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CPR II Exam #2 > Renal Pathology II > Flashcards

Renal Pathology II Flashcards

1
Q

What is Hereditary Nephritis?

A

It’s a group of heterogenous familial renal diseases associated with mutations in collagen genes and manifest mostly as glomerular injury.

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2
Q

What 2 diseases are classified as Hereditary Nephritidies?

A

Alport syndrome

Thin basement membrane disease (benign familial hematuria)

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3
Q

What symptoms predispose many patients (85%) to developing a hereditary nephridity?

A

Family history of hematuria or recurrent hematuria in childhood

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4
Q

What is the clinical manifestation of Alport syndrome?

A

Hematuria with progression to CRF, along with:

  • nerve deafness
  • various eye disorders: lens dislocation, posterior cataracts and corneal dystrophy
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5
Q

What is the progression of Alport syndrome?

A

Approx. 90% of affected males (X-linked disease) will progress to ESRD by 40 y/o.

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6
Q

What is the pathogenesis of Alport syndrome?

A

Mutations in genes coding for subunits of collagen IV, which is crucial for GBM, lens and cochlea.

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7
Q

What is the morphological appearance of the GBM on EM in Alport syndrome?

A

Irregular thickening of BM

Lamination of lamina densa

Foci of rarefraction

*Considered to appear “moth-eaten”

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8
Q

At what age do most patients present with Alport syndrome? What is the major presentation? AT what point does it progress to RF?

A

Hematuria (gross or microscopic) generally at age 5-20 y/o and renal failure by 50 y/o in men

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9
Q

Thin basement membrane disease’s presentation:

A

Often ASX with microscopic hematuria. If proteinuria is present, it is mild to moderate.

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10
Q

Thin basement membrane disease is “characterized by…”

A

Hematuria due to thinned GBM, only approx. 150-250 nm.

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11
Q

What us the progression of Thin basement membrane disease?

A

Renal function is unremarkable and progression to ESRD is uncommon.

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12
Q

What is the pathogenesis of Thin basement membrane disease?

What is the inheritance (homo- or hetero-)?

A

Mutations in genes encoding a3 or a4 chains of type IV collagen.

Mostly are heterzygous.

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13
Q

Which systemic diseases can cause secondary renal diseases that present with Nephrotic syndrome? (4)

A

Diabetic nephropathy
SLE
Hep C (MPGN type I)
HIV nephropathy (FSGS)

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14
Q

Which systemic diseases can cause secondary renal diseases that present with acute nephritic syndrome - or hematuria? (4)

A

SLE
Bacterial endocarditis (acute proliferative GN)
Goodpasture syndrome
Henoch-Schonlein purpura (IgA nephropathy)

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15
Q

30% of ESRF patients are due to:

A

Diabetic kidney disease. 40% of DM patients will progress to ESRD.

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16
Q

What are the 2 major processes that play a role in the development of diabetic glomerular lesions?

A

A metabolic defect linked to hyperglycemia

Hemodynamic effects associated with glomerular hypertrophy

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17
Q

What is the major morphological appearance of diabetic nephropathy? (3 features)

A

Diffuse capillary BM thickening

Diffuse mesangial sclerosis

**Nodular glomerulosclerosis

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18
Q

How do kidneys appear grossly in end-stage diabetic nephrosclerosis?

A

Diffuse granular, pitted surface

Marked thinning of renal cortex

Irregular cortical depressions, secondary to pyelonephritis

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19
Q

What are the typical renal system lesions associated with diabetic nephropathy?

A
  1. Glomerular lesions
  2. Vascular lesions
  3. Pyelonephritis
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20
Q

What is the classic appearance of SLE on EM?

On PAS:

A

EM:
“Wire loops”
Subendothelial dense deposits that are focal and diffuse

PAS stain:
Increase in cellularity
Glomerular size is enlarged and appears “stuffed” in Bowman’s capsule
Reduced size of urinary space

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21
Q

Henoch-Schonlein purpura

What disease is it related to?

A

Childhood syndrome consisting of purpura, abdominal pain and GI bleeding, and arthralgias along with renal abnormalities.

