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Pathology Term 5 > Week 1 - RENAL > Flashcards

Week 1 - RENAL Flashcards

Normal Pathophysiology, Glomerulonephritis, Acute Renal Failure, Chronic Renal Failure

1
Q

Which kidney is higher?

A

Left

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2
Q

True or False?

Lobulations are prominent in the adult kidney

A

False

-more prominent in fetal kidney

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3
Q

Where are the glomeruli, distal tubules and loop of henle located?

A

glomeruli –> cortex

distal tubules/loop of henle –> medulla - renal pyramid

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4
Q

What is the most distal part of the nephron? and where is it located?

A

renal papillae

-tip of the renal pyramids

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5
Q

What are the 3 layers of the glomerulus?

A
  1. inner endothelial layer
  2. basement membrane
  3. podocytes (foot processes)
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6
Q

Outline the filtration membrane

A

endothelium
-big holes –> stops only cells (everything else filtered out)

basement membrane
-stops all large proteins (globulins)

foot processes
-stops smallest proteins (albumin)

**therefore only water and solutes come out of filtration membrane

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7
Q

What is the pathogenesis of oliguria in nephritic syndrome?

A

-marked inflammation cuses obstruction/compression to glomerular capillaries –> little urine produced (but there is hematuria, proteinuria as well)

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8
Q

Compare nephritic and nephrotic syndorme?

A

Nephritic

  • inflammation –> oliguria
  • damage to all 3 layers of filtration membrane (endothelium, basement membrane and foot processes)
  • cells, blood, proteins in urine
  • proteinuria (non-selective) + hematuria
  • oedema due to salt + water retention –> HTN
  • decreased GFR

Nephrotic

  • no inflammation –> polyuria
  • damage confined to foot processes (therefore no hematuria/proteinuria)
  • only albuminuria (selective proteinuria)–> oedema
  • lipiduria
  • hyperlipidemia
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9
Q

What is uremia?

A

disease characterised by:

  • fatigue, N/V, encephalopathy –> renal failure
  • increased BUN, creatinine, urea
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10
Q

What is azotemia?

A

increased blood urea nitrogen

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11
Q

What is the pathogenesis of headache in renal failure?

A
  • fluid retention
  • acidosis
  • uremia
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12
Q

What is the pathogenesis of SOB/pallor in renal failure?

A

anemia –> decreased EPO

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13
Q

What is the pathogenesis of N/V in renal failure?

A

renal osteodystrophy

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14
Q

What are some causes of painless/asymptomatic hematuria?

A

DM, IgA nephropathy, TB, cancer, SLE, vasculitis (polyarteritis), HSP, bacterial endocarditis, exercise hematuria

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15
Q

What is proteinuria with casts vs. proteinuria without casts?

A 
with casts (glomerulonephritis)
without casts (UTI)
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16
Q

What is oliguria and anuria and what are the causes?

A
  • oliguria <500mL/day
  • anuria <50mL/day

*dehydration, nephritic syndrome, renal failure, obstruction

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17
Q

What are some causes of polyuria and what is it?

A

> 3L/day

-increased fluid intake, DM, nephrotic syndrome, D. insipidus, osmotic

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18
Q

Where does ADH mainly act on?

A

collecting duct

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19
Q

What is the glomerular filtrate?

A

180L/day

  • mostly reabsorbed (only 1-2L urine/day)
  • 1.2L blood filtrated/min
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20
Q

What are the immunological causes of glomerulonephritis?

A
  • glomerular Ag (anti GBM) –> autoimmune; crescentic
  • non-glomerular Ag (complement activation due to Ab against Ag in glomerulus) –> insitu*, SLE, strep A
  • circulating immune complex deposition (Ag/Ab) –> SLE, infections
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21
Q

What are the morphological types of glomerulonephritis?

A
  • diffuse –> all glomeruli
  • focal –> some glomeruli
  • global –> whole glomerulus
  • segmental –> part of glomerulus
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22
Q

What is the commonest cause of glomerular damage?

A

immune-mediated

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23
Q

What are the 2 types of immune complex deposition in glomerulus?

A

Linear –> insitu

Granular (lumpy) –> circulating (irregular) **more common

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24
Q

What are the 3 characteristic features of nephrotic syndrome?

