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Renal 2 Test 1 > Renal Pathology Puthoff Lecture > Flashcards

Renal Pathology Puthoff Lecture Flashcards

1
Q

What do kidneys do?

A
  • Excrete certain waste products of metabolism
  • Precisely regulate the body’s concentration of water, salt, calcium, phosphorus and other/cations/anions
  • Serve as an endocrine organ–elaborating erythropoietin, renin, PGs, and regulating vitamin D metabolism
  • Convert mor than 1700 L of blood prepay into the highly specialized, concentrated fluid known as urine
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2
Q

The glomerulus is what kind of organ

A

microvascular

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3
Q

The most common cause of end stage renal disease (ESRD) and second most cause? other causes?

A
  • Diabetes is most common cause
  • High BP is 2nd
  • Other problems that cause kidney failure include: autoimmune diseases, such as Lupus and IgA nephropathy
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4
Q

Are most people with ESRD old or young? What ethnic groups most affected?

A
  • young–63% under age 65
  • Hispanics and Asian Americans fastest growing ethnic groups newly diagnosed with ESRD
  • Currently more than 20 million Americans have some level of chronic kidney disease related to diabetes; as diabetes increases, demand for dialysis will too
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5
Q

CKD associated with what vitamin deficiency and what disease

A
  • Folate

- which is associated with hyperhomocystenimia which is also associated with an increased risk for stroke/ASCVD

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6
Q

What happens if you only have one kidney?

A
  • the single nephron GFR goes up and over time will lead to glomerulosclerosis
  • Also causes elaboration of renin that occurs from golblat phenomenon?
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7
Q

The kidneys are what kind of organs? (intraperotineal or retroperitoneal?) at what level?

A

retroperitoneal

at the level of T12

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8
Q

Why is right kidney lower than left?

A

because of its position under the liver on the right

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9
Q

Where is the Renal angle?

A

Between lower border of 12th rib and lateral border of elector spinae muscle–Renal colic pain starts from this angle down and forwards to groin (CVA)–goes about to L2

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10
Q

How common are renal cysts?

A
  • Common–More than 50% of those over 50% have parenchymal kidney cysts
  • Generally small, contain serous fluid, unremarkable dilations of proximal tubules
  • Often small and asymptomatic and are generally incidental findings, but can become quite large
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11
Q

Types of cysts (not all are small and unremarkable!!)

A
  • simple cysts
  • multilocular–subdivisions, some with smooth muscles in the wall
  • dysplastic kidney–congenital anomalies
  • adult and juvenile polycystic disease
  • cystic tumor–some renal cell carcinomas can become cystic and have hemorrhagic areas
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12
Q

How do most diseases/disroders of the kidney present?

A

-hematuria–SCHITTT: stones, congenital anomalies, hemologic abnormalities like coagulopathies, infection, trauma, tumor, tuberculosis
-proteinuria
-edema
-mass
-HTN
-oliguria
-anuria
-asymptomatic
increased serum/urine creatinine
-decreased creatinine clearance
-increased serum BUN

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13
Q

By the time you palpate a mass for RCC what has happened?

A

the tumor has already metastasized if it is palpable

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14
Q

Single most important question to ask patient suspected of having renal disease and why is this the most important question?

A

Have you had this before?

-Because distinct differences between acute and chronic kidney diseases

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15
Q

Common imaging techniques of the kidney and associated GU organs

A
  • US
  • KUB–plain Ab film (not as common any more)
  • Renal tomography
  • IVP (not as common anymore bc associated with anaphylaxis and more invasive)
  • Retrograde pyelography

Other techniques to evaluate the ureter, bladder or urethra

  • Cystography
  • Voiding urethrography
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16
Q

Additional imaging techniques of the kidney

A
  • CT scan
  • MRI, MRA
  • Rdionuclide imaging
  • Renal angiography
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17
Q

Techniques utilized on renal biopsy material

A
  • light microscopy: standard stain (H&E), other (PAS, silver stains)
  • Flouorescence microscopy (variety of targeted immunologic entities–glomerular diseases)
  • Electron microscopy (transmission)
  • *WITH URINALYSIS
  • Other techniques: increasingly, molecular and genetic analyses
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18
Q

Passage of materials through a membrane by a physical force

A

filtration

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19
Q

Osmosis is the diffusion of water across what kind of membrane

A

semipermeable–necessary for osmosis bc it restricts the movement of certain solutes allowing solvent to pass through but water can pass freely

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20
Q

Glomerulus is?