IgA nephropathy, because IgA deposits are commonly found in the mesangium.

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22
Q

GN associated with bacterial endocarditis clinically:

On histology:

On immunofluorescence:

A

Hematuria and proteinuria of various degrees. An acute nephritic presentation is not uncommon, or even progression to RPGN in rare circumstances.

Vary from focal, to global exudative and proliferative, and may have an MPGN pattern.

Glomerular immune deposits.

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23
Q

Microscopic polyangiitis and Granulomatosis with polyangiitis can also cause…

A

Glomerular lesions

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24
Q

How is Acute tubular injury characterized clinically?

A

Acute renal failure and often evidence of tubular injury in the form of necrosis of tubular epithelial cells.

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25
Q

What are the 2 major causes of Acute tubular injury?

A
  1. Ischemia due to interrupted blood flow. This can be from microscopic polyangiitis, malignant HTN, or microangiopathies.
  2. Direct toxic injury to the tubules by endogenous (Mb, Hb, Ig, etc.) or exogenous (drugs, contrast, etc.) sources.
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26
Q

Simply put, the pathogenesis in both ischemic and nephrotoxic ATI is believed to be from:

How does each play a role in decreasing urine output and GFR?

A

Tubular injury and persistent and severe distrubances in blood flow.

Tubular injury causes interstitial inflammation, sloughing of cells and tubular backleak, all of which cause decreased urine output, obstruction and decreased GFR.

Ischemia causes vasoconstrction, which reduces GFR also.

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27
Q

What cells are highly susceptible to ischemia? Why?

A

Proximal tubular epithelial cells, due to their high energy requirements

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28
Q

Clinical course of Acute tubular injury (3 phases)

A

It is variable, however 3 phases exist:

Initiation
-oliguria at 36 hrs.

Maintenance

  • oliguric crisis w/ uremia
  • hyperkalemia often a clinical issue

Recovery

  • large urine vol (up to 3 L/day)
  • large water, Na+ and K+ loss
  • hypokalemia
  • susceptibility to infection
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29
Q

What is the prognosis for Acute tubular injury?

A

Varies, but if the toxin does not cause significant damage to other organs (liver or heart), they can be OK. 95% of those pts. recover.

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30
Q

What toxin is associated with Acute tubular injury?

A

Ethylene glycol

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31
Q

Tubulointerstitial nephritis is a group of…

What is it “characterized by”?

A

Group of renal diseases that are insidious and characterized by azotemia and inability to concentrate urine.

It can be acute or chronic.

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32
Q

Etiologies of primary tubulointerstitial nephritis

A 
Infection
Toxins
Metabolic DZs
Physical factors (chronic obstruction, etc.)
Neoplasms (Bence-Jones proteins)
Immunologic reactions
Vascular diseases
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33
Q

Morphologic appearances of acute vs. chronic of tubulointerstitial nephritis

A

Acute - interstitial edema, leukocyte infiltration and tubular injury.

Chronic - infiltrate of mostly mononuclear leukocytes, prominent interstitial fibrosis and tubular atrophy

34
Q

85% of UTIs are from:

Other possible bacteria:

A

Enteric bacteria (E coli)

Proteus, Klebsiella, Enterobacter spp.

35
Q

95% of cases of cystitis are from:

A

Inflammation (bacterial) of urinary bladder mucosa

36
Q

Chronic pyelonephritis definition

A

Recurrent or continuous long-term chronic infection of the kidney w/ resulting damage to pelvis/calyces and parenchyma that can cause anatomic distortion.

37
Q

What causes pyelonephritis?

What is a predisposing anatomic defect?

What are predisposing medical conditions?

A

> 95% arise via ascending infection from the bladder to the kidneys

Vesicoureteral reflux and associated intrarenal reflux

DM, pregnancy

38
Q

3 major complications of pyelonephritis

A

Papillary necrosis
Pyelonephrosis
Perinephric abscess

39
Q

Morphological hallmarks of acute pyelonephritis (4)

A

Patchy interstitial suppurative inflammation

Intratubular aggregates of neutrophils

Neutrophilic tubulitis

Tubular necrosis

40
Q

Acute pyelonephritis is almost always the result of:

A

Ascending cystitis infection combined with a predisposing anatomic defect

41
Q

What is vesicoureteral reflux?

