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MBBS IV - Junior Clerkship WCS > JC78 (Medicine) - Glomerular, Tubulo-interstitial diseases and AKI > Flashcards

JC78 (Medicine) - Glomerular, Tubulo-interstitial diseases and AKI Flashcards

1
Q

3 standard histopathological tests for kidney biopsies

A

Light microscopy with staining

Immunofluorescence

Electron microscopy

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2
Q

List all staining techniques for light microscopy exam of kidney biopsy

A

Haematoxylin and eosin (H&E, for nuclei and cytoplasm)

Periodic acid-Schiff (for basement membrane and PAS-positive material)

Period acid silver- methenamine

Masson Trichome (for fibrosis, deposits)

Congo red (for amyloidosis)

Enzyme techniques

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3
Q

Masson-Trichrome stain

  • Usage and color changes when binding to different molecules?
A

Kidney fibrosis - blue

Kidney deposits - orange to red

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4
Q

List all primary glomerular diseases

Categorize into non-proliferative and proliferative

A

Non-proliferative:

  • Minimal change nephrotic syndrome
  • Membranous nephropathy
  • Focal segmental glomerulosclerosis
  • Thin membrane disease

Proliferative:

  • IgA Nephropathy
  • Membranoproliferative GN
  • Crescentic GN
  • IgM Nephropathy
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5
Q

List secondary glomerular diseases

Categorize into proliferate and non-proliferative causes

A

Non-proliferative

  • Diabetic nephropathy
  • Hypertensive nephrosclerosis
  • Amyloidosis
  • Light/heavy chain deposition disease
  • Alport’s syndrome
  • Infection-related membranous glomerulopathy
  • HIV nephropathy (FSGS or collapsing glomerulopathy)
  • Drug-induced glomerulopathy
  • Malignancy-associated nephropathy
  • Reflux nephropathy

Proliferative:

  • Lupus nephritis
  • Post-streptococcal GN
  • Hepatitis B or C- related membranoproliferative GN
  • Systemic vasculitis
  • Goodpasture syndrome
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6
Q

6 general presentations of glomerulonephritis

A
  1. Asymptomatic microscopic hematuria/ proteinuria
  2. Macroscopic hematuria
  3. Acute nephritic syndrome
  4. Nephrotic syndrome
  5. Rapidly progressive glomerulonephritis
  6. Chronic glomerulonephritis/ CKD
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7
Q

Asymptomatic hematuria

  • Presentation
  • Severity of proteinuria
  • Classical histopathological feature
A

Incidental finding of macroscopically/ microscopically detected RBC in urine, usually dysmorphic RBC
Normal GFR, no systemic disease

Proteinuria: variable, usually <1g/day

Feature:
Dysmorphic RBC/ Acanthocytes with ring-formed cell bodies + multiple blebs
RBC casts

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8
Q

Macroscopic haematuria

  • Presentation
  • D/dx
A

Presentation:
Episodic, painless, macroscopic hematuria
Glomerular disease - brown/ smoky urine with no clots

D/dx:

  1. Urological: Stones/ tumor
  2. Renal: Glomerulonephritis, Acute interstitial nephritis, Polycystic kidney disease
  3. Infection: Cystitis, TB, Schistosomiasis
  4. Glomerular causes: IgA Nephropathy, Alport’s syndrome, Thin Membrane Disease (benign familial hematuria)
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9
Q

Alport syndrome

  • Inheritance
  • Pathogenesis
  • Presentation
A

Inheritance: X-linked dominant

Pathogenesis: Mutation in type IV collagen genes, affect auditory sensory cells and glomeruli

Presentation:

  • High tone deafness*
  • Macroscopic Hematuria
  • Renal failure
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10
Q

How to differentiate 3 glomerular causes of macroscopic hematuria?

A
  1. Any gross hematuria?
    - Common in IgA Nephropathy and Alport syndrome
    - Rare in Thin basement membrane disease
  2. Family history of CKD:
    - Alport syndrome: Renal failure, high-tone deafness in male (X-link dominance)
    - IgA Nephropathy: Runs in family, no clear inheritance pattern
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11
Q

First-line investigations for hematuria

A

Basic:

  • Renal function test
  • Urine culture, AFB
  • Urine cytology
  • Urinalysis

Imaging:

  • X-ray or CT KUB
  • USG/ Doppler ultrasound
  • Cystoscopy
  • IV pyelogram/ retrograde pyelogram
  • CT urogram

D/dx tests:

  • Pure tone audiometry for Alport’s syndrome
  • Kidney biopsy for significant proteinuria (>1g/day)
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12
Q