A

capillary loops between afferent and efferent arterioles

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21
Q

Most filtration occurs at which end of capillary bed? and osmosis/colloid osmotic pressure occurs at which end?

A
  • filtration= arteriolar

- osmosis=venule via plasma proteins

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22
Q

Osmotic vs oncotic pressure

A
  • osmotic=pressure developed by solutes dissolved in water working across selectively permeable membrane
  • oncotic=colloid osmotic pressure which is form of osmotic pressure exerted by proteins (albumin) in a blood vessel’s plasma that pulls water into circulatory system
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23
Q

Typical normal pattern for serum protein electrophoresis

A
  • positive pole=large quantities of albumin (small molecule) migrates fastest towards positive pole
  • positive to negative pole order: albumin, alpha1, alpha2, beta, gamma
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24
Q

Multiple myeloma serum protein electrophoresis findings

A

-IgG plasma cell malignancy dyscrasia with kappa light chains

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25
Q

Bence-Jones proteins effects on kidneys

A

-deposition of light chains in tubules which causes lots of tubular damage and can ultimately cause chronic renal failure

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26
Q

organs involved in causing edema in congestive heart failure

A

-kidney and liver

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27
Q

Nephrotic syndrome

A

-generalized edema

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28
Q

What can cause generalized edema

A
  • kidney failure
  • heart (congestive heart failure)
  • Liver (not producing enough plasma proteins)
  • GI proteins (caused by losing proteins–protein losing enteropathies)
  • Lungs–because of its effect on the heart
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29
Q

What are the compartments or major morphologic components of the kidney?

A
  • Glomeruli
  • Tubules
  • Interstitium
  • Vessels
  • Tubules and vessels are in interstitium)
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30
Q

Is diabetes primarily what kind of disease?

What about hypertension?

A
  • diabetes=GLOMERULAR disease (microvasculature) manifestations
  • HTN=vascular (arteriolar) disease manifestations (TUBULOINTERSTITIAL DISEASE)
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31
Q

The general category of glomerular disorders is considered due to ____ disease

A
  • immunologic (primary or secondary)

- but diabetes effect on kidney is largely hemodynamic not immunologic in terms of diabetic nephropathy

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32
Q

is glomerulonephritis due to infection? Difference bw glomerulonephritis and glomerulopathy

A
  • in most cases no! but may have inflammatory infiltrates

- they are the same

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33
Q

How does the interstitium react to chronic kidney disease?

A

-by becoming fibrotic and may see some degree of inflammation and some edema of the interstitium as well

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34
Q

What diseases do you see nephrosclerosis?

A
  • HTN
  • diabetes
  • other disorders that affect blood vessels
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35
Q

difference between azotemia and uremia?

A

-uremia is azotemia PLUS a constellation of clinical findings and biochemical abnormalities resulting from renal damage

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36
Q

Acute Kidney injury

A
  • Rapid decline in GFR
  • Most severe form exhibit oliguria or anuria
  • May result from glomerular, interstitial, vascular or acute tubular injury (ATN)
  • Can be reversible, or progress to CKD
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37
Q

CKD

A
  • mild–clinically silent
  • more severe–uremia
  • defined with diminished GFR
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38
Q

ESRD

A

-GFR

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39
Q

Which disorders are characteristic of glomerular disease? And which disorders are characteristic of tubulointerstitial disease? Which are characteristic of both?

A

-Glomerular: nephritic syndrome, nephrotic syndrome, ASYMPTOMATIC hematuria or proteinuria

Tubulointerstitial: UTI, UT obstruction, renal tumors, nephrolithiasis

BOTH: renal tubular defects and acute renal failure

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40
Q

difference between neprholithiasis and nephrocalcinosis

A
  • nephrolithiasis is kidney stones

- nephrocalcinosis is dystrophic calcification of kidney parenchyma

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41
Q

Why do you see lipids in nephrotic syndrome?

