathology of postinfectious glomerulonephritis seen on light microscopy, fluorescence microscopy, and electron microscopy

A

Light: diffuse endocapillary proliferation, leukocytic infiltration

Fluorescence: granular IgG and C3 in GBM and mesangium; granular IgA in some cases

Electron: primarily subepithelial humps; subendothelial deposits in early stages

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34
Q

Most frequent clinical presentation and pathogenesis of Goodpasture syndrome

A

Presents as rapidly progressive glomerulonephritis

Pathogenesis: anti-GBM COL4-A3 antigen

35
Q

Goodpasture syndrome findings on microscopy

A

Light: extracapillary proliferation with crescents; necrosis

Fluorescence: linear IgG and C3; fibrin in crescents

Electron: no deposits; GBM disruptions; fibrin

36
Q

Most frequent clinical presentation and pathogenesis of chronic glomerulonephritis

A

Presents as chronic renal failure; pathogenesis is variable

37
Q

Chronic glomerulonephritis findings on microscopy

A

Hyalinized glomeruli

Fluorescence microscopy may be granular or negative

38
Q

Most frequent clinical presentation and pathogenesis of membranous nephropathy

A

Presents as nephrotic syndrome

Pathogenesis: in-situ immune complex formation; PLA2R antigen — in most cases of primary disease

39
Q

Microscopy findings with membranous nephropathy

A

Light: diffuse capillary wall thickening

Fluorescence: granular IgG and C3; diffuse

Electron: subepithelial deposits

40
Q

Most frequent clinical presentation and pathogenesis of minimal change disease

A

Presents as nephrotic syndrome

Pathogenesis unknown (possibly podocyte injury)

41
Q

Minimal change disease findings on microscopy

A

Light: normal; lipid in tubules

Fluorescence: negative

Electron: loss of foot processes; no deposits

42
Q

Most frequent clinical presentation and pathogenesis of focal segmental glomerulosclerosis

A

Presents as nephrotic syndrome; nonnephrotic proteinuria

Pathogenesis unknown

43
Q

FSGS findings on microscopy

A

Light: focal and segmental sclerosis and hyalinosis

Fluorescence: IgM + C3 in many cases

Electron: loss of foot processes, epithelial denudation

44
Q

Most frequent clinical presentation and pathogenesis of membranoproliferative glomerulonephritis (MPGN) type I

A

Presents with mixed pattern of nephritic/nephrotic syndrome

Pathogenesis = immue complex

45
Q

MPGN type I findings on microscopy

A

Light: mesangial proliferative or membranoproliferative patterns of proliferation; GBM thickening; splitting

Fluorescence: IgG++ C3; C1q ++C4

Electron: subendothelial deposits

46
Q

Most frequent clinical presentation and pathogenesis of dense deposit disease (MPGN type II)

A

Presents as hematuria and chronic renal failure

Pathogenesis: autoantibody; alternative complement pathway activation

47
Q

MPGN type II findings on microscopy

A

Light: mesangial proliferative or membranoproliferative patterns of proliferation; GBM thickening; splitting

Fluorescence: C3 [no C1q or C4]

Electron: dense deposits (intramembranous)

48
Q

Most frequent clinical presentation and pathogenesis of IgA nephropathy

A

Presents as recurrent hematuria or proteinuria

Unknown pathogenesis

49
Q

IgA nephropathy findings on microscopy

A

Light: focal mesangial proliferative glomerulonephritis; mesangial widening

Fluorescence: IgA +/- IgG, IgM, and C3 in mesangium

Electron: Mesangial and paramesangial dense deposits

50
Q

Pathogenesis of acute proliferative glomerulonephritis (diffuse)

A

Immune complex injury triggered by exogenous bacterial, viral, or fungal Ag

Historically antecedent infection by beta-hemolytic strep — specific nephritogenic strains of Lancefield Group A

51
Q

Microscopic findings in pts with acute proliferative glomerulonephritis

A

Marked hypercellularity — ranges from simple mesangial to complex endocapillary cell infiltrate

Leukocyte infiltration: exudative within glomerular tuft

[subepithelial humps, granular deposits of IgG, IgM, C3 along GBM]

52
Q

Describe presentation of acute proliferative glomerulonephritis (post-strep) in children

A

Generally ages 6-10

Typically 1-4 wks after pharyngitis or skin infection

Often SpeB (streptococcal pyogenic exotoxin B)

Often presents with malaise, fever, nausea, oliguria, and hematuria 1-2 weeks after recovery from sore throat

Dysmorphic red cells or RBC casts; mild proteinuria, periorbital edema, and mild/moderate HTN

53
Q

Describe presentation of acute proliferative glomerulonephritis (post-strep) in adults

A

More atypical and aggressive course

May exhibit sudden HTN or edema, frequently with elevated BUN

54
Q

Clinical course of acute proliferatieve glomerulonephritis (post-strep) in children vs. adults

A

Children tend to clear in 6-8 weeks; renal biopsy generally not indicated. Most recover completely with conservative therapy and no long term sequelae

Only 60% of adults recover completely with no sequelae; higher percentage than children progress to rapidly progressive GN, prolonged time to resolution, and progress to chronic glomerulonephritis

55
Q

Describe microscopic findings of crescentic glomerulonephritis (RPGN)

A

Collapsed, compacted glomerular tufts

Crescent-shaped mass of proliferating visceral and parietal epithelial cells

Rather rapid obliteration of urinary space

Infiltrates of macrophages and leukocytes

Characteristic wrinkling and disruption of GBM

56
Q

Types of RPGN

A

Type I = Anti-GBM Ab (renal-limited)

Type II = immune complex (idiopathic or post-infectious glomerulonephritis)

Type III = pauci-immune (ANCA-associated or idiopathic)

57
Q

What condition is associated with type I RPGN?

