Acute Kidney Failure Flashcards

1
Q

Broad categories of AKF aetiologies

A

Pre-renal

Intrinsic (renal)

Post-renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pre-renal causes of AKF

A

Decreased blood flow to kidney –> Renal ischaemia

  • Hypovolemia
  • Hypotension
  • HF
  • Liver cirrhosis –> hepatorenal syndrome
  • Renal artery stenosis
  • Renal vein thrombosis (can’t drain properly –> stasis –> ischaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Classic lab findings in pre-renal AKF

A

Orine osmolarity: >500

Urine Na+: 20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Intrinsic (renal) causes of AKF

A

Damage to glomeruli, renal tubules, or interstitium due to:

  • Glomerulonephritis –> damage to glomeruli
  • Acute tubular necrosis –> damage to renal tubues
  • Acute interstitial nephritis –> damage to interstitium

Other causes:

  • Rhabdomyolysis
  • Tumour lysis syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Features of Nephrotic syndrome

A
  • Oedema
  • Proteinuria
  • Hypoalbuminaemia (serum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Features of Nephritic Syndrome

A
  • Haematuria
  • HTN
  • Oliguria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of glomerulonephritis

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
  • Thin basement membrane disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Features of minimal change disease

A
  • Presents as nephrotic syndrome

- Tx with corticosteroids, does not progress to chronic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Features of Focal segmental glomeruloscleross

A
  • Affects glomeruli - segments of sclerosis
  • Increased hyaline, homogenous pink, seen on EM
  • Associated with HIV, Heroin abuse, or inherited Alport’s Syndrome
  • 20-30% cases unknown cause
  • 50% patients progress to total renal failure
  • Tx: corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Features of Membranous glomerulonephritis

A
  • Presents as nephrotic OR nephritic syndrome
  • Usually associated with auto-antibodies to phospholipase A2 receptors
  • Other associations include: SLE, malaria, Hep B, bowel and lung cancers, Penicillamine
  • Prognosis: rule of thirds
  • — 1/3 patients remain with MGN indefinitely
  • — 1/3 remit
  • — 1/3 progress to total renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Thin basement membrane disease

A
  • Inherited condition, AD
  • Thin glomerular basement membrane seen on EM
  • Benign condition
  • Causes persistent microscopic haematuria, +/- mild proteinuria
  • Good prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Key causes of intrinsic renal failure, of glomerular origin?

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
  • Thin basement membrane disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Features of Acute Tubular Necrosis

A
  • Necrosis of the epithelial cells forming the renal tubules
  • One of the most common causes of ARF
  • Causes: HTN, nephrotixicity (usually drugs)
  • Presence of “muddy brown casts” of epithelial cells = pathognomonic for ATN
  • Tx is of underlying cause
  • Because of usual rapid turnover of epithelial cells of renal tubules, once underlying cause treated, recovery usually within 7-21 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Common nephrotixic drugs causing direct renal tubule injury

A

Proximal tubule

  • Gentamycin (Aminoglycoside Abx)
  • Amphotericin B
  • Cisplatin
  • Radiocontrast media
  • Immunoglobulins
  • Mannitol
Distal tubule
- NSAIDs
- ACEIs
- Cyclosporins
Litium salts
- Cyclophosphamide
- Amphoteracin B

Tubular obstruction

  • Sulphonamides
  • Methotrexate
  • Aciclovir
  • Triamterene
  • Diethylene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Features of Interstitial Nephritis

A
  • Nephrtis affecting the interstitium surrounding renal tubules
  • Common causes: Infection, drug reactions (most cases)
  • Time delay from exposure to offending drug - development of interstitial nephritis can be 5/7 to 5/12
  • Symptoms: sometimes asymptomatic
  • Varied: Dysurua, electrolyte imbalances, metabolic acidosis, lower back pain
  • Allergic reaction type: fever, rash, enlarged kidneys
  • Chronic IN: Nausea, vomiting, fatigue, w/loss, electrolyte imbalances
  • Tx: remove offending agent, ensure hydration
  • Chronic type: No cure, will progress to ARF –> dialysis –> renal transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Classic lab findings in intrinsic (renal) ARF

A
  • Urine osmolarity: >350
  • Urine Na+: >20
  • Fe/Na+: >2%
  • BUN/Cr:
17
Q

Post renal causes of ARF

A
Urinary obstruction
- Benign prostatic hyperplasia
- Kidney stones
- Bladder stone
- Bladder / urethral malignancy
- Obstructed urinary catheter
Must always rule out urinary retention
18
Q

Basic investigations to rule out urinary retention

A
  • Post-void residual scan: 50-100ml suggests neurogenic bladder dysfunction
  • Renal USS –> hydronephrosis
  • BT abdo –> Hydronephrosis or bladder distension
19
Q

Classic findings in post-renal causes of AKF

A

Urine osmolarity: 40
Fe/Na+: >4%
BUN/Cr: >15

20
Q

Process involved in hepatorenal syndrome

A

Pre-renal cause of AKF

Cirrhosis with portal HTN –> Damaged hepatic cells release vasoactive substances –> Splanchnic vessel dilation –> Decreased pressure sensed by juxtaglomerular apparatus –> RAS activation –> RAS activation insufficient to combat splanchnic dilation –> Chronic ‘underfilling’ of renal arteries –> From RAS activation, subsequent renal/Na+ activity = ASCITES, and renal vasoconstriction = Hepatorenal syndrome

21
Q

Diagnostic definition of acute kidney injury

A

Abrupt loss of kidney function occuring over 7 days

If any one of the following is present:

Increased serum Cr by >0.3 mg/dl (>22umol/L) within 48 hours

Increased serum Cr to >1.5 X baseline, occuring within the prior 7 days

Urine volume