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Pathology > Kidney Path > Flashcards

Kidney Path Flashcards

1
Q

nephrotic syndrome

A 
severe proteinuria
hypoalbuminemia
generalized edema
hyperlipidemia
lipiduria
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2
Q

nephritic syndrome

A 
hematuria
azotemia
oliguria
hypertension
proteinuria
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3
Q

causes of nephrotic syndrome

A 
Minimal Change Disease (MCD)
Membranous Glomerulonephritis
(MGN)
Focal Segmental
Glomerulosclerosis (FSGS)
Membranoproliferative
Glomerulonephritis (MPGN)
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4
Q

Minimal Change Disease (MCD)

A

n most frequent cause of the nephrotic
syndrome in children
n glomeruli have normal appearance under
the light microscope, but electron
microscopy reveals diffuse loss of visceral
epithelial foot processes

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5
Q

what is universal to nephrotic syndrome

A

fusion of podocytes

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6
Q

Minimal Change Disease (MCD) path

A

current evidence points to a disorder of T cells
-elaborate factors (IL-8, TNF, etc.?) that affect
nephrin synthesis

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7
Q

Minimal Change Disease (MCD) gold standard for diagnosis

A

EM

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8
Q

Minimal Change Disease (MCD) immunofluorescence?

A

no

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9
Q

Minimal Change Disease (MCD) clinical course

A

Insidious development of nephrotic syndrome in
otherwise healthy child (peak age, 2-6)
-Usually follows respiratory infection or prophylactic
immunization; assoc. w/atopic disorders
Selective proteinuria (mainly albumin)
Good prognosis
>90% respond to short course of corticosteroids
<5% develop chronic renal failure after 25 years

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10
Q

Membranous Glomerulonephritis

MGN

A 
most common cause of
nephrotic syndrome in
adults (peak age, 30-50)
n glomeruli appear normal
early in the disease, but
develop diffuse thickening
of the capillary walls
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11
Q

Membranous Glomerulonephritis

(MGN) path

A

form of chronic immune complex nephritis
-idiopathic forms (85% of cases) are mainly autoimmune
*antibodies react to antigens in the glomerulus components, or to
antigens that have become trapped there
-may also be due to circulating complexes of known exogenous
or endogenous antigen
the membrane attack complex of complement (C5b-C9)
activates mesangial and epithelial cells, causing them to
liberate proteases and oxidants that damage glomerular
capillaries

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12
Q

Membranous Glomerulonephritis

(MGN) key to dianosis

A

silver stain

detects collagen in BM

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13
Q

Membranous Glomerulonephritis

(MGN) clinical course

A

Insidious development of nephrotic syndrome
Proteinuria is nonselective and does not respond
to corticosteroid therapy
Variable course
40% suffer progressive disease ending in renal failure
after 2-10 years
10-30% follow benign course with partial or complete
remission

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14
Q

Focal Segmental

Glomerulosclerosis (FSGS)

A

characterized by sclerosis affecting some
but not all glomeruli and involving only
segments of each glomerulus
most well-known association is with HIV
patients and IV drug users, but occurs in
all ages (more common in African-
American populations)

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15
Q

Focal Segmental

Glomerulosclerosis (FSGS) path

A

unknown (some have suggested it is an
aggressive variant of minimal change
disease)
circulating mediator is likely responsible
-proteinuria recurs soon after renal transplant

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16
Q

Focal Segmental

Glomerulosclerosis (FSGS) diagnosis

A

IF usually isn’t done, but detects IgM and

C3 in sclerotic segments

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17
Q

Focal Segmental

Glomerulosclerosis (FSGS) clinical course

A

May be a primary disease or result from other
forms of GN (esp. IgA nephropathy)
Proteinuria is nonselective and has poor
response to corticosteroid therapy
Higher incidence of hematuria and hypertension
(more likely to evolve from nephritic syndromes)
Prognosis is poor, with children faring slightly
better than adults
-50% suffer renal failure after 10 years

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18
Q

Membranoproliferative

Glomerulonephritis (MPGN)

A

may be nephritic, nephrotic, or mixed
characterized by alterations in the GBM
and mesangium plus proliferation of
glomerular cells

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19
Q

Membranoproliferative

Glomerulonephritis (MPGN) Type I

A

(2/3rds of cases)
Circulating immune complexes of unknown antigen
-Associated with hepatitis B and C, SLE, infected
atrioventricular shunts, chronic lymphocytic leukemia