A

At the vesicoureteral junction, the ureter is supposed to enter obliquely, but in reflux, there is not an oblique entrance of the ureter, and predisposes pts. to bacteria traveling up the ureters during micturition.

42
Q

Papillary necrosis cause: DM

M-to-FM ratio:
Time course:
Infection:
Calcification?

A

M-to-FM ratio: 1:3
Time course: 10 yrs
Infection: 80%
Calcification? Rare

43
Q

Papillary necrosis cause: analgesic nephropathy

M-to-FM ratio:
Time course:
Infection:
Calcification?

A

M-to-FM ratio: 1:5
Time course: 7 yrs of abuse
Infection: 25%
Calcification? Frequent

Almost all papillae effected

44
Q

Papillary necrosis cause: obstruction

M-to-FM ratio:
Time course:
Infection:
Calcification?

A

M-to-FM ratio: 9:1
Time course: variable
Infection: 90%
Calcification? Frequent

45
Q

Gross appearance of papillae in DM vs. analgesic nephropathy

A

DM: pale grayish necrosis limited to papillae

Analgesic nephropathy: red-brown necrotic papillae sloughed into calyces

46
Q

What percentage of pts. with chronic pyelonephritis did ESRD result?

A

10-20% required transplant/dialysis, but those numbers are decreasing due to less prevalence of DZ in US

47
Q

What causes polar scarring of the kidney?

A

VUR with chronic pyelonephritis

48
Q

What bacteria is associated with Xanthogranulomatous pyelonephritis?

A

Proteus spp.

49
Q

2 most common causes of AKI

A
  1. Pyelonephritis

2. Tubulointerstital nephritis induced by drugs/toxins

50
Q

Clinical representation of Tubulointerstital nephritis induced by drugs/toxins (3)

What can complicate it?

A

Fever
Eosinophilia
Interstitial renal parenchymal infiltrates

Complicated by papillary necrosis

51
Q

What is the progression of Tubulointerstital nephritis induced by drugs/toxins?

A

With cessation of drugs and therapy for infection, renal function can stabilize or improve.

A small percent with analgesic nephropathy may develop urothelial carcinoma of renal pelvis.

52
Q

Benign nephrosclerosis is a…. instead of a….

A

General process, not a specific diagnosis

53
Q

Benign nephrosclerosis definition:

What is the result?

A

Morphologic changes associated with hyaline sclerosis of renal arterioles and small arteries.

Multi-focal ischemia of the kidney parenchyma supplied by the sclerotic vessels.

54
Q

Benign nephrosclerosis severity in the following conditions:

Increasing age:
HTN:
DM:

A

Increasing age: mild changes
HTN: mod-severe changes
DM: mod-severe changes

55
Q

Pathogenesis of benign nephrosclerosis (2)

A

Medial and intimal thickening in response to hemodynamic changes, aging, etc.

Hyaline protein depositions in arteriolar walls.

56
Q

Morphologic changes in benign nephrosclerosis (3)

A

Hyaline arteriosclerosis
Fibroelastic hyperplasia
Ischemic atropy

57
Q

What is the progression of benign nephrosclerosis?

A

Not usually associated with renal insufficiency, but there are some exceptions:

  • AAs may have renal insufficiency
  • when superimposed on severe HTN
  • diabetic nephropathy
58
Q

Pathologic effects of malignant HTN on the kidneys (2)

They lead to…

A

Ischemia to the kidneys
Elevated renin

Both lead to a perpetuating cycle of damage and HTN

59
Q

Malignant arteriosclerosis =

A

Malignant nephrosclerosis in the kidneys

60
Q

Hyperplastic arteriolitis is an…

What is it associated with?

