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CPR EXAM 2 > 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
Diseases associated with glomerular subepithelial humps seen on microscopy
Acute glomerulonephritis
26
Diseases associated with epimembranous glomerular deposits on microscopy
Membranous nephropathy Heymann glomerulonephritis
27
Diseases associated with subendothelial glomerular deposits seen on microscopy
Lupus nephritis Membranoproliferative glomerulonephritis
28
Disease associated with mesangial deposits on microscopy
IgA nephropathy
29
Immune mechanisms of glomerular injury
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
30
Descriptive patterns/distributions in categorization of glomerular disorders
Diffuse = involves all glomeruli Focal = involves only subset of glomeruli Segmental = of affected glomeruli, only portions are affected Global = involves entire glomerulus
31
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 _____
Focal segmental glomerulosclerosis (FSGS); tubulointerstitial fibrosis
32
Most frequent clinical presentation and pathogenesis of postinfectious glomerulonephritis
Most frequent clinical presentation = nephritic syndrome Pathogenesis = immune complex mediated; circulating or plated antigen
33
Glomerular pathology of postinfectious glomerulonephritis seen on light microscopy, fluorescence microscopy, and electron microscopy
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
34
Most frequent clinical presentation and pathogenesis of Goodpasture syndrome
Presents as rapidly progressive glomerulonephritis Pathogenesis: anti-GBM COL4-A3 antigen
35
Goodpasture syndrome findings on microscopy
Light: extracapillary proliferation with crescents; necrosis Fluorescence: linear IgG and C3; fibrin in crescents Electron: no deposits; GBM disruptions; fibrin
36
Most frequent clinical presentation and pathogenesis of chronic glomerulonephritis
Presents as chronic renal failure; pathogenesis is variable
37
Chronic glomerulonephritis findings on microscopy
Hyalinized glomeruli Fluorescence microscopy may be granular or negative
38
Most frequent clinical presentation and pathogenesis of membranous nephropathy
Presents as nephrotic syndrome Pathogenesis: in-situ immune complex formation; PLA2R antigen — in most cases of primary disease
39
Microscopy findings with membranous nephropathy
Light: diffuse capillary wall thickening Fluorescence: granular IgG and C3; diffuse Electron: subepithelial deposits
40
Most frequent clinical presentation and pathogenesis of minimal change disease
Presents as nephrotic syndrome Pathogenesis unknown (possibly podocyte injury)
41
Minimal change disease findings on microscopy
Light: normal; lipid in tubules Fluorescence: negative Electron: loss of foot processes; no deposits
42
Most frequent clinical presentation and pathogenesis of focal segmental glomerulosclerosis
Presents as nephrotic syndrome; nonnephrotic proteinuria Pathogenesis unknown
43
FSGS findings on microscopy
Light: focal and segmental sclerosis and hyalinosis Fluorescence: IgM + C3 in many cases Electron: loss of foot processes, epithelial denudation
44
Most frequent clinical presentation and pathogenesis of membranoproliferative glomerulonephritis (MPGN) type I
Presents with mixed pattern of nephritic/nephrotic syndrome Pathogenesis = immue complex
45
MPGN type I findings on microscopy
Light: mesangial proliferative or membranoproliferative patterns of proliferation; GBM thickening; splitting Fluorescence: IgG++ C3; C1q ++C4 Electron: subendothelial deposits
46
Most frequent clinical presentation and pathogenesis of dense deposit disease (MPGN type II)
Presents as hematuria and chronic renal failure Pathogenesis: autoantibody; alternative complement pathway activation
47
MPGN type II findings on microscopy
Light: mesangial proliferative or membranoproliferative patterns of proliferation; GBM thickening; splitting Fluorescence: C3 [no C1q or C4] Electron: dense deposits (intramembranous)
48
Most frequent clinical presentation and pathogenesis of IgA nephropathy
Presents as recurrent hematuria or proteinuria Unknown pathogenesis
49
IgA nephropathy findings on microscopy
Light: focal mesangial proliferative glomerulonephritis; mesangial widening Fluorescence: IgA +/- IgG, IgM, and C3 in mesangium Electron: Mesangial and paramesangial dense deposits
50
Pathogenesis of acute proliferative glomerulonephritis (diffuse)
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
Microscopic findings in pts with acute proliferative glomerulonephritis
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
Describe presentation of acute proliferative glomerulonephritis (post-strep) in children
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
Describe presentation of acute proliferative glomerulonephritis (post-strep) in adults
More atypical and aggressive course May exhibit sudden HTN or edema, frequently with elevated BUN
54
Clinical course of acute proliferatieve glomerulonephritis (post-strep) in children vs. adults
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
Describe microscopic findings of crescentic glomerulonephritis (RPGN)
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
Types of RPGN
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
What condition is associated with type I RPGN?
