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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
# **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
*Segmental necrosis and GBM breaks --> **“Crescents”** *IF: **(“lumpy bumpy”)** pattern of immune complex disease
26
Microscopic Findings: * Segmental necrosis and GBM breaks -> **“Crescents”** and * **Diffuse proliferation and leukocyte exudation** * Mesangial proliferation * Immunofluorescence: Characteristic granular **(“lumpy bumpy”)** Features of?
**Immune Complex-Mediated progressive GN (Type II)**
27
pathogenesis of **Lupus Nephritis**: Deposition of **-------------** within the glomeruli -> Inflammatory response --> Proliferation of the **--------------, --------------- and/or -----------**, but also **------------** of the glomeruli, in severe cases
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
28
Most common type of Lupus Nephritis
Diffuse Lupus Nephritis (Class IV) | * (35-60% of patients) and most serious form
29
Micro features of Diffuse Lupus Nephritis (Class **---**): * Extensive **-----------------** immune complexes --> Circumferential thickening of the capillary wall **(“---------------”)** * Involvement of **>--%**of glomeruli
**(Class IV)** * Extensive **sub-endothelial** immune complexes -> Circumferential thickening of the capillary wall **(“wire loops”)** * Involvement of **>50%** of glomeruli
30
CF of Diffuse Lupus Nephritis (Class IV)
1) Haematuria, 2) moderate to severe Proteinuria, 3) Hypertension and 4) Renal Insufficiency
31
# * Lupus Nephritis **----------** Lupus Nephritis (Class **--**): - Immune complexes in the mesangium
**Minimal Mesangial** Lupus Nephritis **(Class I)**: * Immune complexes in the mesangium
32
# * Lupus Nephritis **----------------** Lupus Nephritis (Class **---**): * Immune complexes in the mesangium * Mild to moderate increase in the mesangial matrix and cellularity
**Mesangial Proliferative** Lupus Nephritis **(Class II)**:
33
**-------------** Lupus Nephritis (Class **---**): - Complete sclerosis of greater than 90% of glomeruli
**Advanced Sclerosing** Lupus Nephritis **(Class VI)**:
34
CF of Advanced Sclerosing Lupus Nephritis (Class VI)?
End-stage Renal Disease
35
**------------** Lupus Nephritis (Class **---**): * Diffuse thickening of the glomerular capillary wall, due to deposition of **sub-epithelial** immune complexes
**Membranous** Lupus Nephritis **(Class V)**:
36
Membranous Lupus Nephritis (Class **----**): * Diffuse thickening of the **---------------**, due to deposition of **-------------** immune complexes
Membranous Lupus Nephritis **(Class V):** * Diffuse thickening of the **glomerular capillary wall,** due to deposition of **sub-epithelial** immune complexes
37
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
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
**-----------**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
**Focal** Lupus Nephritis **(Class III)**:
39
CF of Focal Lupus Nephritis (Class III)
From mild microscopic Haematuria and Proteinuria to ---> **erythrocyte casts** and Acute, Severe Renal Insufficiency
40
causes of pauci-immune Crescentic glomerulonephritis
Systemin Vasculitis 1) Microscopic Polyangiitis 2) Wegnes Granulomatosis
41
Microscopic Findings: * Segmental necrosis and GBM breaks --> “**Crescents”** * Lack of anti-GBM Abs or Immune Complexes (IF & EM) features of?
Pauci-immune Crescentic GN
42
Lab findins of Pauci-immune GN?
**ANCA** in serum
43
Inflammatory reactions of the tubules and interstitium --> ------------
Tubulo-Interstitial Nephritis
44
Ischaemic or toxic tubular injury --> **-----------**
Acute Tubular Injury
45
Causes of Tubulo-Interstitial Nephritis
* **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
Causes of Acute Pyelonephritis | * Ischaemic or toxic tubular injury
Enteric gram (-) rods (e.g. E. coli, Proteus, Klebsiella, etc.)
47
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?
Acute Pyelonephritis
48
# **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
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
CF of Acute Pyelonephritis
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
Predisposing factors of Acute Pyelonephritis
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
Patho of Acute Pyelonephritis -Bacterial spread to the kidney by: 1) **----------------** 2) **-----------------**
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
Complication of Acute Pyelonephritis
1) Papillary necrosis 2) Pyonephrosis 3) Peri-Nephric Abscess | * p.45 (explanation)
53
**---------**: Total or almost complete obstruction and **accumulation of pus in pelvis**, calyces and ureter
Pyeonephrosis
54
**----------**: Disorder in which chronic tubulo- interstitial inflammation and renal scarring are associated with pathologic involvement of the **pelvi-calyceal system**
Chronic Pyelonephritis
55
causes of Chronic Pyelonephritis
2 forms: 1) Chronic obstructive Pyelonephritis 2) Chronic Reflux-associated Pyelonephritis
56
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?
Chronic Pyleonephritis
57
# * 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
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
CF of Chronic Obstructive Pyelonephritis
* Insidious Onset or * Manifest as Acute Recurrent Pyelonephritis, with: - Back pain - Fever - Frequent **Pyuria (puss in pee)**
59
Cf of Chronic Reflux Nephropathy
1) Hypertension, in children 2) Loss of tubular function --> Polyuria and Nocturia
60
What is observed on imaging in a px w/ Chronic Pyelonephritis
* **Asymmetrically contracted Kidney** * Blunting and deformity of the Calyceal system (**Caliectasis**)
61
Cause of Drug-induced Interstitial Nephritis
1) Synthetic Penicillins (e.g. Methicillin, Ampicillin, etc.) 2) NSAIDs 3) Diuretics (e.g. Thiazides)
62
CF of Drug-Induced Interstitial Nephritis
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
cause of Chronic Obstructive Pyelonephritis
* Bilateral (Congenital Anomalies of the Urethra) * Unilateral (e.g. Calculi)
64
Causes of Reflux Nephropathy | * Chronic Reflux-associated Pyelonephritis
**UTIs** (on Congenital vesico-ureteral Reflux and Intra-renal reflux) | * Mostly children
65
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)
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
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**
**IgE** and **cell mediated immune reaction**
67
causes of Acute tubular injury
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
CF of Acute tubular Injury
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
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
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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