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20
Q

Membranoproliferative

Glomerulonephritis (MPGN) Type II

A

Less clear, but serum of patients has a factor called C3
nephritic factor (C3NeF)
Activates the alternative complement pathway by stabilizing
C3 convertase
hypocomplementemia, but normal C1, C2, C4

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21
Q

Membranoproliferative

Glomerulonephritis (MPGN) key to diagnosis

A

“doubled” GBM on silver stain

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22
Q 
Membranoproliferative
Glomerulonephritis (MPGN) EM varies by type
A 
Type I: subendothelial
deposits
Type II: dense
deposits in center of
GBM and under
endothelium
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23
Q

Causes of Nephritic Syndrome

A 
Acute Proliferative (Poststreptococcal)
Glomerulonephritis (PGN)
Rapidly Progressive (Crescentic)
Glomerulonephritis (RPGN or CrGN)
IgA Nephropathy (Berger Disease)
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24
Q 
Acute Proliferative (Poststreptococcal)
Glomerulonephritis (PGN)
A

Typically caused by immune complexes of
exogenous or endogenous antigens
-Prototype exogenous pattern = 1-4 weeks after a
streptococcal infection
*Only “nephritogenic” strains of group A β-hemolytic
streptococci associated
*Most cases follow skin or pharynx infection
Children affected more frequently than adults

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25
Q 
Acute Proliferative (Poststreptococcal)
Glomerulonephritis (PGN) path
A 
Immune complex formation, but unclear if
complexes are simply trapped as they
pass through the glomerulus, or if C3 is
deposited on GBM before IgG
subepithelial humps
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26
Q 
Acute Proliferative (Poststreptococcal)
Glomerulonephritis (PGN) Clinical Course
A

Abrupt onset, with malaise, slight fever, nausea, and
nephritic syndrome
Hematuria: urine appears smoky brown
Hypocomplementemia; elevated serum antistreptolysin
O titers in poststreptococcal cases
Children: complete recovery in most (95%)
Adults: complete recovery (60%); many develop RPGN
or chronic GN

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27
Q 
Rapidly Progressive (Crescentic)
Glomerulonephritis (RPGN or CrGN)
A

Clinical syndrome (not a specific etiologic form of
GN)
Characterized by rapid and progressive loss of
renal function associated with severe oliguria
and (if untreated) death from renal failure in
weeks to months
All types demonstrate crescents (proliferation of
parietal cells/migration of monocytes into
Bowman’s space)

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28
Q 
Rapidly Progressive (Crescentic)
Glomerulonephritis (RPGN or CrGN) type I
A

anti-GBM disease
Type IV collagen is target
Linear deposits of IgG (sometimes C3 also) on GBM
In some patients, anti-GBM antibodies also bind to pulmonary
alveolar capillary basement membranes = GOODPASTURE
SYNDROME
-Goodpasture antigen is noncollagenous component of Type IV
collagen
-Males > females; peak age is 20-40 y.o.
-Pulmonary involvement precedes renal disease
*Pulmonary hemorrhage and recurrent hemoptysis
-Plasmapheresis is beneficial (removes pathogenic antibodies)
Least common of all CrGN types

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29
Q 
Rapidly Progressive (Crescentic)
Glomerulonephritis (RPGN or CrGN) Type II CrGN
A

Complication of any immune complex nephritides
(PGN, SLE, IgA nephropathy)
Granular IF pattern

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30
Q 
Rapidly Progressive (Crescentic)
Glomerulonephritis (RPGN or CrGN) Type III GrGN (pauci-immune type CrGN)
A

Component of a systemic vasculitis, like microscopic
polyangiitis or Wegener granulomatosis, or idiopathic
Most have serum ANCAs
No anti-GBM antibodies or immune complexes

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31
Q 
Rapidly Progressive (Crescentic)
Glomerulonephritis (RPGN or CrGN)
A

Crescents obliterate the Bowman’s space

and compress the glomeruli

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32
Q 
Rapidly Progressive (Crescentic)
Glomerulonephritis (RPGN or CrGN) clinical course
A

Typical nephritic syndrome, but oliguria and
azotemia more pronounced
Rapid progression to severe renal failure; longterm
dialysis or transplantation required
Prognosis roughly related to crescent number
(<80% crescents means better prognosis) and
type

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33
Q

IgA Nephropathy (Berger Disease)