A

Goodpasture syndrome

58
Q

What conditions are associated with type II RPGN?

A

Lupus nephritis
Henoch-schonlein purpura
IgA nephropathy

59
Q

What conditions are associated with type III RPGN?

A

Granulomatosis with polyangiitis

Microscopic polyangiitis

[50% of primary renal diseases associated with RPGN have a type III pauci-immune pattern on immunofluorescence studies]

60
Q

what renal diseases are treated with plasmapheresis?

A

Goodpasture

TTP

61
Q

Most common cause of nephrotic syndrome (in primary glomerular disease) in children

A

Minimal-change disease

62
Q

What is the difference in pathogenesis of nephrotic syndrome in primary vs. secondary renal disease?

A

Primary:
Characteristic kidney pathologic changes in the absence of associated systemic disease — so ONLY the kidney is affected. Primary kidney disease is by far the most common cause of nephrotic syndrome in children (usually MCD)

Secondary:
Systemic diseases causing nephrotic disease (e.g., DM, SLE); with characteristic alterations in histomorphology. Secondary causes are more frequent in ADULTS

63
Q

Leading etiologies of nephrotic syndrome in systemic disease

A

DM and SLE are most common

Others: amyloidosis, drugs (NSAIDs, penicillamine), infection (malaria, syphilis, hep B and C, HIV), malignant disease, bee-sting allergy, hereditary nephritis

64
Q

About 75% of cases of membranous glomerulopathy are ______

Primary or secondary?

A

Primary!

[secondary causes include certain drugs, underlying malignancy, SLE, infection, other autoimmune dz,etc]

65
Q

Multiple proteins are found in the urine of people with membranous glomerulopathy, in other words the proteinuria is said to be _____

A

Nonselective

66
Q

Clinical course of membranous glomerulopathy

A

Proteinuria persists in 60% of pts

40% of these develop renal insufficiency

10% progress to ESRF

67
Q

Is MCD usually associated with selective or nonselective proteinuria?

A

Selective! Meaning primarily albuminuria

68
Q

A characteristic feature of MCD is a dramatic response to _____ therapy

A

Corticosteroid

69
Q

Most common overall cause of nephrotic syndrome in US adults

A

Primary FSGS

[note greater incidence in Hispanic and African-American pts]

70
Q

The 5-10% of MCD cases in children that does not respond to corticosteroid therapy generally exhibits ____ upon biopsy

A

FSGS

71
Q

How does the clinical presentation of idiopathic FSGS differ from MCD and other podocytopathies?

A

Higher incidence of hematuria, reduced GFR, and HTN

Proteinuria tends to be nonselective

Generally there is poor response to corticosteroids

Significant progression to CKD with at least 50% developing ESRD within 10 years

72
Q

Patients with HIV that are found to have a glomerulopathy are most likely to have _____

A

FSGS

73
Q

Which types of MPGN are most common in kids vs. adults?

A

MPGN type I Primary = most cases present in children or young adults; common presentation is nephrotic syndrome

MPGN type I Secondary = almost exclusively in adults; frequently associated with chronic antigenemia

74
Q

MPGN type I secondary has notably been a reflection of renal glomerular disease in patients with what other conditions?

A

Hepatitis C with cryoglobulinemia

Chronic immune complex disorders such as SLE endocarditis

Certain malignancies (CLL, lymphomas, melanoma)

75
Q

Which is more common, MPGN I or II?

A

MPGN I is more common

76
Q

___ is a more dominant clinical finding in MPGN type II, in contrast to the proteinuria seen in MPGN type I

A

Hematuria

77
Q

Which disease is associated with alternative pathway complement activation?

A

MPGN II (dense deposit disease)

C3NeF (nephritic factor) IgG autoantibody binds C3 convertase, leading to continuous activation of alternative pathway

Would see low levels of circulating complement

78
Q

Most common type of glomerulonephritis worldwide (Not in US!!)

A

IgA nephropathy

More common in Caucasians and Asians > African Americans

Male predominance

79
Q

Renal IgA nephropathy not associated with systemic disease

A

Berger disease

80
Q

IgA nephropathy associated with systemic disease, often exhibiting skin manifestations and involvement of abdominal viscera other than the kidney

A

Henoch-Schonlein purpura (HSP)

81
Q

IgA nephropathy has known associations with ____ enteropathy and ____ disease

A

Gluten; liver

82
Q

Clinical outcomes of IgA nephropathy

A

Recurrent episodes of hematuria without progression of renal disease in a majority of pts

Acute nephritic syndrome with HTN in 5-10%

Acute renal failure in 1-2%, associated wtih HTN, edema, oliguria, and crescenteric glomerulonephritis (RPGN)

Chronic renal failure in 15-40% as a slowly progressive disease over 20 year period

83
Q

What condition is MOST likely to progress to chronic glomerulonephritis?

A

Crescentic glomerulonephritis (RPGN) — 90%

[others include FSGS, membranoproliferative, IgAN, membranous nephropathy]

Renal II Cumulative Final (20 decks)

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