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Nephrology > Hematuria > Flashcards

Hematuria Flashcards

1
Q

Causes of red urine (with a U/A negative for heme)

A
  1. Food (beets, rhubarb)
  2. Food dyes
  3. Antibiotics (rifampin, nitrofurantoin, metronidazole, sulfa)
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2
Q

What does a urine dip positive for blood mean when there are NO RBC’s on microscopy?

A
  1. Heme-positive (hemolysis) - free hemoglobin
  2. Myoglobin positive (ie: rhabdo) - check serum CK
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3
Q

Define hematuria

A

More than 5 RBC’s on urine microscopy (per microL of urine)

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4
Q

How do you distinguish renal vs. lower urinary system bleeding?

A

Renal:

  • Dark cola urine
  • Proteinuria (>1g)
  • RBC casts (because RBCs are being deformed as they pass through the glomerulus)
  • Deformed RBC on microscopy

Lower urinary (i.e.: pelvic collecting system, ureter, bladder, urethra):

  • Bright red urine - LUTS (dysuria, frequency)
  • Renal colic
  • History of trauma
  • Blood clots present
  • RBCs are NOT deformed
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5
Q

Classic symptoms of glomerulonephritis:

A
  1. Dark urine 2. Oliguria 3. Edema 4. Hypertension
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6
Q

DDx for glomerulonephritis:

A
  1. IgA nephropathy (Berger disease) 2. Post-infectious glomerulonephritis 3. Lupus nephritis 4. Henoch-Schonlein purpura (HSP) 5. Hereditary nephritis (Alport Syndrome) 6. Hemolytic uremic syndrome (HUS)
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7
Q

True or False: Hematuria in glomerulonephritis is typically PAINLESS

A

True

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8
Q

DDx for abdominal mass:

A
  1. Tumour (Wilms) 2. Hydronephrosis 3. Polycystic kidney disease 4. Renal vein thrombosis
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9
Q

Hereditary causes of hematuria:

A
  1. Hereditary nephritis (Alport syndrome)
  2. SLE
  3. Thin glomerular basement membrane disease
  4. IgA nephropathy
  5. Atypical (D-) HUS
  6. Polycystic kidney disease
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10
Q

Genetic disorders associated with hematuria:

A
  1. VACTERL association (R = renal)
  2. Zellweger syndrome (cerebrohepatorenal syndrome)
  3. Tuberous sclerosis
  4. von Hippel Lindau syndrome
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11
Q

Classic features of glomerular injury:

A
  1. Proteinuria 2. Hematuria 3. Oliguria 4. Hypertension 5. Edema
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12
Q

Post-infectious glomerulonephritis:

A
  • typical onset 10d post infection (usually GAS pharyngitis or impetigo, but also moraxella)
  • pathophys is immune-mediated to bacterial proteins trapped in capillaries
  • most common in children 2-12 years (M>F)
  • sudden onset
  • Low C3 only!
  • resolves within 6-8 wks (acute phase)
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13
Q

Which type of glomerulonephritis typically has isolated low C3?

A

Post-infectious GN

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14
Q

Features of hypertensive encephalopathy:

A
  • headache (severe) - altered LOC - seizures - hypertension - blurred vision
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15
Q

When does hematuria resolve in post-infectious GN?

A

1-2 years!

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16
Q

Diagnosis of post-infectious GN?

A
  • documented recent infection (throat swab, ASOT) - low C3 - classic findings of acute GN
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17
Q

Most likely diagnosis for recurrent painless gross hematuria?

A

IgA nephropathy

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18
Q

Most common glomerular disease in children?

A

IgA nephropathy

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19
Q

Presentation of igA nephropathy

A
  • occurs with URTI - recurrent and self-resolving - more common in males - typically benign course during childhood
20
Q

Long-term consequences of IgA nephropathy?

A
  • ESRD in 30% 15-20 years after onset
21
Q

Treatment of IgA nephropathy:

A
  • Hypertension management (ACEi) - Minimize proteinuria (ACEi) - Steroids for significant proteinuria - fish oil? (anti-inflammatory)
22
Q

What is benign familial hematuria?

A
  • inherited AD disorder - microscopic hematuria - benign course usually - due to thin basement membrane Also known as: thin basement membrane disease
23
Q

What is Alport syndrome? (aka hereditary nephritis)

A
  • genetic condition leading to progressive basement membrane destruction over time
  • due to abnormal type 4 collagen
  • associated with hearing loss and cataracts
  • typically presents with asymptomatic microscopic hematuria (although can also present as gross hematuria with URTIs)
  • slowly progressive renal disease
24
Q

What is the genetic basis for Alport syndrome?

A

Heterogeneous genetic aetiology of genes coding for type 4 collagen X-linked disease in 85% of cases

25
Q

What type of hearing loss is associated with Alport syndrome?

A

BILATERAL sensorineural hearing loss Hearing loss is progressive over time (just like the renal disease)

26
Q

Pathognomonic ophtho finding in Alport syndrome?