A
  • massive albuminuria
  • hypoalbuminemia
  • hyperlipidemia

*non-inflammatory

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25
Q

What is the commonest secondary cause of nephrotic syndrome?

A

DM

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26
Q

What are the primary glomerular diseases of nephrotic syndrome?

A
  1. minimal change disease (MCD)
  2. focal segmental glomerulosclerosis (FSGS)
  3. membranous GN (MGN)
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27
Q

What is the commonest type of nephrotic syndrome in children?

A

minimal change GN
AKA: nil disease; lipoid nephrosis

*80% nephrotic synd. in kids

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28
Q

What is the etiology of minimal change GN?

A

-idiopathic; destruction of podocytes

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29
Q

What is the microscopy of minimal change GN?

A

normal routine microscopy

-loss of foot processes only visible on electron microscopy**

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30
Q

What is the prognosis of minimal change GN?

A
  • spontaneous remission in majority

- some may progress to chronic renal failure or focal segmental glomerulosclerosis (FSGS)

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31
Q

What is the morphology of FSGS?

A
  • segmental collapse necrosis
  • IgM deposit
  • podocyte damage (like MCD)
  • protein casts
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32
Q

What is collapsing glomerulopathy?

A

When FSGS becomes severe and the whole glomerulus is affected –> HIV; drugs, etc

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33
Q

True or False?

FSGS is associated with NHL

A

False

-HL

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34
Q

What are the secondary causes of FSGS?

A
  • HIV
  • HL
  • IgA nephropathy
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35
Q

What are the primary and secondary causes of membranous GN?

A

primary:
-autoantibody to podocyte Ag

secondary:
-HBV, SLE, malignancy, gold/mercury poisoning, drugs (anti-inflamm.)

36
Q

What is the pathogenesis of membranous GN?

A
  • Ab against podocyte Ag
  • directly activating complement (C3, C5b-C9)
  • only proteinuria
  • no inflammation*
37
Q

How do lab + clinical findings of membranous GN differ to MCD lab/clinical findings?

A

MCD –> selective proteinuria (only albumin)

membranous GN –> damage is increased - non-selective proteinuria (albumin + globulin); hematuria maybe present; still NO inflammation

38
Q

Why is membranous GN known as ‘wire loop’?

A

-morphologically, glomerular capillaries appear like thick wires due to marked deposition of antibodies

39
Q

What is the morphology of membranous GN?

A
  • wireloop thick BM (some damage)
  • sub-epithelial humps of IgG + C3, effacement of foot processes
  • no inflammation –> nephrotic
  • protein casts
40
Q

What is the commonest type of nephrotic syndrome in adults?

A

membranous GN

41
Q

What are the characteristic features of nephritic syndrome?

A
  • oliguria
  • hematuria
  • azotemia
  • HTN
  • non-selective proteinuria
42
Q

What are the primary glomerular diseases in nephritic syndrome?

A
  1. post-strep proliferative GN
  2. IgA nephropathy
  3. rapidly progressive GN
43
Q

What is the commonest cause of nephritic syndrome in children?

A

acute post-strep diffuse proliferative GN (‘post infectious GN’)

44
Q

What is the etiology of post-strep proliferative GN?

A
  • autoimmune
  • GABH strep (Type 12 - nephritogenic sp)
  • other bacteria/virus, etc can cause it too
45
Q

What is the pathogenesis of post-strep proliferative GN?

A
  • 1-4wks post-infection
  • insitu immune complex depostion - C3/IgG coarse subepithelial deposits –> inflammation with neutrophil infiltration/mesangial cell proliferation –> compression of glomerular capillaries –> oliguria + severe damage –> hematuria/non-selective proteinuria
46
Q

What is the lab findings in post strep proliferative GN?

A
  • oliguria
  • hematuria
  • RBC casts
  • non-selective proteinuria
  • decr. serum complements (C3 - hypocomplementemia)
47
Q

What is the morphology of post-strep proliferative GN?

A
  • diffuse, hypercellular glomeruli with neutrophils
  • inflammation
  • collapsed capillaries (narrow/non-patent**)
  • RBC casts
48
Q

What is a common cause of recurrent hematuria in Young?

A 
IgA nephropathy (Berger's disease)
-males, Asia-Pacific, Infections*
49
Q

What is the etiology of IgA nephropathy?

A
  • abnormal IgA
  • Abs formed against glycosylated IgA
  • congenital
50
Q

What is secondary IgA nephropathy?