A

Most common glomerular disease, and one of
most common causes of recurrent hematuria
Usually affects children and young adults (mostly
males)
Typical presentation = gross hematuria that
occurs 1-2 days after a nonspecific respiratory
tract infection; disappears, but recurs every few
months

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34
Q

IgA Nephropathy (Berger Disease) path

A

Genetic or acquired abnormality of IgA
production and clearance
-IgA synthesis is increased in response to respiratory
or GI exposure to antigen
*IgA nephropathy occurs with increased frequency in patients
with celiac sprue and liver disease
-IgA and IgA complexes are entrapped in the
mesangium, where they activate the alternative
complement pathway and cause glomerular injury
Proposed to be a variant of Henoch-Schönlein purpura

35
Q

IgA Nephropathy (Berger Disease) clinical course

A 
Typically presents with loin pain, gross
hematuria; usually after respiratory,
gastrointestinal, or urinary infection
Some develop slow progression to chronic
renal failure in 20 years
36
Q

Hereditary Nephritis

A

Group of hereditary familial renal diseases
Best studied is Alport syndrome
-GBM defect due to mutation in type IV collagen components
-Nephritis accompanied by nerve deafness and eye disorders,
including lens dislocation, posterior cataracts, and corneal
dystrophy
-Males affected more frequently, more severely
Patients present at age 5-20 y.o., and develop renal
failure by 20-50 yoa
Heterogenous inheritance (X-linked, autosomal
recessive, or autosomal dominant)

37
Q

Chronic Glomerulonephritis

A 
The final stage of many forms of
glomerular disease; characterized by
progressive renal failure, uremia, and
untimely death
Usually from rapidly progressive GN, focal glomeulosclerosis, membranoproliferative GN
38
Q

signs & symptoms of Chronic Glomerulonephritis

A 
decreased renal acuity
cramps
restless leg
sleep disturbances
bone disease
itching
anemia
39
Q

Chronic Glomerulonephritis morphology

A

Kidneys small with

granular surface

40
Q

Chronic Glomerulonephritis clinical course

A 
Usually undiscovered until late
in its course, when symptoms
of renal insufficiency develop
(proteinuria, hypertension,
azotemia, anasarca, anemia,
anorexia)
Urinalysis: broad waxy casts
Dialysis and renal
transplantation required
41
Q

Chronic Diabetic Glomerulopathy risk factors

A

Poor glycemic control
hypertension
diabetic retinopathy (high
correlation)

42
Q

Diabetic Glomerulopathy path

A 
Nonenzymatic glycosylation (NEG)
-glomerular and tubular BMs
-arterioles (efferent 1st)
osmotic damage to glomerular capillary
endothelial cells
- glucose → osmotically active sorbitol
hyperfiltration damage to mesangium
 diabetic microangiopathy
43
Q

Diabetic Glomerulopathy clinical features

A

Microalbuminuria
-first lab manifestation (usually after ~10 y of poor
glycemic control)
-microalbuminuria dipsticks detect albumin levels 1.5-8
mg/dL
increased susceptibility to acute and chronic
pyelonephritis
infarction of renal papillae = papillary necrosis
most common cause of chronic renal failure in
U.S.

44
Q

Renal amyloidosis

A

B-2 microglobulin

45
Q

Acute Pyelonephritis

A 
if obstruction prevents draining, the renal
pelvis, calyces, and ureter may fill with
exudate = pyonephrosis
-pus under pressure
may develop ischemic and suppurative
necrosis of the renal pyramid tips =
papillary necrosis
-more common in diabetics
papillary necrosis
46
Q

Acute Pyelonephritis clinical course

A

Fever, chills, malaise
Dysuria, frequency, and urgency
Costovertebral angle (CVA) tenderness
Urinalysis shows WBC casts and pyuria

47
Q

Chronic Pyelonephritis

A 
Due to recurrent infections promoted by
chronic obstruction or reflux
-Chronic Obstructive Pyelonephritis
-Chronic Reflux-Associated Pyelonephritis
Important cause of chronic renal failure
48
Q

Chronic Pyelonephritis morphology

A 
Uneven scarring of
the pelvis and/or
calyces
-Leads to blunted
calyces
49
Q

Chronic Pyelonephritis clinical course

A

Unnoticed until renal insufficiency begins;
may cause hypertension
n Some develop FSGS

50
Q

Acute Drug-Induced Interstitial

Nephritis (aka, Acute TIN)