A

Anterior lenticonus (the lens protrudes anteriorly in a cone shape)

27
Q

Treatment of Alport syndrome

A

Supportive

ACE-inhibitors for proteinuria

Renal transplantation eventually

28
Q

What is Goodpasture disease?

A
  • Autoantibodies to type IV collagen in the lungs and kidney
  • Results in ‘pulmonary-renal syndrome’
  • Key features:
  1. Acute pulmonary hemorrhage (large)
  2. Acute, progressive glomerulonephritis
29
Q

What do the antibodies in Goodpasture disease target in the kidney?

A

The glomerular basement membrane (GBM)

“anti-GBM antibodies”

30
Q

What type of glomerulonephritis is Goodpasture disease?

A

Crescentic

31
Q

Clinical presentation in Goodpasture’s

A
  1. Hemoptysis (pulmonary hemorrhage - sometimes life threatening)
  2. Glomerulonephritis (rapidly progressive with classic proteinuria, hematuria, hypertension)
    • Occasionally, children will present with ONLY renal manifestations
32
Q

Laboratory findings Goodpasture disease

A
  • anti-GBM antibodies in the serum
  • NORMAL C3
  • Positive ANA (some - may indicate more severe disease)
  • Renal biopsy findings consistent with disease
33
Q

Diagnosis of Goodpasture disease

A
  1. Clinical presentation
    1. Pulmonary hemorrhage with glomerulonephritis
  2. Anti-GBM antibodies in the serum
  3. Characteristic renal biopsy findings
34
Q

DDx for pulmonary-renal syndrome

A
  1. Lupus
  2. Goodpasture’s
  3. HSP
  4. Wegener’s (granulomatosis with polyangiitis)
35
Q

Treatment of Goodpastures

A

*Untreated, outcome is poor*

  • High-dose steroids (IV methylpred)
  • Cyclophosphamide
  • Plasmapharesis

Typically - disease will still progress to ESRD despite therapy

36
Q

Wegener granulomatosis is also known as:

A

granulomatosis with polyangiitis (GPA)

37
Q

What is vasculitis?

A

Inflammation of the blood vessels

Can involve small (capillaries), medium (renal and coronary arteries) or large (aorta) vessels

Most are idiopathic (some are autoimmune)

Pattern of inflammation on histology can be helpful for diagnosis

38
Q

What type of antibodies is Wegeners/Granulomatosis with polyangiitis (GPA) associated with?

A

ANCA = antineutrophilic cytoplasmic antibodies

39
Q
A
40
Q

What type of vessels are affected in Wegeners (GPA)?

A

Small vessels (ie: capillaries, venules)

41
Q

Clinical presentation of granulomatosis with polyangiitis?

A
  • All ages
  • In children - average is 14 years
  • More common in females
  • Get necrotizing granulomas of the upper and lower respiratory tract and kidneys
    • It is unclear why the lungs and kidneys are targeted in these types of vasculitis
  • A type of ‘pulmonary-renal’ syndrome
42
Q

Is Wegeners antibody or immune-complex mediated?

A

Antibodies! (ANCA)

On biopsy, there are NOT many immune complexes

43
Q

Clinical presentation of Wegeners?

A
  • General symptoms: fever, malaise, weight loss, arthralgia and myalgia
  • Upper respiratory tract:
    • chronic sinusitis, otitis media, nasal ulceration, epistaxis, hearing loss
    • Saddle-nose deformity
  • Lower respiratory tract:
    • Cough, wheeze, hemoptysis, shortness of breath
    • Subglottic stenosis
  • Renal:
    • Hematuria, proteinuria, hypertension
  • Other features: skin and eye involvement
44
Q

Diagnosis of Wegeners:

A
  • Imaging:
    • CXR - may be normal
    • CT chest - nodules, cavitations, mediastinal lymphadenopathy
  • Biopsy:
    • Renal, sinus or lung biopsy with granulomas
  • Bloodwork:
    • specific anti-PR3 ANCA antibodies
    • ANCA is positive in 90%
    • Elevated CRP, ESR, WBC and platelets
    • Normocytic anemia (inflammatory)
45
Q

Treatment of Wegeners:

A

Immune suppression is the goal…

Acute/Induction:

  1. Steroids
  2. Cyclophosphamide (usually given with steroids)
  3. Rituximab is sometimes used

Maintenance (once remission is achieved):

  1. Methotrexate
  2. Azathioprine
  3. Mycophenolate mofetil
  4. Septra for PCP prophylaxis
46
Q

Complications of Wegeners:

A

Acute:

  • pulmonary hemorrhage
  • upper airway obstruction due to subglottic stenosis

Chronic:

  • Orbital and optic nerve involvement
  • Hearing loss
  • Chronic lung disease with scarring, recurrent infections and cavitations
  • End-stage renal disease

Nephrology (1 decks)

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