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patho II > Renal I (b) - Nephritic Syndrome > Flashcards

Renal I (b) - Nephritic Syndrome Flashcards

1
Q

IG-A Nephropathy is aka?

A

Berger Disease

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2
Q

IG-A Nephropathy is one of the most common causes of micro/macoscopic ————

A

Haematuria

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3
Q

There is an increased frequency of developing IG-A Nephropathy in px w/ ———- ?

A

Coeliac disease

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4
Q

IG-A Nephropathy (Berger disease)

Pathogenesis:
Respiratory or GI tract infections (in genetically susceptible individuals) –> ————- –> Deposition of ——— and ———— in the ————– –> Activation of the alternative complement pathway –> Initiation of glomerular injury

A

Respiratory or GI tract infection (in genetically susceptible individuals) –> Increased IgA synthesis —> Deposition of IgA and IgA-containing immune complexes in the Mesangium –> Activation of the alternative complement pathway –> Initiation of glomerular injury

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5
Q

Morphology:
* Normal glomeruli
* Mesangial widening and segmental inflammation of some glowmruli (Focal proliferative GN)
LM: Mesengial proliferation
IF: Mesangial IgA deposits, often w/ C3

Features of?

A

IG-A Nephropathy (Berger disease)

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6
Q

Microscopic Findings:
* Mesangial cell proliferation
* Segmental endo-capillary proliferation
* Segmental glomerulosclerosis and adhesion
* Focal accumulation of hyaline
* Focal presence of glomerular crescents
* Tubular atrophy with interstitial fibrosis
* Mesangial hypercellularity
* mesangial IgA depositis on IF

features of?

A

IG-A Nephropathy (Berger disease)

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7
Q

CF of Berger disease (IG-A Nephropathy)

A

1) Macro-Haematuria after respiratory/GI tract infection (>50%)
2) Micro-haematuria +/- proteinurea (30-40%)
3) 5-10 % –> Typical Nephritic Syndrome

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8
Q

25-50% of cases of Berger’s disease –> Development of ————–

A

Chronic Renal Failure

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9
Q

Alport syndrome is an X-linked dominant disease caused by mutations in genes encoding ———-?

A

a5 type IV collagen

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10
Q

Morphology
(Electron Microscopy):
* Irregular foci of thickening and thinning and splitting of GBM–> “Basket-weave” appearance

Features of?

A

Alport Syndrome

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11
Q

Alport Syndrome

EM: Irregular thickening and thinning and splitting of the GBM –> ————— appearance

A

“Basket weave”

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12
Q

CF of Alprot syndrome

A

1) Eye disorders (e.g. Lens dislocation, Posterior
Cataracts, Corneal dystrophy)
2) Slowly progressing Proteinuria
3) Gross or microscopic Haematuria
4) Nerve Deafness

* Can’t see, Can’t pee, Can’t hear a bee

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13
Q

menomic : Can’t see, Can’t pee, Can’t hear
what CM do these stand for+ which disorder is this?

A

1) Gross or microscopic Haematuria
2) Slowly progressing Proteinuria
3) Nerve Deafness
4) Eye disorders (e.g. Lens dislocation, Posterior
Cataracts, Corneal dystrophy)

Alport Syndrome

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14
Q

causes of Rapidly progressive Glomerulonephritis

A

Goodpasture syn., post-infectious GN, SLE

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15
Q

What distinctive microscopic feature identifies Rapidly progressiVe Glomerulonephritis

A

“Crescents”

aka Rapidly progressive (Crescentic) GN

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16
Q

Calssification of Rapidly progressive GN

A

1) Type I (Anti-GBM Antibody)
2) Type II (Immune Complex)
3) Type III (Pauci-Immune)

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17
Q

CM of Rapidly progressive GM

A

1) Rapid and progressive loss of renal function
2) Severe Oliguria
3) Signs of Nephritic Syndrome

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18
Q

In Rapidly progressive GM the presence of < 80% of “Crescents” –> [Better/poor] prognosis

A

Better

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19
Q

what organs are involved in Goodpasture syndrome ?