A

Adverse reaction to drugs that begins ~15 days (range,
2-40 days) after exposure
-Synthetic antibiotics, especially penicillins
-Diuretics (thiazides)
-Nonsteroidal anti-inflammatory agents (phenylbutazone)

51
Q

Acute Drug-Induced Interstitial

Nephritis (aka, Acute TIN) path

A

Drugs acts as haptens that covalently bind to
cytoplasmic or extracellular component of tubular cells
and become immunogenic
eosinophils in the urine help support the
diagnosis

52
Q

Acute Drug-Induced Interstitial

Nephritis (aka, Acute TIN) Clinical Course

A

Fever
Eosinophilia (may be transient)
Rash (only ~25% of patients)
Renal abnormalities: hematuria, minimal or no
proteinuria, leukocytouria
A rising serum creatinine level or acute renal failure with
oliguria develops in about 50% of cases (esp. elderly)
Withdrawal of offending drug results in recovery (may
take months)

53
Q

Analgesic Nephropathy

A 
Seen in patients consuming large
quantities of analgesics
-Most consume mixtures containing some
combination of phenacetin, aspirin,
acetaminophen, caffeine, and codeine for long
periods
papillary necrosis
54
Q

Analgesic Nephropathy clinical course

A 
Chronic renal failure (more common in
those with preexisting renal disease),
hypertension, anemia
Increased incidence of transitional cell
carcinoma
55
Q

Acute Tubular Necrosis

A

The most common cause of acute renal failure
Characterized by destruction of tubular epithelial
cells
Generally a reversible lesion that arises in a
variety of clinical settings:
Ischemic Type = due to decreased blood flow (e.g.,
severe hemorrhage, shock, dehydration)
Nephrotoxic Type = death of tubular cells due to
poisons, drugs

56
Q

Acute Tubular Necrosis: Nephrotoxic Type

A

Aminoglycosides (#1 cause) and other drugs
IV radiographic contrast agents (#2 cause)
Heavy metals (e.g., mercury, gold, lead)
Organic solvents (e.g., carbon tetrachloride)
Ethylene glycol
Mushroom poisoning
Pesticides
Myoglobin (from crushing injuries)

57
Q

Acute Tubular Necrosis Clinical Course

A

Oliguria and elevation of blood urea nitrogen and
creatinine
Metabolic acidosis and hyperkalemia
Urinalysis: dirty brown granular casts and
epithelial casts
Prognosis is excellent in nephrotoxic ATN if
patient survives the disease responsible

58
Q

normal BUN & creatinine

A

BUN: 7-18 mg/dL
creatinine = 0.6-1.2 mg/dL
Ratio should be ~15:1

59
Q

Pre-renal azotemia

A

caused by a decrease in cardiac output to kidneys (e.g., blood loss,
CHF) that ↓GFR
BUN:Cr > 15

60
Q

Renal (intrinsic) azotemia

A

caused by damage to the kidneys (e.g., ATN, chronic renal failure)
BUN:Cr ≤ 15

61
Q

Post-renal azotemia

A

↓GFR due to obstruction and increased tubular pressure causes backdiffusion
of urea into blood
BUN:Cr > 15
**persistent obstruction will lead to renal azotemia

62
Q

Benign Nephrosclerosis

A 
term for the renal
changes observed in
benign hypertension
-always associated with
hyaline
arteriolosclerosis
* homogeneous, pink
hyaline thickening of
the vessel lumen
63
Q

Benign Nephrosclerosis morphology

A 
kidneys atrophy --> grain
leather appearance
does not cause severe
damage to kidneys
-↓ GFR
-loss of concentrating
ability
64
Q

Malignant nephrosclerosis

A

associated with malignant hypertension
-always associated with hyperplastic
arteriolosclerosis

65
Q

Malignant nephrosclerosis morphology

A

small, pinpoint petechial hemorrhages
cover the kidney surface
-“flea-bitten kidney”

66
Q

Malignant nephrosclerosis clinical course

A

Diastolic pressure >120 mm Hg, papilledema,
encephalopathy, cardiovascular abnormalities, renal
failure
At onset, there is marked proteinuria and hematuria, but
no significant alteration in renal function
-quickly progresses to renal failure, so treat as medical
emergency
~50% survive 5 years; 90% of deaths caused by uremia

67
Q

Simple Cysts

A 
occur as multiple or single
cystic spaces in renal cortex
-~1-5 cm in diameter; filled with
clear fluid
no clinical significance;
common postmortem finding
main importance is
differentiation from tumors
(usually simply via ultrasound)
68
Q