A

-bc when kidney is stressed it tries to make more proteins and the pathway it goes into makes lipoproteins that deposit primarily in proximal tubule

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42
Q

Glomerular disease characterized by severe proteinuria (albumin) (more than 3.5gm/day–less in children), severe edema, hyperlipidemia, and lipiduria

A

Nephrotic syndrome

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43
Q

Glomerular disease dominated by acute onset of grossly visible hematuria, mild to moderate proteinuria, and hypertension. Proteinuria and edema common but not as severe

A

-Nephritic syndrome

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44
Q

signs of nephritic syndrome with rapid decline (days-weeks) in glomerular filtration rate (GFR). Implies severe glomerular injury

A
  • Rapidly progressive glomerulonephritis
  • nephritic
  • protein in urine but LESS than 3.5 gm/day;
  • normal protein in urine is about UPTO 150mg/day
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45
Q

Isolated urinary abnormalities

A

-glomerular hematuria and/or subnephrotic range proteinuria

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46
Q

Where do you find endothelial cells?

A

-line ALL blood vessels

47
Q

Where are podocyte foot processes located?

A

-directly on basement membrane which deep to the podocyte cells

48
Q

Morphology of glomerulus

A

-initial nephron segment consists of a glomerulus and bowman’s capsule (together make up the renal corpuscle) that captures and funnels the glomerular filtrate, the initial urinary stream into the tubular system

49
Q

PAS stains what?

A

glycoproteins

50
Q

Three layers of the basement membrane

A
  • lamina densa
  • lamina rara interna
  • lamina rara externa
  • within that are negatively charged anions–among those are HEPARIN which is how charge selectivity occurs
51
Q

HEMATURIA, azotemia, oliguria, edema, HTN

A

Nephritic syndrome

52
Q

Acute nephritic, proteinuria, and acute renal failure

A

RPGN

53
Q

> 3.5 gm/day PROTEINURIA, hypoalbuminemia, hyperlipidemia, lipiduria

A

Nephritic syndrome

54
Q

Azotemia–>uremia progressing for months to years

A

Chronic renal failure

55
Q

Glomerular hematuria and/or subnephrotic proteinuria

A

Isolated urinary abnormalities

56
Q

edema usually seen in nephritic or nephrotic syndrome?

A

-NEPHROTIC

57
Q

Pathologic responses of the glomerulus to injury

A
  • hypercellularity
  • basement membrane
  • Hyalinosis and sclerosis
58
Q

Pathologic responses of the glomerulus to injury–hypercellularity

A
  • proliferation of native cells (mesangial cells, endothelial cells and visceral epithelial cells) and infiltrates of inflammatory cells (neutrophils, macrophages, etc mononuclear cells, etc)
  • crescents: occur in Bowman’s space–both necrotizing elements and cellular elements
59
Q

Pathologic responses of the glomerulus to injury—-Basement membrane

A
  • thickening (breaks, sclerotic regions)
  • deposits (electron dense deposits)
  • glomerulus BM is not the same as glomerular filtration membrane!!
  • glomerulus BM is PART of glomerular filtration
60
Q

Pathologic responses of the glomerulus to injury—-Hyalinosis and sclerosis

A
  • Hyaline change

- sclerosis: acellular sclerotic pattern that involves small vessels of the microvasculature of glomerulus

61
Q

Primary Glomerulonephropathies

A
  • Acute Proliferative Glomerulonephritis (usually DIFFUSE)
  • RPGN
  • Membranous Glomerulopathy
  • Minimal change disease (lipoid necrosis/ mills disease)
  • Focal Segmental glomerulosclerosis
  • Membranoproliferative Glomerulonephritis (mesangial-capillary GN)–Dense deposit disease
  • IgA nephropathy (acute FOCAL GN)
  • Chronic Glomerulonephritis–End stage
62
Q

Systemic diseases with glomerular involvement

A
  • Lupus
  • Diabetes

Not as common:

  • Amyloidosis
  • Goodpasture
  • Microscopic polyarteritis/angiitis
  • Wegener granulomatosis
  • Henoch-schonlein purpura (IgA systemic disease!)
  • Bacterial endocarditis
63
Q

Systemic diseases with glomerular involvement–Heriditary disorders

A
  • Alport syndrome
  • Thin Basement membrane disease
  • Fabry disease
64
Q

Immune complexes in the glomerulus Subepithelial humps

A

acute glomerulonephritis

65
Q

Immune complexes in the glomerulus–epimembranous depostis

A

Membranous nephropathy

Herman glomerulonephritis

66
Q

Immune complexes in the glomerulus–SUBENDOTHELIAL DEPOSITS

A

Lupus nephritis

Membranoproliferazive glomerulonephritis

67
Q

Immune complexes in the glomerulus–Mesangial deposits

A
  • -Acute focal proliferative GN!