A

Kidney and Lungs

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20
Q

what stain is used to demeonstrate Renal BM?

A

jones’ Methenamine Silver stain (JMS)

* Same as PAS

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21
Q

Microscopic features:
- Areas of necrosis with rupture of capillary loops
- “Wire loop” lesion of Lupus Nephritis
- Epithelial Crescent
- IF: Fibrinogen Ab

Feautres of?

A

Rapidly progressive (Crescentic) GM

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22
Q

Macroscopic Features:
* Enlarged and pale kidneys
* Petechial, cortical located haemorrhages

Microscopic Findings:
* Formation of “Crescents”, by the proliferation parietal cells and the infiltration of monocytic inflammatory cells
* IF: Strong staining of linear IgG and C3 deposits, along the GBM
* EM: Focal disruptions of the GBM
* Treatment: Plasmapheresis

Features of?

A

Anti-glomerular BM Antibody-mediated Crescentic GN

*type I class of Rapidly progressive GN

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23
Q

On IF of Anti-Glomerular BM Antibody-mediated Crescentic GN , Strong staining of linear ——- and ———– deposits, along the GBM are found

A

Strong staining of linear IgG
and C3 deposits, along the GBM

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24
Q

Lab finding of Anti-Glomerular BM Antibody-mediated Crescentic GN

A

Serum anti-GBM Antibodies

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25
Q

Immune Complex-Mediated progressive GN (Type II)

Microscopic Findings:
* Segmental necrosis and GBM breaks –> ”———–“ and
* Diffuse proliferation and leukocyte exudation (Post Infectious Glomerulonephritis, SLE)
* Mesangial proliferation (IgA Nephropathy, HenochSchönlein Purpura)
* IF: Characteristic granular (“—————”) pattern of immune complex disease

A

*Segmental necrosis and GBM breaks –> “Crescents”
*IF: (“lumpy bumpy”) pattern of immune complex disease

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26
Q

Microscopic Findings:
* Segmental necrosis and GBM breaks -> “Crescents” and
* Diffuse proliferation and leukocyte exudation
* Mesangial proliferation
* Immunofluorescence: Characteristic granular (“lumpy bumpy”)

Features of?

A

Immune Complex-Mediated progressive GN (Type II)

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27
Q

pathogenesis of Lupus Nephritis:
Deposition of ————- within the glomeruli -> Inflammatory response –> Proliferation of the ————–, ————— and/or ———–, but also ———— of the glomeruli, in severe cases

A

Deposition of DNA-anti-DNA complexes within the glomeruli –> Inflammatory response ->Proliferation of the endothelial, mesangial and/or epithelial cells, but also necrosis of the glomeruli, in severe cases

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28
Q

Most common type of Lupus Nephritis

A

Diffuse Lupus Nephritis (Class IV)

* (35-60% of patients) and most
serious form

29
Q

Micro features of Diffuse Lupus Nephritis (Class —):
* Extensive —————– immune complexes –>
Circumferential thickening of the capillary wall
(“—————”)
* Involvement of >–%of glomeruli

A

(Class IV)
* Extensive sub-endothelial immune complexes -> Circumferential thickening of the capillary wall
(“wire loops”)
* Involvement of >50% of glomeruli

30
Q

CF of Diffuse Lupus Nephritis (Class IV)

A

1) Haematuria,
2) moderate to severe Proteinuria,
3) Hypertension and
4) Renal Insufficiency

31
Q

* Lupus Nephritis

———- Lupus Nephritis (Class –):
- Immune complexes in the mesangium

A

Minimal Mesangial Lupus Nephritis (Class I):
* Immune complexes in the mesangium

32
Q

* Lupus Nephritis

—————- Lupus Nephritis (Class —):
* Immune complexes in the mesangium
* Mild to moderate increase in the mesangial matrix
and cellularity

A

Mesangial Proliferative Lupus Nephritis (Class II):

33
Q

————- Lupus Nephritis (Class —):
- Complete sclerosis of greater than 90% of glomeruli

A

Advanced Sclerosing Lupus Nephritis (Class VI):

34
Q

CF of Advanced Sclerosing Lupus Nephritis (Class VI)?