Goodpasture syndrome
58
What conditions are associated with type II RPGN?
Lupus nephritis Henoch-schonlein purpura IgA nephropathy
59
What conditions are associated with type III RPGN?
Granulomatosis with polyangiitis Microscopic polyangiitis [50% of primary renal diseases associated with RPGN have a type III pauci-immune pattern on immunofluorescence studies]
60
what renal diseases are treated with plasmapheresis?
Goodpasture | TTP
61
Most common cause of nephrotic syndrome (in primary glomerular disease) in children
Minimal-change disease
62
What is the difference in pathogenesis of nephrotic syndrome in primary vs. secondary renal disease?
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
Leading etiologies of nephrotic syndrome in systemic disease
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
About 75% of cases of membranous glomerulopathy are ______ | Primary or secondary?
Primary! [secondary causes include certain drugs, underlying malignancy, SLE, infection, other autoimmune dz,etc]
65
Multiple proteins are found in the urine of people with membranous glomerulopathy, in other words the proteinuria is said to be _____
Nonselective
66
Clinical course of membranous glomerulopathy
Proteinuria persists in 60% of pts 40% of these develop renal insufficiency 10% progress to ESRF
67
Is MCD usually associated with selective or nonselective proteinuria?
Selective! Meaning primarily albuminuria
68
A characteristic feature of MCD is a dramatic response to _____ therapy
Corticosteroid
69
Most common overall cause of nephrotic syndrome in US adults
Primary FSGS [note greater incidence in Hispanic and African-American pts]
70
The 5-10% of MCD cases in children that does not respond to corticosteroid therapy generally exhibits ____ upon biopsy
FSGS
71
How does the clinical presentation of idiopathic FSGS differ from MCD and other podocytopathies?
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
Patients with HIV that are found to have a glomerulopathy are most likely to have _____
FSGS
73
Which types of MPGN are most common in kids vs. adults?
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
MPGN type I secondary has notably been a reflection of renal glomerular disease in patients with what other conditions?
Hepatitis C with cryoglobulinemia Chronic immune complex disorders such as SLE endocarditis Certain malignancies (CLL, lymphomas, melanoma)
75
Which is more common, MPGN I or II?
MPGN I is more common
76
___ is a more dominant clinical finding in MPGN type II, in contrast to the proteinuria seen in MPGN type I
Hematuria
77
Which disease is associated with alternative pathway complement activation?
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
Most common type of glomerulonephritis worldwide (Not in US!!)
IgA nephropathy More common in Caucasians and Asians > African Americans Male predominance
79
Renal IgA nephropathy not associated with systemic disease
Berger disease
80
IgA nephropathy associated with systemic disease, often exhibiting skin manifestations and involvement of abdominal viscera other than the kidney
Henoch-Schonlein purpura (HSP)
81
IgA nephropathy has known associations with ____ enteropathy and ____ disease
Gluten; liver
82
Clinical outcomes of IgA nephropathy
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
What condition is MOST likely to progress to chronic glomerulonephritis?
Crescentic glomerulonephritis (RPGN) — 90% [others include FSGS, membranoproliferative, IgAN, membranous nephropathy]

CPR EXAM 2 (52 decks)

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