- IgA nephropathy!!

68
Q

Immune mechanisms of glomerular injury

A
  • Ab mediated (in situ immune complex deposition)–fixed, intrinsic tissue Ags OR planted Ags
  • Circulating immune complex deposition (Endogenous or exogenous Ags)
  • Cell mediate immune injury
  • Activation of alternative complement pathway
69
Q

Ab mediated Glomerular injury

A
  • deposition, circulating immune complexes sub endothelial
  • In situ deposition on BM
  • In situ deposition on foot processes–Heymann
70
Q

Difference between Diffuse, focal, segmental and global

A
  • diffuse involves all glomeruli
  • Focal involves only subset of glomeruli
  • Segmental means only portions of the affected glomeruli involved
  • global means it involves entire glomerulus
71
Q

Once GFR is reduced to 30-50% what happens?

A

-regadless of the stimulus underlying disease it results in FSGS and tubulointerstitial fibrosis even though it may not start as such

72
Q

Proteinuria in nephrotic syndrome vs FSGS

A
  • nephrotic is selective proteinuria–mostly just albumin

- FSGS is nonselective

73
Q

Immune complex injury triggered by exogenous bacterial, viral or fungal Ag
Historically antecedent of Group A hemolytic stop; specific nephritogenic strains of Lacefield group A

A

Acute proliferative Glomerulonephritis

74
Q

Diffuse proliferative glomerulonephritis characterized by

A
  • marked hypercellularity: ranges from simple mesangial to complex endocapillary cell infiltrate
  • Leukocyte infiltration: exudate within glomerular tuft
75
Q

EM: sub epithelial hump of immune complex; neutrophil in lumen

A

Acute proliferative glomerulonephritis

76
Q

Acute proliferative glomerulonephritis IF findings

A

Granular deposits of IgG, IgM, and C3 in mesangium and along the GBM corresponding to sub epithelial humps

77
Q

Acute proliferative glomerulonephritis children clinical presentation

A
  • ages 6-10
  • typically 1-4 wks following pharyngitis or skin infection
  • often but not invariably strep B
  • often present with malaise, fever, nausea, oliguria, and hematuria 1-2 wks after recovery from sore throat; dysmorphic RBC cast, mild proteinuria (
78
Q

Acute proliferative glomerulonephritis –adults clinical

A
  • more typical and aggressive course

- may see sudden HTN or edema with elevated BUN

79
Q

Acute proliferative glomerulonephritis children vs adults clinical course

A
  • Children clear in 6-8 wks–renal biopsy not indicated

- 95% recover completely;

80
Q

Acute proliferative glomerulonephritis associated with what infections besides strep B?

A
  • other bacterial (immunoglobulin feature with some staph infections)
  • viral
  • sequel to parasitic infx
81
Q

What do you see in nephritic syndrome

A

-MAY exhibit nephritic syndrome with systemic disorders but typically seen in setting of post infectious disease and exudative GN, and syndromic clinical features helpful in dx of crescentic GN

82
Q

Where do crescent formations occur?

A

-Bowmans space bw parietal (modified squamous cells) and visceral epithelial cells

83
Q

Crescentic GN characteristic of what disorder?

A
  • RPGN
  • crescent shaped mass of proliferating visceral and parietal epithelial cells
  • Rather rapid obliteration of urinary space
  • infiltrates of macrophages & leukocytes
  • PAS stain
84
Q

RPGN Type 1

A

ANTI-GBM Ab

  • Renal limited
  • Goodpastures syndrome (kidney and lung hemorrhage)
85
Q

RPGN Type 2

A

IMMUNE COMPLEX
-Idiopathic
-postinfectious GN
-Lupus nephritis
-Henoch Schönlein Purpura (systemic IgA disease)
-IgA nephropathy (renal limited IgA disease)
other

**Not all of these start out as RPGN!! They may be acute and focal and progress to RPGN later

86
Q

Type 3 RPGN

A

PAUCI IMMUNE

  • ANCA associated (anti neutrophil cytoplasmic associated)
  • Idiopathic
  • Granulomatosis with polyangiitis–wegners associated with ANCA
  • Microscopic polyangiitis
87
Q

50% of PRIMARY renal diseases (so not lupus or Heoch schnolen bc these are systemic) associated with RPGN have what type of RPGN on IF

A

Type III (paci immune) on IF

88
Q

Type I RPGN characterized by

A

-anti-GBM Ab-induced disease characterized by LINEAR deposits of IgG and many cases C3 in GBM

89
Q

What happens when anti GBM Abs cross react with lung alveolar BM?