A

End-stage Renal Disease

35
Q

———— Lupus Nephritis (Class —):
* Diffuse thickening of the glomerular capillary wall, due to deposition of sub-epithelial immune complexes

A

Membranous Lupus Nephritis (Class V):

36
Q

Membranous Lupus Nephritis (Class —-):
* Diffuse thickening of the —————,
due to deposition of ————- immune
complexes

A

Membranous Lupus Nephritis (Class V):
* Diffuse thickening of the glomerular capillary wall, due to deposition of sub-epithelial immune complexes

37
Q

Focal Lupus Nephritis (Class —-):
* Lesions in < –% of the glomeruli
* Segmental or global distribution, within each glomerulus
* Active lesions: Swelling and proliferation of
———- and ———– cells, neutrophilic infiltrates, —————, capillary thrombi

A

Focal Lupus Nephritis (Class III):
* Lesions in < 50% of the glomeruli
* Segmental or global distribution, within each glomerulus
* Active lesions: Swelling and proliferation of
endothelial and mesangial cells, neutrophilic infiltrates, fibrinoid deposits, capillary thrombi

38
Q

———–Lupus Nephritis (Class —):
* Lesions in < 50% of the glomeruli
* Segmental or global distribution, within each
glomerulus
* Active lesions: Swelling and proliferation of
endothelial and mesangial cells, neutrophilic
infiltrates, fibrinoid deposits, capillary thrombi

A

Focal Lupus Nephritis (Class III):

39
Q

CF of Focal Lupus Nephritis (Class III)

A

From mild microscopic Haematuria and Proteinuria to —> erythrocyte casts and Acute, Severe Renal Insufficiency

40
Q

causes of pauci-immune Crescentic glomerulonephritis

A

Systemin Vasculitis
1) Microscopic Polyangiitis
2) Wegnes Granulomatosis

41
Q

Microscopic Findings:
* Segmental necrosis and GBM breaks –> “Crescents”
* Lack of anti-GBM Abs or Immune Complexes (IF & EM)

features of?

A

Pauci-immune Crescentic GN

42
Q

Lab findins of Pauci-immune GN?

A

ANCA in serum

43
Q

Inflammatory reactions of the tubules and interstitium –> ————

A

Tubulo-Interstitial Nephritis

44
Q

Ischaemic or toxic tubular injury –> ———–

A

Acute Tubular Injury

45
Q

Causes of Tubulo-Interstitial Nephritis

A
  • Pyelonephritis
  • Toxins (e.g. Drugs, Analgesics, Heavy Metals, etc.)
  • Metabolic diseases (e.g. Hypokalaemic-, Oxalate-, Acute Phosphate-Nephropathy, etc. )
  • Chronic Urinary Tract Obstruction
  • Neoplasms (e.g. Multiple Myeloma)
46
Q

Causes of Acute Pyelonephritis

* Ischaemic or toxic tubular injury

A

Enteric gram (-) rods (e.g. E. coli, Proteus,
Klebsiella, etc.)

47
Q

Macroscopic Features:
* Discrete, pale, raised abscesses on the surface

Microscopic Findings:
* Intra-parenchymal liquefactive necrosis, with abscess development
* Prominent, intra-tubular, neutrophil cell infiltrates
* Extension into the collecting ducts, resulting in
the formation of the white cell casts in the urine

featurs of?

