Renal Flashcards

1
Q

Red blood cell casts?

A

Glomerulonephritis

Renal ischaemia and infarction

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2
Q

White blood cell casts?

A

Acute pyelonephritis

Interstitial nephritis

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3
Q

Granular (muddy-brown) casts?

A

Acute tubular necrosis

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4
Q

Hyaline casts?

A

Common, non-specific

Vigorous exercise, dehydration

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5
Q

Epithelial casts?

A

Acute tubular necrosis

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6
Q

Waxy casts?

A

Advanced chronic kidney disease

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7
Q

Fatty casts?

A

Nephrotic syndrome

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8
Q

What causes ATN?

A
Acute tubular necrosis causes:
Ischaemic 
 - Hypovolaemic shock
 - Sepsis
Nephrotoxic
 - drugs
 - pigment nephropathy
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9
Q

What is pigment nephropathy?

A

Toxic action of heme-containing pigment on kidneys.
This can be from myoglobin or haemoglobin
i.e. rhabdomyolysis or intravascular haemolysis
Leads to ATN

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10
Q

CKD Stages in terms of eGFR?

A

eGFR measured inmL/min/1.73m^2

Stage 1 = =>90
Stage 2 = 60-90 mild
Stage 3a = 30-45 mild/moderate
Stage 3b = 45-60 moderate/sever
Stage 4 = 15-30 severe
Stage 5 = <15 (Kidney failure)
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11
Q

Who should be offered testing for CKD, and what testing?

A

People are at risk if they have:

  • Diabetes
  • Cardiovascular disease
  • HTN
  • AKI

Tests:

  • eGFRcreatinine
  • ACR (albumin:creatinine ratio)
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12
Q

What is ACR and why useful in CKD?

A
Albumin:creatinine ratio
Useful as the higher it is, the worse CKD  
<3 normal
3-30 moderate
30+ severe

Combined with eGFR, to determine G and A stage of CKD

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13
Q

Aim for blood pressure ranges in CKD?

A

<140/90

If they have diabetes or ACR>70
then <130/80

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14
Q

How to treat HTN in CKD?

A

ACE or ARBs
NOT aldosterone antagonists
Take eGFR readings before starting, and 1-2 weeks after starting

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15
Q

Who should be investigated for AKI?

A

Acutely unwell and one of:

  • CKD
  • Heart failure
  • Liver disease
  • Diabetes
  • Hx of AKI
  • oliguria
  • hypovolaemia
  • sepsis
  • nephrotoxic drugs
  • recent use of iodinated contrast agents
  • > 65
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16
Q

Nephrotoxic drugs?

A
NSAIDs
Aminoglycosides
ARBs
ACEi
Diuretics
17
Q

Diagnosis of AKI if?

A

If:

  • Inc in creatinine of 26micromol/L in 48 hrs
  • Inc in creatinine of 50% in 7 days (25% in kids and young people)
  • Dec in urine output <0.5ml/kg/hr for 6 hrs (8 in young)
18
Q

Stages in AKI?

A

Stage 1
Creatinine:
50-99% rise in 7 days OR >26 micromol/L rise in 48hrs Urine output:
<0.5ml/kg/hr for >6hrs

Stage 2
Creatinine:
 100-199% rise in 7 days OR 2-2.9 X baseline rise                 in 7 days          
Urine Output:
 <0.5ml/kg/hr for >12hrs
Stage 3:
Creatinine:
200% or more rise in 7 days            
Urine Output:
<0.3ml/kg/hr for >24hrs 
Anuria >24hrs
19
Q

Life threatening complications of AKI?

A

Acute pulmonary oedema
Metabolic acidosis
Hyperkalaemia

20
Q

Treating hyperkalaemia steps?

A
  1. If hyperkalaemia and ECG changes - IV calcium gluconate
    2a. If hyperkalaemia >6.5 - nebulised salbutamol
    2b. If hyperkalaemia 6-6.5 - IV insulin-glucose (dextrose)
21
Q

What produces renin?

A

Juxtaglomerular apparatus -
synthesised as prorenin - 50-90% of circulating renin
Some is cleaved and stored as renin

22
Q

Renin released controlled by?

A

Pressure changes in afferent arteriole
Sympathetic tone
Chloride and osmotic conc. in distal tubule
Local prostaglandin and nitric oxide release

23
Q

Angiotensin II does what?

A

Systemic vasoconstriction
Sodium & water retention
Thus increase blood pressure

24
Q

Why is Vitamin D affected by kidney disease?

A

Kidneys produce enzyme that activates cholecalciferol (vit D).
NB vitamin D increases calcium uptake, so without it, poor bone mineralization

25
Q

Why are NSAIDs nephrotoxic?

A

Inhibit COX-1 and COX-2.
These enzymes responsible for catalyzing prostaglandin synthesis.
PGs maintain renal blood flow and GFR