8.14 Proteinuria, Nephrotic & Nephritic Syndrome Flashcards

1
Q

What structures of the glomeruli is normally damaged?

A
  • Basal membrane
  • epithelium
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2
Q

Normal urine protein

A

<150 mg/d

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3
Q

Why don’t you normally get albumin and IgG in urine?

A

Molecules are to big in normal instances

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4
Q

Mechanisms preventing protein loss

A
  • physical filtration barrier (proteins = macromolecules)
  • electrical barrier (protein negatively charged)
  • tubular reabsorption ±1.5 g/d LMW proteins filtered reabsorbed by proximal tubule
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5
Q

If there is tubular damage what happens?

A

Glomerulus “holes” gets bigger and albumin leak
Holes between prodocytes processes become bigger

Proteinuria = glomeruli damage

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6
Q

NB Quantification of urinary protein

A

Semi-quantitive: only roughly
- Urine dipstick
- sulphosalicylic acids

Quantitative:
- 24hr urine collection (not very acurate)
- spot sample urine protein: creatine ratio (UPCR)

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7
Q

What protein does urine dipsticks pick up?

A

Only pick up Albumin when it is in excess of >300 mg/day
NO OTHER PROTEIN; not immunoglobulins

Trace = <300mg/day

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8
Q

What proteins does sulfosalicylic acid (SSA)?

A

ALL proteins

If urine dip ➖ & SSA ➕ = not albumin but IMMUNOGLOBULINS

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9
Q

Why is the 24hr urine protein sample collection not used anymore?

A
  • inaccurate
  • cumbersome
  • cannot be used in out pt setting
  • UPCR have perfect correlation with the 24hr protein (when pt is in steady state)
  • there it doesn’t matter how much urine is used for the test, the results will stay the same (not nesseasary for 24hr urine collection)
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10
Q

Causes of proteinuria

A

Non-pathological / functional = hemodynamic effects on kidney
- heart failure
- fever
- strenuous exercise
- autostaic proteinuria (young women)

Pathological
- overflow proteinuria (Bens-jones / immunoglobins light chain in urine)
- Glomerular damage (leak albumin)
- tubular damage (>1.5 reabsorbed)

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11
Q

Glomerular injury

A

1. Infam
- cells infiltrate kidney and damage
- swelling
- leaks proteins and other blood component (RBC, WBC) = Nephritis / Glomerular nephritis

2. Structural damage
- to podocytes
- genetic causes (missing structural podocytes)
- only protein leaks
- Nephrotic syndrome

Asym haematuria/proteinuria ➡️ Acute glomerulonephritis / nephrotic syndrome

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12
Q

NB Nephritis syndrome
Def

A
  • haematuria ± proteinuria
  • renal failure
  • oedema
  • hypertention
  • Oliguria (<400 ml/day)
  • RBC cast pathonemonic of NS

Proteinuria >3.5 g/day = can’t diagnose without THIS!!!

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13
Q

Glomerular disease
Causes

A

Needs to exclude secondary cause first
Slide 23

Primary Diagnosis of exlusion
- Membranous GN
- FSGS
- Mesangiocapillary GN
- Minimal change disease

Secondary
- DM
- SLE
- Infec: HIV, Hep B & C
- pre-eclampsia
- drugs
- amyloids
- malignancies

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14
Q

Finish on slides

A

‼️

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