A

Acute Pyelonephritis

48
Q

Acute Pyelonephritis

Macroscopic Features:
* Discrete, ——–, raised ————- on the surface

Microscopic Findings:
* —————— liquefactive necrosis, with abscess development
* Prominent, intra-tubular, ————–
* Extension into the collecting ducts, resulting in
the formation of the —————- in the urine

A

Micro:
* Discrete, pale, raised abscesses on the surface

Macro:
* Intra-parenchymal liquefactive necrosis, with abscess development
* Prominent, intra-tubular, neutrophil cell infiltrates
* Extension into the collecting ducts, resulting in
the formation of the white cell casts in the urine

49
Q

CF of Acute Pyelonephritis

A

1) Pain at the costo-vertebral angle
2) Generalised Signs and Symptoms of infection:
- Chills
- Fever
- Malaise

3) Dysuria, Frequency and Urgency
4) Turgid urine (Pyuria)

50
Q

Predisposing factors of Acute Pyelonephritis

A

1) Benign Prostatic Hyperplasia and Uterine Prolapse (Ouflow obstruction)
2) DM
3) Vesico-Ureteral Reflux (Incompetence of VesicoUreteral Orifice); i. Congenital defect, ii. Acquired
(Spinal Cord Injury, Neurogenic Bladder Dysfunction
[DM])

51
Q

Patho of Acute Pyelonephritis
-Bacterial spread to the kidney by:
1) —————-
2) —————–

A

Bacterial spread to the kidney by:
1) Ascending infection : Mucosal adhesion of the bacteria –> Colonisation of the distal Urethra –> Movement against urine flow –> Extension to the Urinary Bladder and Kidneys
2) Haematogenous dissemniation : In the course of Septicaemia or Infective Endocarditis

52
Q

Complication of Acute Pyelonephritis

A

1) Papillary necrosis
2) Pyonephrosis
3) Peri-Nephric Abscess

* p.45 (explanation)

53
Q

———: Total or almost complete obstruction and accumulation of pus in pelvis, calyces and ureter

A

Pyeonephrosis

54
Q

———-: Disorder in which chronic tubulo- interstitial inflammation and renal scarring are associated with pathologic involvement of the pelvi-calyceal system

A

Chronic Pyelonephritis

55
Q

causes of Chronic Pyelonephritis

A

2 forms:
1) Chronic obstructive Pyelonephritis
2) Chronic Reflux-associated Pyelonephritis

56
Q

Macroscopic Features:
* Irregular scarring; Coarse, discrete, cortico-medullary scars
* Dilated, blunted, or deformed calyces
* Flattened papillae

Microscopic Findings:
* Uneven interstitial fibrosis
* Mixed inflammatory cell infiltrates
* Dilatation of tubules, with atrophy of the lining
epithelium
* Presence of intraluminal colloid (PAS[+]) casts –> Resemblance to Thyroid tissue [“Thyroidization”]
* Hyaline Arteriolosclerosis (Hypertension)
* Focal Segmental Glomerulosclerosis

features of?

A

Chronic Pyleonephritis

57
Q

* Chronic Pyelonephritis

Macroscopic Features:
* —————; Coarse, discrete, cortico-medullary scars
* Dilated, blunted, or deformed ——-
* Flattened ————–

Microscopic Findings:
* Uneven interstitial fibrosis
* Mixed inflammatory cell infiltrates
* Dilatation of tubules, with atrophy of the lining
epithelium
* Presence of ——————- –> Resemblance to Thyroid tissue [”————–”]
* Hyaline Arteriolosclerosis (Hypertension)
* Focal Segmental Glomerulosclerosis

A

Macroscopic Features:
* Irregular scarring; Coarse, discrete, cortico-medullary scars
* Dilated, blunted, or deformed calyces
* Flattened papillae

Microscopic Findings:
* Uneven interstitial fibrosis
* Mixed inflammatory cell infiltrates
* Dilatation of tubules, with atrophy of the lining
epithelium
* Presence of intraluminal colloid (PAS[+]) casts –> Resemblance to Thyroid tissue [“Thyroidization”]
* Hyaline Arteriolosclerosis (Hypertension)
* Focal Segmental Glomerulosclerosis

58
Q

CF of Chronic Obstructive Pyelonephritis

A
  • Insidious Onset or
  • Manifest as Acute Recurrent Pyelonephritis, with:
  • Back pain
  • Fever
  • Frequent Pyuria (puss in pee)
59
Q