First-line investigations/ evaluations for proteinuria

A
  1. Dipstix - screening for proteinuria
  2. Spot urine quantitative analysis: Urine protein- creatinine ratio
  3. Timed urine (24h)

Dipstick for screening
Quantitative analysis for monitoring and further Ix of positive dipstick

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13
Q

Standard urinary dipstick

  • Mechanism
  • Cut-offs for 5 different levels of positive dipstix for albumin
A

Mechanism:

  • Measures albumin concentration via colorimetric reaction between albumin and tetrabromophenol blue
  • Different shades of green for concentrations of albumin

Cut-offs: (mg/dL)

  • Negative
  • Trace: 15-30
  • 1+ = 30-100
  • 2+ = 100-300
  • 3+ = 300-1000
  • 4+ = >1000
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14
Q

Urine protein to creatinine Cut-off for nephrotic proteinuria

A

> 3.5mg/mg = nephrotic

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15
Q

Causes of false positive proteinuria

A

Strenuous exercise in 24h (myoglobinuria)
Concomitant systemic infection or UTI
High output state: Fever, pregnancy, hypertension
Haematuria

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16
Q

Orthostatic proteinuria

  • Define
  • Severity of proteinuria
  • Diagnostic test
A

Increased protein excretion in upright position. No proteinuria in supine position

Usu. <1g/day, may exceed 3g/day

Split urine collection (no proteinuria over night when supine, proteinuria during daytime when upright)

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17
Q

Acute nephritic syndrome

  • Presentation
  • Severity of proteinuria
  • Most common cause
A

Abrupt onset of macroscopic hematuria
Oligouria
Acute renal failure
Fluid retention - edema, hypertension

Urinary protein <3g/day

Most common cause:
- Post-streptococcal GN

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18
Q

Post-streptococcal GN

  • Typical demographic
  • Pathogenesis
  • Presentation
  • Ix
  • Tx
A

Demographic: Usu. children between age 2-10

Pathogenesis: Streptococcal antigen deposit in glomerulus during infection, with delayed host immune response

Presentation:

  • Gross hematuria, Oligouria, HT, edema develop 7 days to 12 weeks after streptococcal infection (throat/ skin)
  • Spontaneous resolution: diuresis within 1-2weeks, normal renal function within 4 weeks

Ix:

  • Total hemolytic complement activity, C3 concentrations (low)
  • Antibodies against Streptolysin O

Tx:
Penicilin, supportive therapy, temporary dialysis

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19
Q

D/dx acute nephritic syndrome with low C3 complement concentration

A

Post-streptococcal GN
Lupus nephritis
Membranoproliferative glomerulonephritis

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20
Q

Nephrotic syndrome

  • Severity of proteinuria
  • Presentation
A

Massive proteinuria >3.5g/day

Presentation:
Generalized edema - Periorbital edema, ankle edema
Hypoalbuminemia (<30g/dL) - Muehrcke’s bands in fingers
Hyperlipidemia and lipiduria, Xanthelesma
Massive proteinuria - Frothy urine

21
Q

Primary kidney diseases asso. with nephrotic syndrome

A

Primary non proliferative:
Focal segmental glomerulonephritis
Membranous glomerulopathy
Minimal change disease