A
  • associated with celiac/liver disease

- due to lack of removal of IgA from the body

51
Q

What is the morphology of IgA nephropathy?

A
  • IgA containing immune deposits
  • C3 in mesangium
  • high serum IgA1
52
Q

What are the clinical features of IgA nephropathy?

A
  • episodic, asymptomatic hematuria –> microscopic hematuria (40%); massive hematuria (40%)
  • usually following infections
53
Q

What is rapidly progressive GN AKA?

A

Crescentic GN

N.B. not a separate disease –> ANY GN may result in RPGN

54
Q

What is RPGN? and its microscopic features?

A 
acute, severe, rapidly progressive renal failure (WEEKS)
Micro:
-crescent (inflamm exudate)
-compressed glomerular capillary
-mixed casts within tubules
55
Q

Why is it called crescentic GN?

A
  • severe inflammation in glomerulus

- inflamm fluid/exudate secreted from glomerulus into bowman’s capsule –> crescent formation of inflammatory exudate

56
Q

What is the pathogenesis of edema in nephritic syndrome?

A
  • oliguria/decreased GFR

- salt and water retention –> HTN

57
Q

What % of crescentic/RPGN leads to chronic GN? and post-streptococcal GN?

A

crescentic –> 90% - poor prognosis

post-strep GN –> 1%

58
Q

What is acute renal failure?

A
  • acute deterioration of renal function - oliguria, anuria, uremia
  • decreased GFR (<20ml/min) –> BUN + Creatinine increased
59
Q

What is the commonest type of acute renal failure?

A

Pre-renal (60%)

others: intrinsic/renal (30%) + post-renal (10%)

60
Q

What are the pre-renal causes of renal failure?

A
  • hypovolemia, shock, dehydration, cardiac failure

- microangiopathy –> DIC, HUS, TTP, etc- arterial block emboli

61
Q

What are the renal causes of renal failure?

A
  • acute tubular necrosis
  • acute glomerulonephritis
  • acute tubulointerstitial nephritis
  • infiltrations, malignancy, tubular obstructions –> drugs, Hb, myoglobin, myeloma proteins, etc
62
Q

What are the post-renal causes of renal failure?

A

-urinary tract obstruction –> stones, UTI, tumours, bladder, prostate

63
Q

What is FENa% and its interpretation?

A

Fractional Excretion of sodium –> % of sodium filtered by the kidney what is excreted in the urine

  • <1% = pre-renal
  • > 1% = renal
  • > 4% = post-renal
64
Q

What is acute tubular necrosis?

A
  • acute tubular injury (ATI)
  • necrosis of tubular epithelium –> fall as epithelial casts
  • *commonest cause of renal ARF**
65
Q

What are the 2 types of acute tubular necrosis?

A
  1. Ischaemic type
    - obstruction to BVs
    - patchy (PCT + DCT)
    - hypovolemia, shock, DIC, HUS, TTP, etc
  2. Toxic type
    - due to toxins
    - PCT only*
    - drugs, toxins, mercury, CCL4, radiocontrast, Hb, myoglobin, bilirubin, immunoglobulins
    - REVERSIBLE* –> dialysis
66
Q

How do the cells of the DCT compare to PCT cells?

A

DCT cells are typically flatter in appearance

67
Q

What is microscopy of acute tubular necrosis (toxic) and (ischaemic)?

A

Toxic:

  • normal glomerulus
  • necrotic PCT –> NO nuclei
  • normal DCT (protein cast inside)

Ischaemic:

  • epithelial sloughing (all tubules)
  • pyknosis of nuclei in both PCT/DCT –> patchy
  • epithelial casts
  • pink appearance
68
Q

What is benign nephrosclerosis?

A
  • AKA hypertensive nephropathy/vascular nephrosclerosis
  • arteriolosclerosis (hyperplastic + hyaline)
  • pathogenesis (increased hydrostatic pressure - BP)
  • glomerulosclerosis –> atrophy –> fine granular surface (orange peel) - cortical atrophy**
  • African race –> apolipoprotein L1 mutation (trypanosoma resistance)
69
Q

What is the gross and microscopic appearance of benign nephrosclerosis?