A

Adaptive response of arterioles that are irreversibly injured

Associated w/ renal failure

61
Q

Gross manifestations of kidneys with malignant HTN

A

“Flea-bitten” appearance of renal hemorrhages

62
Q

BP of malignant HTN

A

180/120

63
Q

Clinical features of malignant HTN (5)

A 
Papilledema
Retinal hemorrhages
Encephalopathy
CV abnormalities
Renal failure
64
Q

What large vessel disease is possible curable?

What does it resemble?

A

Renal a. stenosis

Resembles pts. w/ essential HTN

65
Q

Pathophysiology of unilateral renal a. stenosis lead to… (4)

A

Stenosis -> renin release -> +RAAS which leads to:

CV hypertrophy
Systemic VC
Increased BV
Renal Na+ and fluid retention

66
Q

Most common etiology of renal a. stenosis:

What etiology is more common in women?

A

70% from atherosclerosis

Fibromuscular dysplasia

67
Q

Thrombotic microangiopathies include clinical syndromes with… (2)

A

Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS)

68
Q

What causes TTP and HUS?

A

Certain triggers cause excessive activation of platelets, including thrombi in capillaries and arterioles in various tissue beds, including the kidneys.

69
Q

What are the features of HUS and TTP? (3)

What are the consequences of HUS and TTP? (3)

A

Thrombi in capillaries and arterioles and renal failure
Microangiopathic hemolytic anemia
Thrombocytopenia

Vascular obstructions
Vasoconstriction
Ischemia

70
Q

Endothelial injury triggers that may cause HUS/TTP (5)

A 
Bacterial toxins
Cytokines
Viruses
Some meds
Anti-endothelial Abs
71
Q

Typical HUS is associated with…

Who does it affect?

What other bacteria can cause it?

A

Mostly associated w/ diarrhea as a consequence of eating food contaminated w/ Shiga-like toxin (E. coli)

Mostly kids, but can be in some adults.

Shigella spp.

72
Q

Atypical HUS is associated with…

A

Inherited mutations of proteins that regulate complement.
Multiple acquired causes of endothelial injury, usually in adults.

Antiphospholipid syndrome, pregnancy, systemic sclerosis, malignant HTN, chemo, kidney radiation, etc.

73
Q

TTP is caused by…

Involvement of what system is paramount in TTP?

A

Inherited or acquired deficiencies of ADAMTS13, a protease that regulates function of vWF; leads to unregulated platelets aggregation

Neurologic involvement is prominent in TTP

74
Q

Classic features of TTP (5)

Who is more likely to get TTP?

A 
Fever
Neurological SX**
Microangiopathic hemolytic anemia
Thrombocytopenia
Renal failure (50% of pts.)

Adults <40 y/o; more common in females

75
Q

Atheroembolic renal disease cause…

SX depend on…

A

Embolization of fragments of plaques from aorta and renal a. into intrarenal vessels in older pts. w/ atherosclerosis, especially post-op on the aorta, etc.

Clinical SX depend on the number of emboli and pre-existing state of renal function.

76
Q

What are the SX of Atheroembolic renal disease? (6)

A 
Flank pain
Hematuria
HTN
Arrhythmia
N/V
Oliguria
77
Q

Most renal infarcts are due to…

Underlying process is…

A

Embolism

Mural thrombosis from left heart usually, but can be from endocarditis, aortic aneurysms or atherosclerosis

78
Q

Sickle cell nephropathy is seen in pts. w/…

What is the presentation?

How many exhibit proteinuria?

A

The disease and may manifest in pts. w/ sickle trait also.

Generally hematuria and hyposthenuria with papillary necrosis

30% proteinuria that is usually sub-nephrotic range; however, some may progress to full nephrotic syndrome progressing to glomerulosclerosis

79
Q

What nephrotic process occurs in the kidney diffuse cortical necrosis?

A

Diffuse cortical necrosis with coagulative necrosis of glomeruli and tubules

80
Q

What causes diffuse cortical necrosis? (3)

They lead to…

A

Obstetric emergencies
Sepsis
Surgical complications

… which lead to systemic hypoperfusion or hypoxia

CPR II Exam #2 (20 decks)

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