A

Pulmonary hemorrhage occurs in addition to renal disease (Goodpassure’s syndrome)

90
Q

Good pasture Ag is a

IF pattern

A

peptide within non collagenous regions of collagen type IV

-Anti-IgG localized to glomerular BM with DIFFUSE LINEAR staining

91
Q

Goodpastures and gene associations

A
  • high prevalence with certain HLA subtypes and haplotypes (HLADRB1) in RPGN patients
  • genetic predisposition to autoimmunity
92
Q

Tx for Goodpastures

A

-Plasmapheresis to remove pathogenic circulating Abs is part of Tx regimen which is effective in conjunction with immunosuppressive Tx

93
Q

Type II vs Type III RPGN

A
  • Type II immune complex deposition RPGN associated with acute proliferative GN, lupus nephritis and IgA nephropathy
  • -Type I=celluar proliferation within glomerular tufts occurs in addition to crescent formation; IF studies reveal GRANULAR pattern of immune complex deposition
  • Type II pts DO NOT RESPOND to plasmapheresis
  • Type III defined by lack of anti GBM Abs or immune complexes by IF or EM
  • Most pts with type III (pauci immune) have circulating antineutrophil cytoplasmic Abs (ANCA)
94
Q

Renal syndrome where basic defect is increased permeability of glomeruli to plasma proteins resulting in proteinuria

A

Nephrotic syndromes

95
Q

Major clinical features of nephrotic syndrome

A
  • Severe proteinuria (>3.5 gm/day)
  • Hypoalbuminemia
  • Edema; common to start with periorbital but becomes GENERALIZED
  • Hyperlipiemia–elevated serum cholesterol & lipoproteins
96
Q

Causes of Nephrotic syndrome in children vs adults

A
  • Children usually Minimal change disease (children usually get it from PRIMARY glomerular disease 95% like minimal change disease)
  • Adults usually FSGS and Membranous glomerulopathy (more often associated with systemic disease compared to children but 60% still from primary disease)
97
Q

Massive increase in urinary protein in nephrotic syndrome is due to

A

diffuse changes in the majority of glomeruli

  • GBM becomes diffusely leaky or porous to proteins especially albumin which is both a small protein and represents half the total protein in blood
  • But in NS the generalized increase in GBM porosity to proteins does not allow RBCs to transmit into urinary space (size and charge selectivity)
98
Q

Primary vs secondary renal disease in nephrotic syndrome

A
  • Primary: only kidney is affected (renal etiology); MOST common cause of NEPHROTIC syndrome in children
  • Secondary: systemic diseases causing nephrotic renal disease (DM, SLE) with alterations in renal histomorphology; more frequent in adults (40% of cases)
99
Q

PURE protein disorders (rarely exhibit hematuria)

A
  • Minimal Change disease
  • Membranous Glomerulopathy
  • Focal segmental Glomerulosclerosis (of the 3, this is most likely to have hematuria)
100
Q

Acute Proliferative GN and RPGNs (I, II and III) are nephritic or nephrotic?

A

-Nephritic

101
Q

Leading etiologies of Nephrotic syndrome

A

-DM, and SLE most common
-Infections (malaria, syphillis, Hep B and C, HIV)–typically membranous glomerulopathies
-Malignant disease (carcinoma, lymphoma)–also membranous
-Amyloidosis
Drugs (non steroidal anti-inflammatory, penicillamine)
-Miscallaneous (bee sting allergy, hereditary nephritis)

102
Q

Membranous Glomerulopathy major characteristics

A
  • 75% of cases are primary
  • Autoimmune disease linked to HLA-DQA1 and Abs to renal auto antigen PLA2 receptor with pathophysiologic involvement of complement (primarily MAC) and IgG4
  • Remainder due to drugs, underlying malignancies, SLE, infections, other AI disease
  • 85% are NEPHROTIC! Hematuria and HTN CAN occur (15-35% of cases)
  • NON-selective proteinuria!
103
Q