A

Gross:

  • leathery granularity (orange peel) –> due to glomerular scarring in cortex
  • cortical atrophy

Micro:

  • artery sclerosis
  • glomerular sclerosis
  • narrowed capillary lumen
70
Q

What is the microscopic appearance of kidney in malignant hypertension?

A

fibrinoid necrosis of arteriole

71
Q

What is analgesic nephropathy?

A
  • tubulointerstitial nephritis
  • progressive chronic use of analgesics (phenacetin*)
  • chronic eosinophilic interstitial inflammation with tubular injury
  • renal papillary necrosis, sloughing + calcification (grossly) –> CRF
  • clinical: hematuria, renal colic, mild proteinuria + leukocyturia
  • rare urothelial Ca. of renal pelvis
72
Q

What is NSAID nephropathy?

A
  • NOT analgesic
  • COX inhibition –> decreased PGs –> vasoconstriction –> interstitial nephritis - acute or chronic (like analgesic)

*MCD or MGN

73
Q

What is chronic renal failure and what are the common causes?

A
  • progressive scarring of the kidney from any cause (infection, GN, etc) –> resulting in CRF eventually terminating in ESRD (dialysis/transplantation)
  • HTN + DM = commonest clinical causes
74
Q

What are the 2 major types of CRF?

A
  1. end stage of several types of GN/kidney injury (secondary)
  2. primary (de novo) presentation –> idiopathic
75
Q

What are the clinical features of CRF?

A
  • uremia –> N/V, GI bleeding, anemia, itching (pruritis)
  • metabolic –> acidosis (kussmaul), increased K, BUN, creatinine
  • osteodystrophy –> decreased vit. D = decreased Ca = increased PTH = increased bone lysis
  • endocrine –> hyperparathyroidism (secondary)
  • bleeding –> plt. dysfunction due to uremia (toxins)
  • anemia –> decreased EPO, bleeding, RBC lysis (uremia - toxins)
  • skin pigmentation
  • pericarditis
  • myopathy, neuropathy, coma
76
Q

What is the most important Ix. for chronic kidney disease? and what is the normal value?

A

GFR/eGFR

-normal = 120mL

77
Q

How is eGFR calculated?

A

MDRD formula

  • Modification of Diet in Renal Disease
  • 4 variables: age, gender, ethinicity, serum creatinine

**(140 - age) x Wt/(0.81 x SCr) [x 0.85 if F]

78
Q

Outline CRF staging

A

CRF staging = mL/min/1.73m^2

  1. GFR > 90mL (asymptomatic)
  2. GFR 60-89mL (asymptomatic)
  3. GFR 30-59mL (mild kidney failure)
  4. GFR 15-29mL (moderate)
  5. GFR < 15mL (severe –> ESRD)*–> dialysis/transplant
79
Q

What is the microscopy of ESRD?

A
  1. scarred glomeruli (collagen)
  2. atrophic tubules (no epithelium) with only casts
  3. interstitial inflammation
80
Q

True or False?

Pyelonephritis is usually bilateral

A

False

-unilateral*

81
Q

What is vesicoureteral reflux?

A
  • retrograde transport of urine from bladder to kidney

- due to defective sphincter (deranged vesicoureteral junction)

82
Q

What is pyelonephritis? and what are the causes?

A
  • suppurative tubulointerstitial inflammation
  • acute/chronic; usually unilateral
  • secondary to UTI/UTO, DM, pregnancy
  • vesicoureteral reflux (deranged vesicoureteral junction)** commonest cause
  • papillary necrosis = poor prognosis
83
Q

What are the gross and microscopic features of pyelonephritis?

A

Gross:

  • abscess/pus –> atrophy scarring (large wide irregular scars) –> ESRD
  • small, shrunken

Micro:

  • plenty of inflammatory cells (neutrophils)
  • WBC casts within tubules +tubular atrophy
  • scarring of interstitium
84
Q

What are the clinical features of pyelonephritis?

A
  • fever
  • loin pain
  • pyuria (pus in urine)
85
Q

What are the gross and microscopic features of diabetic nephropathy?

A

Gross:

  • shrunken
  • atrophic
  • prominent pelvic fat
  • papillary necrosis

Micro:

  • necrosis of renal papillae
  • hyaline arterolosclerosis
  • nodular glomerularsclerosis (KW/diffuse)
  • tubular atrophy
  • interstitial inflammation

Pathology Term 5 (6 decks)

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