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1Principles of Biomedicine - MD1 > 147 - Pathophysiology of Acute & Chronic Renal Failure > Flashcards

147 - Pathophysiology of Acute & Chronic Renal Failure Flashcards

1
Q

Definition of acute renal failure

A

Urine flow less than 500 ml/day

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2
Q

Common time-course for chronic renal failure to develop

A

6 months or more

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3
Q

Normal GFR

A

125mL/min, 180L/day

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4
Q

GFR of significant chronic renal failure

A

Under 50mL/minute, under 72L/day

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5
Q

Reversibility of acute and chronic renal failure

A

Acute is often reversible.

Chronic is irreversible

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6
Q

Hallmark of chronic renal failure

A

Creatinine excretion and a decrease in CFR from a loss of functional nephrons

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7
Q

Broad types of nephron pathology

A

Glomerular and tubular. Often a mixed pathology.

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8
Q

Examples of renal endocrine impairment
1
2
3

A

1) Ras (renin-angiotensin system) (excessive activation)
2) Vitamin D activation
3) Epo

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9
Q

Ras endocrine pathologies

A

Excessive activation (but rarely): vasoconstriction can impair RBF; possibility of “malignant hypertension”

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10
Q

Most important endocrine dysfunction in CRF

A

Vitamin D activation.

Leads to a unique pattern of bone disease.

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11
Q

Effects of vitamin D activation in CRF

A

Osteo-dystrophy, renal rickets; exacerbated by hypocalcaemia

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12
Q

Effects of epo dysregulation with CRF

A

CRF seems to be invariably associated with anaemia

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13
Q

Effectiveness of urea in assessing GFR

A

Poor

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14
Q

Proportion of urea that is reabsorbed

A

~50%

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15
Q

What can alter urea in urine without affecting kidneys

A

Diet. Urea is produced from protein

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16
Q

States where urea can be elevated

A

CRF, catabolic states, steroid use, cachexia in cancer

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17
Q

What suppresses urea excretion?

A

Malnutrition, liver disease

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18
Q 
Features of creatinine in GFR assessment 
1
2
3
4
5
A

1 Creatinine production is constant
2 Filtered, but 15% bound to plasma proteins (underestimates GFR)
3 Not reabsorbed
4 Small amount of secretion (overestimates GFR)
5 (2) and (4) tend to cancel out

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19
Q

Normal serum creatinine level

A

50-120 μM/L

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20
Q

What is daily production of creatinine proportional to?

A

Muscle mass

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21
Q

What is equal to creatinine filtration?

A

Creatinine excretion

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22
Q

What is equal to creatinine clearance?

A

GFR

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23
Q

Aspects of creatinine that can skew calculation of GFR from creatinine excretion
1
2

A

15% of creatinine is bound to plasma proteins.
Therefore can underestimate GFR>

Some secretion of creatinine occurs. This can overestimate GFR.

These two roughly cancel out.

24
Q

Equation for creatinine clearance

A

UV/P

U = urinary concentration of creatinine 
V = Urine volume/day
P = Plasma concentration of creatinine

Because UV is often constant, can say that creatinine clearance is inversely proportional to creatinine plasma concentration

25
Q

What must you do for plasma creatinine concentrations to be meaningful?

A

Take more than one. People can have normally high creatinine. As creatinine levels should be constant, look for increases in concentration.

26
Q

Net filtration pressure

A

10mmHg from glomerulus into Bowman’s capsule

27
Q 
Features of acute renal failure 
1
2
3
4
A
  • Oliguria
  • Anuria (rarely)
  • GFR falls acutely (hours to days)
  • Easily missed (depending on cause) because of itself may be asymptomatic
28
Q

Types of acute renal failure

A

Pre-renal
Renal
Post-renal

29
Q

Most common cause of acute renal failure

A

Pre-renal.

EG: shock, dehydration.