Primary vs secondary membranous glomerulopathy response to steroid therapy

A
  • primary responds POORLY to steroid therapy; high disease recurrence in transplant patients; in contrast Minimal change disease responds very well to steroids!
  • some evidence that women may have more beingn course
104
Q

Membranous glomerulopathy morphology

A
  • Marked diffuse thickening of capillary walls without increase in cellularity; spikes of silver staining matrix project from basement membrane toward urinary space
  • acellular sclerotic glomerulus
  • Effaced Foot processes
  • Thick basement membrane: 5-20 fold increased thickness
  • subepithelial deposits: dense aggregates IgG (electron dense) along epithelial side of BM
  • Obliterated foot processes overlying dark deposits
  • SPIKE AND DOME!!
  • Lumpy bumpy IgG deposits
105
Q

The only disease where you see ONLY fusion of foot processes

A

Minimal Change disease

106
Q

Membranous Glomerulopathy Clinical Course

A
  • Proteinuria persists in 60% of patients
  • 40% develop renal insufficiency
  • 10% progress to end stage renal failure
  • corticosteroids and immunosuppressive tx NOT efficacious (in contrast to Minimal change disease)
107
Q

MCD clinical characterisitics

A
  • NS presentation–Edema
  • Biopsy–ONLY foot process fusion
  • peak incidence bw 2-6 yrs
  • MCC of NS in children and may follow a respiratory infection or immunization
  • significant evidence that it has immunologic basis
  • associated with Hodgkin lymphoma and other lymphoreticular diseases
  • HTN is rare
  • highly selective proteinuria (albumin mostly)
  • Respond well to corticosteroids and no clinical recurrence–very good prognosis
108
Q

Visceral Epithelial Cell (podocyte) injury

A
  • Abs against epithelial cell Ags, certain toxins, cytokines or other factors cause injury, resulting in foot process effacement (fusion or simplification)
  • can be Associated with detachment of epithelial cells and protein leakage through defective GBM and filtration slits
109
Q

Nephritic or nephrotic
MPGN Type I
MPGN Type II (dense deposit)
IgA nephropathy

A

type 1: mixed
type 2: hematuria, renal failure
IgA nephropathy: recurrent hematuria

110
Q

FSGS involves what part of kidney

A

not just bowman’s capsule but has a sclerosing pattern that extends deep into the glomerular tufts as well

111
Q

FSGS types/classifications

A
  • idiopathic/primary
  • other known conditions/associations
  • often a secondary glomerular event!!
  • adaptive response to loss of renal mass
  • uncommon inherited forms/mutations in genes that encode proteins localized to podocyte slit diaphragms
  • can be associated with HIV
  • Often a SECONDARY event in contrast to membranous and minimal change disease
  • adaptive response to glomerular injury–leads to FSGS
112
Q

Idiopathic FSGS epidemiology and clinical course

A
  • idiopathic accounts for 35% of adults with NS–10% NS in children
  • Primary FSGS most common overall cause of NS syndrome now in US adults ; greater incidence among Hispanics and African Americans
  • 5-10% of MCD in children that does NOT respond to steroid tx exhibit FSGS upon biopsy (but children overall have better prognosis than adults in this disorder)
  • FSGS also occurs in other disease settings and is generally a Dx that implies poor prognosis, as progressive renal disease occurs over time
  • 20% of pts follow unusually rapid course with massive proteinuria and renal failure within 2 years
113
Q

FSGS different from MCD and other podocytopathies how?

A
  • higher incidence of hematuria, reduced GFR, and HTN
  • Proteinuria is nonselective (large serum proteins equally part of exhibited proteinuria, as well as smaller proteins, i.e. albumin)
  • Poor response to steroids
  • significant progression to CKD with at least 50% developing ESRD within 10 years
114
Q

FSGS HIV associated Nephropathy

A
  • HIV can directly and indirectly cause renal disease including acute renal failure and/or acute interstitial nephritis
  • collapsing variant of FSGS
  • occurs in 5-10% of pts, more frequently in African americans and caucasians

Renal 2 Test 1 (16 decks)

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