Cf of Chronic Reflux Nephropathy

A

1) Hypertension, in children
2) Loss of tubular function –> Polyuria and Nocturia

60
Q

What is observed on imaging in a px w/ Chronic Pyelonephritis

A
  • Asymmetrically contracted Kidney
  • Blunting and deformity of the Calyceal system (Caliectasis)
61
Q

Cause of Drug-induced Interstitial Nephritis

A

1) Synthetic Penicillins (e.g. Methicillin, Ampicillin, etc.)
2) NSAIDs
3) Diuretics (e.g. Thiazides)

62
Q

CF of Drug-Induced Interstitial Nephritis

A

About 15 days, after exposure to the Drug, with:
1) Fever
2) Eosinophilia
3) Haematuria
4) Minimal or no Proteinuria
5) Leukocyturia (indication of UTI)
6) Serum Creatinine elevated or Acute Kidney Injury
with Oliguria (50% of cases)

63
Q

cause of Chronic Obstructive Pyelonephritis

A
  • Bilateral (Congenital Anomalies of the Urethra)
  • Unilateral (e.g. Calculi)
64
Q

Causes of Reflux Nephropathy

* Chronic Reflux-associated Pyelonephritis

A

UTIs (on Congenital vesico-ureteral Reflux and Intra-renal reflux)

* Mostly children

65
Q

Patho of Reflux Nephropathy:
* Superimposition of an ———- on Congenital Vesico-Ureteral Reflux and intra-renal reflux -> Renal damage –> ——— and ————–>
Chronic Renal Insufficiency (in cases of ——— involvement)

A

Superimposition of an urinary tract infection
on Congenital Vesico-Ureteral Reflux and
intra-renal reflux –> Renal damage –>Scarring and Atrophy –> Chronic Renal Insufficiency (in cases of bilateral involvement)

66
Q

Patho of Drug induced Intertitial Nephritis :
* Covalent binding of drug (acts as hapten) to cytoplasmic or extra-cellular component of tubular cells –> Acquisition of immunogenicity –> ——- and ———— to tubular cells or their basement membranes**

A

IgE and cell mediated immune reaction

67
Q

causes of Acute tubular injury

A

1) Acute Kidney Injury (Oliguria; Urine Output: <400mL/day)
2) Severe Glomerular disease
3) Diffuse Renal Vascular Diseases (Thrombotic Microangiopathies, Microscopic Polyangiitis)
4) Acute Drug-induced Allergic Interstitial Nephritis
5) Ischaemic Acute Tubular Injury –> Generalised or localised reduction in blood flow; Marked Hypotension and Shock
6) Nephrotoxic Acute Tubular injury: Various Poisons (e.g.Heavy Metals, Organic Solvents, some Antibiotics etc.)

68
Q

CF of Acute tubular Injury

A

1) Oliguria (cases of Acute Kidney Injury), Anuria or even non-oliguric (milder) cases
2) Decreased GFR
3) Electrolyte abnormalities
4) Acidosis
5) Signs and Symptoms of Uraemia and Fluid Overload

69
Q

Ischaemic Acute Tubular Injury:
Morphology
* Mainly affected segments: Straight portion of the
————— and —————–
* —————- and sloughing of brush borders
* Detachment of tubular cells from BM
* Vacuolisation of cells
* —————— casts (mainly ———— protein or Uromodulin) in the distal tubules and collecting
ducts
* —————- of the interstitium
* Mild, mixed inflammatory cell infiltrates

A

Ischaemic Acute Tubular Injury:
* Mainly affected segments: Straight portion of the
proximal tubule and ascending thick limb
* Blebbing and sloughing of brush borders
* Detachment of tubular cells from BM
* Vacuolisation of cells
* Proteinaceous casts (mainly Tamm-Horsfall protein or Uromodulin) in the distal tubules and collecting ducts
* Generalised oedema of the interstitium
* Mild, mixed inflammatory cell infiltrates

patho II (29 decks)

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