30
Q

Pre-renal acute renal failure

A

Anything that drops blood pressure to the point where no filtration occurs across glomerulus and Bowman’s capsule

31
Q

Systemic perfusion pressure at which ARF occurs

A

Under 70mmHg

32
Q

Glomerular hydrostatic pressure at which ARF occurs

A

Under 45mmHg

33
Q 
Examples of causes of pre-renal ARF
1
2
3
4
5
A 
– Shock 
– Sepsis 
– Haemolysis
– Rhabdomyolysis 
– Nephrotoxic drugs (actually cause tubulo-interstitial nephritis, a renal cause)
34
Q 
Examples of things that can cause intrinsic renal ARF
1
2
3
4
A

•Glomerular disease

•Interstitial nephritis (Tubulo-interstitial)
–Inflammatory reaction, often drug-related

•Tubular damage
–ischemia

•Acute tubular necrosis, vascular obstruction

•toxins
-antibiotics, X-ray contrast media, myoglobin

35
Q

ATN

A

Acute tubular necrosis.

So common as to be almost synonymous with ARF.

36
Q

Most common renal cause of ARF

A

Acute tubular necrosis

37
Q

Things that can cause acute tubular necrosis

A

Ischaemia, toxins

38
Q 
Effects of acute tubular necrosis
1
2
3
4
A

•oliguria (

39
Q

Main concern with CRF

A

Accumulation of toxic metabolites, EG creatinine.

Loss of hormonal function of kidneys (EG: vitamin D, epo, renin)

40
Q

Main concern with ARF

A

Accumulation of H+ and K+ ions. Leads to acidosis and hyperkalaemia.

41
Q

Treatment of ARF

A

Rehydration.

42
Q

Post-renal ARF

A

•Outlet Obstruction
–Ureteric, cystic or urethral
–stones, clots, fibrosis, tumors

43
Q

Treatment of post-renal ARF

A

Not just rehydration. Also need to remove the obstruction.

44
Q 
Features of chronic renal failure
1
2
3
4
5
A
  • Irreversible loss of renal function
  • Reduction in functional renal mass
  • Develops over months to years (highly variable rates of decline)
  • Aka “uraemia”
  • Leads to End-Stage Renal Disease (ESRD)
45
Q

Effect of CRF on glomeruli
1
2 a, b, c

A 
•Remaining nephrons hypertrophy
•Glomerular hyperfiltration
–loss of functional reserve
–glomerular hypertension
–further damage and glomerulosclerosis
46
Q

Uremia
1
2
3 a, b, c

A 
•Accumulation of “uremic” toxins
•Mostly urea, but not exclusively
•Symptomatic with under 30% of renal function
–Fatigue
–Loss of appetite
–Skin pigmentation (lemon)
47
Q 
Main causes of CRF
1
2
3
4
A

1) Diabetes
2) Hypertension
3) Chronic glomerulonephritis
4) Polycystic kidney disease

48
Q

Salt and water imbalances in CRF
1
2

A 
•Predominantly glomerular disease
–Sodium retention and hypertension
•Predominantly tubular disease
–Sodium wasting and low BP
–Impaired concentrating ability & polyuria
49
Q

Potassium in CRF

A

–Tends to rise, especially late-stage
–Higher in diabetes
–If rapidly rises, can lead to arrhythmia

50
Q 
pH in CRF
1
2
3
4
5
A

–Falls i.e. H+ accumulates; failure to excrete non-volatile acids
•Produced at high rate in normal metabolism
•Excretion requires high GFR
•Reduced ammonia production
•Low [HCO3-]

51
Q

Calcium and phosphate in CRF
1
2
3

A
  • Reduced phosphate excretion
  • Still reabsorbs same amount of phosphate, while secretion is decreased
  • Leads to rise in [PO4] (should be 1 - 1.3 milimols)
  • Reciprocal reduction in [Ca]
52
Q

Part of nephron that transports phosphate

A

Epithelial pump in proximal tubule.

Clears ~1 milimol/day

53
Q

Effect of elevated phosphate in CRF

A

Calcium phosphate can begin precipitating (EG on bones)

54
Q

Effect of CRF on vitamin D3

A

–Reduced renal mass and Vit D activation
–Hyperphosphatemia
–Renal “rickets”: osteomalacia with fractures and subperiosteal resorption

55
Q

Hormonal effect of high phosphate

A

High parathyroid hormone release.

Leads to excessive osteoclastic activity.

56
Q

Osteomalacia

A

Similar to osteoporosis.

If there is low serum Ca2+, then body starts taking Ca2+ from bones.

57
Q

Renal osteodystrophy

A

Combination of low serum Ca2+, leading to body taking Ca2+ from bones. Also increased PTH leads to excessive osteoclast activity

1Principles of Biomedicine - MD1 (157 decks)

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