Primary Proliferative:
Membranoproliferative glomerulonephritis
IgA nephropathy (sometimes)
~~~

22
Q

Systemic causes of Nephrotic syndrome

A

DM
SLE
Amyloidosis

Secondary membranous nephropathy:

  • Infection: HBV, HCV, HIV, Malaria, Syphillis
  • Malignancy: lymphoma, adenocarcinoma, myeloma
  • Drugs: penicillamine, gold, mercury, NSAIDs, Probenecid
23
Q

First-line investigations for nephrotic syndrome

Generic Tx

A

Blood:

  • CBC with differential
  • Renal function test
  • Urine protein analysis - urine protein: creatinine ratio >3.5

D/dx cause:
- Fasting glucose for DM
- Ig pattern for SLE, amyloidosis
- Secondary membranous nephropathy:
HBsAg, Anti-HCV, Anti-HIV,
Tumor screening with CXR, FOBT, tumor markers
- Idiopathic membranous nephropathy - Anti-PLA2R

Tx:
Corticosteroids, Calcineurin inhibitors for refractory cases

24
Q

Diagnostic marker for idiopathic membranous nephropathy

A

Anti-PLA2R

M-type Phospholipase A2 receptor used as target antigen

25
Q

Glomerular diseases/ diseases that do not require kidney biopsy before dx

A

Children (<12) with steroid-sensitive nephrotic syndrome or Post-streptococcal GN

Idiopathic membranous nephropathy (PLA2R +ve)
ANCA vasculitis (MPO or PR3 +ve)
Anti-glomerular basement membrane disease
Alport disease, Fabry disease
Familial focal and segmental glomerulosclerosis
SLE

26
Q

Rapidly progressive glomerulonephritis (RPGN)

  • Presentation
  • ## Histopathological feature
A

Presentation:

  • Glomerulonephritis: hematuria, proteinuria, RBC casts
  • Rapid kidney failure in days to weeks
  • Other organs: e.g. Pulmonary hemorrhage in Goodpasture’s, Hepatic failure in leptospirosis

Histological feature:
Cellular crescents - Glomerulus periphery is replaced by circumferential layer of fibro-cellular proliferation/ Crescent

26
Q

RPGN

  • Underlying etiologies
A 
Renal:
Pauci-immune GN (systemic vasculitis)
Anti-GBM disease/ Goodpastrue syndrome 
Crescentic IgA Nephropathy 
Acute post-infectious GN

Multisystem diseases:

  • Systemic vasculitides
  • Cryoglobulinemia
  • SLE
27
Q

RPGN

First-line investigations

A 
Basic: 
CBC with differentials 
RFT, electrolytes 
Urine protein quantification 
Urine sediments

Underlying cause:
- Autoimmune markers:
ANCA, Anti-GBM, ANA, Anti-dsDNA, C3/C4 concentration
- CXR and DLCO for pulmonary involvement in Goodpasture’s

28
Q

RPGN

Generic Tx

A

Systemic corticosteroids +/- immunosuppressants

Plasmapheresis for Anti-GBM Ab removal

29
Q

Chronic glomerulonephritis

  • Presentation
  • 1 major etiology
A

Progressive kidney function loss with glomerular inflammation
Proteinuria, hematuria, hypertension
Kidney atrophy

Etiology: Tubulointerstitial diseases

30
Q

Chronic glomerulonephritis

  • First-line Ix with typical findings
  • Tx
A

Ix:
CBC - NcNc anaemia
Renal: High serum urea, creatinine, PO4
Hypocalcemia, Hyperkalemia, Metabolic acidosis
USG - Kidney atrophy
Urine protein quantification - Proteinuria

Tx:
Supportive
RRT if CKD stage 5

31
Q

Tubulointerstitial diseases

  • Presentation
  • Major entities/ types
A

Presentation: due to interstitial inflammation and tubular dysfunction

  • Loss of renal function
  • Abnormal urine sediment (WBC, Protein)
  • Electrolyte disturbance
  • Acid-base disorders

Entities:

  • Acute interstitial nephritis
  • Chronic interstitial nephritis
  • Potassium-wasting tubular disorders
  • Renal tubular acidosis
32
Q

First-line investigations for AKI

A
  • Visual: Color/ Turbidity/ Volume
  • Chemical (Urine dipstick): pH/ Special gravity/ Glucose/ Protein/ Ketones/ Blood/ Leukocyte esterase/ Nitrite/ Bilirubin/ Urobilinogen
  • Microscopic (Urine sediment): RBC/ WBC/ Epithelial cells/ Microorganisms/ Casts/ Crystals

Renal function test (RFT)
• Plasma creatinine level
• Plasma urea level / Blood urea nitrogen (BUN)
• Plasma Urea: Creatinine ratio / BUN: Creatinine ratio
• Glomerular filtration rate (GFR)

Urine albumin-to-creatinine ratio (ACR)/ Urine albumin/ Urine total protein

33
Q

Clinical/ Biochemical definitions of AKI

A

Acute kidney injury (AKI) is defined by any of the following

  • Increase in serum creatinine ≥ 0.3 mg/dL (≥ 26.5 μmol/L) within 48 hours (OR)
  • Increase in serum creatinine to ≥ 1.5x from baseline which is known or presumed to have occurred within the prior 7 days (OR)
  • Urine volume < 0.5 mL/kg/hr for 6 hours
34
Q

Risk factors of AKI

A 