Dialysis-associated cystic change

A

occur in patients with end-stage renal disease that
have undergone prolonged dialysis
present in both cortex and medulla, and may bleed,
causing hematuria
increase risk for adenomas and adenocarcinomas

69
Q 
Autosomal Dominant (Adult)
Polycystic Kidney Disease
A 
multiple expanding cysts
of both kidneys that
destroy underlying
parenchyma
important cause of
chronic renal failure
(~10% of cases)
70
Q 
Autosomal Dominant (Adult)
Polycystic Kidney Disease path
A

caused by inheritance of an autosomal dominant
polycystin (PKD) gene, either PKD1 (90% of
families) or PKD2
-both genes encode proteins of unknown function, but
have homology to those involved in cell-cell or cellmatrix adhesion
pressure of expanding cysts leads to
ischemic atrophy of renal parenchyma

71
Q 
Autosomal Dominant (Adult)
Polycystic Kidney Disease clinical course
A 
usually does not produce symptoms until
the 4th decade
-flank pain; "heavy, dragging sensation"
-intermittent gross hematuria
-superimposed hypertension and urinary
infection are most important complications
Berry aneurysms of the circle of Willis
present in 10-30% of patients
- high incidence of subarachnoid hemorrhage
Asymptomatic liver cysts in 1/3rd of
patients
72
Q 
Autosomal Dominant (Adult)
Polycystic Kidney Disease prognosis
A 
better than
other most chronic
renal diseases
-slow progression; renal
failure occurs, on
average, at 50 yoa, but
variable
- treat with renal transplantation
73
Q 
Autosomal Recessive (Childhood)
Polycystic Kidney Disease path
A

rare polycystic kidney disease with perinatal,
neonatal, infantile, and juvenile categories
caused by inheritance of two mutated copies of
the fibrocystin gene (PKHD1)
- unknown function, but may be a receptor with role in
collecting-duct and biliary differentiation

74
Q 
Autosomal Recessive (Childhood)
Polycystic Kidney Disease presentation
A

numerous small cysts in the cortex and medulla;
give kidney sponge-like appearance
- all cysts derive from collecting tubules

75
Q 
Autosomal Recessive (Childhood)
Polycystic Kidney Disease clinical course
A 
perinatal and neonatal
forms are most common
- cysts present at birth
- may die quickly from
pulmonary or renal failure
- patients surviving infancy
develop liver cirrhosis
76
Q

Urolithiasis

Renal Calculi, Stones

A

stones may arise at any level in the urinary
tract, but the kidney is the most common site
affect 5-10% of Americans in their lifetime
- men > women; peak age: 20-30s
-most commonly contain calcium oxalate (70%),
followed by magnesium ammonium phosphate
(struvite), uric acid, and cystine

77
Q

Urolithiasis

(Renal Calculi, Stones) path

A

increased urine concentration of the
stone’s constituents so that it exceeds
their solubility in urine (supersaturation)
e.g., hypercalciuria associated with calcium
oxalate stones

78
Q

Magnesium ammonium
phosphate (struvite)
stones

A 
associated with UTIs
caused by urea-splitting
bacteria (e.g., Proteus sp.)
bacteria also serve as nidus
for stone formation
79
Q

Uric acid stones

A

predisposition with gout, diseases involving
rapid cell turnover (leukemias), and low urine
pH (<5.5)

80
Q

Cystine stones

A

genetic defect in renal transport of amino acids

81
Q

Urolithiasis

(Renal Calculi, Stones) clinical course

A 
renal or ureteral colic
- flank pain radiating toward the groin
gross hematuria
predispose to bacterial infection; large
stone may cause hydronephrosis
82
Q

Hydronephrosis

A

dilation of the renal pelvis and calyces, with
atrophy of the parenchyma, caused by
obstruction to urine outflow

83
Q

Hydronephrosis morphology

A

kidney may be massively enlarged
renal parenchyma is compressed and atrophied;
papillae are obliterated and pyramids are flattened

84
Q

Hydronephrosis clinical course

A 
complete bilateral obstruction (below ureters)
causes anuridia, but partial bilateral obstruction
causes polyuria (due to defects in tubular
concentrating mechanism)
unilateral obstruction often remains silent for
long period
reversible if obstruction is removed within a few
weeks

Pathology (16 decks)

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