Pre-existing CKD 
Age >50 
Diabetic nephropathy 
Heart failure 
Hypovolemia 
Liver disease 
Sepsis, Trauma, Post-op
Cancer
35
Q

AKI

Categorize etiologies into 3 anatomical groups

A

Pre-renal (>50%)

Intrinsic: Tubular necrosis, Interstitial nephritis, Acute GN/ RPGN

Post-renal (<10%): obstructive pathologies

36
Q

List pre-renal causes of AKI

A

Hypovolemia
• Hemorrhage
• Vomiting/ Diarrhea
• Diuretics

Hypervolemia but low effective circulating volume
• Heart failure with reduced ejection fraction (HFrEF)
(Cardiorenal syndrome)
• Decompensated liver disease with portal hypertension (Hepatorenal syndrome)

Low Afferent arteriole vasodilatation
• NSAIDs: Inhibits COX enzymes and thus decreased synthesis of prostaglandins (PG)
• ACEI/ ARB
• Cyclosporine

37
Q

List intrinsic/ renal causes of AKI

A

Small vessel diseases: Thrombotic microangiopathy, renal atheroembolism, small vessel vasculitis

Large vessel vasculitides:
• Renal artery embolism/ aneurysm/ dissection
• Rena vein thrombosis
• Systemic thromboembolism

Glomerular diseases:
 Proliferative glomerulonephritis (Nephritic pattern)
 Non-proliferative glomerulonephritis (Nephrotic pattern)

Tubular and interstitial disease:
Acute tubular necrosis
Acute interstitial nephritis
Acute urate nephropathy (TLS)

38
Q

List post-renal causes of AKI

A

Obstructive diseases:

  • Bladder outlet obstruction
  • Tumors
  • Renal calculi
  • Papillary necrosis
  • Retroperitoneal fibrosis
39
Q

Management plan for AKI

A
  1. Accurate Dx and reverse underlying cause
  2. Treatment
    Fluid overload - IV Loop or thiazide diuretics

Hyperkalemia
• Restriction of dietary K+ intake, discontinuation of ACEI/ARB and loop diuretics to promote urinary K+ loss

Hypocalcemia
• Restriction of dietary PO43- intake + Calcium carbonate or calcium gluconate if symptomatic

Hyperphosphatemia
• PO4 binding agents

Metabolic acidosis
• Administration of sodium bicarbonate

Acute dialysis: Central vascular access hemodialysis

40
Q

Causes of acute tubular necrosis

A
  • Ischemia
  • Sepsis or shock
  • Endogenous nephrotoxin: Rhabdomyolysis/ Hemolysis/ Multiple myeloma
  • Exogenous nephrotoxin: Contrast nephropathy/ Aminoglycosides/ Cisplatin/ Amphotericin B
41
Q

Causes of acute interstitial nephritis

A
  • Myeloma cast nephropathy

* Drug-induced nephrotoxicity: NSAIDs/ Penicillin/ Rifampicin/ Allopurinol

42
Q

Compare the urinalysis results for proliferative vs non-proliferative glomerular disease

A

Proteinuria + Hematuria + Dysmorphic RBC + RBC casts
o Proliferative glomerular disease (Nephritic pattern)

Heavy proteinuria + NO hematuria
o Non-proliferative glomerular disease (Nephrotic pattern)/ DM nephropathy/ Amyloidosis

43
Q

Ddx high plasma urea-to-creatinine ratio/ high plasma BUN-to-creatinine ratio

A
44
Q

Ddx LOW plasma urea-to-creatinine ratio/ high plasma BUN-to-creatinine ratio

A
45
Q

AKI

S/S and pathogenesis

A

Edema
• ↓ Plasma oncotic pressure due to hypoalbuminemia
• Renal Na+ and water retention in collecting tubules - drop in plasma volume due to interstitial edema&raquo_space; compensatory increase RAAS activation

Hypertension
• Renal Na+ and water retention in collecting tubules - drop in plasma volume due to interstitial edema&raquo_space; compensatory increase RAAS activation

Oliguria/ Anuria

46
Q

Typical electrolyte profile in AKI and pathogenesis

A

Hyponatremia (↓) - Inability to excrete free water

Hyperkalemia (↑): Occurs due to presence of metabolic acidosis

  • Excess H+ are buffered in the cells and electroneutrality is maintained in part by the movement of intracellular K+ into the extracellular fluid
  • Impaired cellular uptake of K+ due to diminished Na+-K+-ATPase pump also contributes to hyperkalemia

Hypocalcemia (↓)

  • Hyperphosphatemia leading to hypocalcemia
  • ↓ Synthesis of calcitriol (1,25-(OH)2D3) in kidneys**

Hyperphosphatemia (↑)
o ↓ Renal excretion of PO43-

47
Q

Typical arterial blood gas profile in AKI

A

Metabolic acidosis + ↑ Anion gap
o Excretion of acid and regeneration of HCO3-is impaired in low GFR
- Impaired H+ and NH4+ excretion due to decreased in number of functioning nephrons in renal failure

o ↑ H+ production in lactic acid or ketoacids in sepsis and trauma

o ↓ HCO3- due to loss from diarrhea or renal tubular acidosis

MBBS IV - Junior Clerkship WCS (131 decks)

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