Renal function, AKI and CKD Flashcards

1
Q

What is clearance?

A

Volume of plasma that can be completely cleared of a marker substance per unit time

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2
Q

What are the 3 criteria that need to be fulfilled for a marker to be used to measure GFR?

A

 Marker is NOT bound to serum proteins
 Freely filtered by the glomerulus
 NOT secreted or reabsorbed by tubular cells

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3
Q

What factors affect creatinine

A
  • Muscularity (proportional to mass)
  • Age
  • Sex (higher in men)
  • Ethnicity (higher in Afro-Caribbean)
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4
Q

What is an alternative endogenous marker used to measure GFR

A

CYSTACIN C

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5
Q

What is PCR and how is it collected

A

• Urine protein: creatinine ratio (PCR):
o This is a quantitative assessment of the amount of proteinuria
o Measurement of creatinine corrects for urinary concentration- since creatinine is released at constant rate into urine

o Two methods to do PCR:
 24hr urine collection (cumbersome and messy; highly inaccurate without patient education)
 Spot urine measurement

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6
Q

What is investigated in a urine dipstick

A

o pH = 4.5 to 8.0
o Specific gravity (density of urine)
o Protein = sensitive to albumin, not BJPs (Bence-Jones Proteins); Zero  Trace  1+ to 4+
o Blood (neg excludes haematuria)
o Leucocyte esterase (negative result is significant – reliably excludes bacteria)
o Nitrite (detects bacteria, esp. Gm negatives – cannot reliably excludes bacteria if -ve)

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7
Q

What to look for in urine microscopy

A
	Crystals		calcium oxalate crystals 	
	RBCs		‘little doughnuts’
	WBCs		‘multi-nucleate cells’
	Casts		‘fuzzy burritos’
	Bacteria 		‘wannabe RBCs’
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8
Q

Difference between AKI and CKD

A

AKI- abrupt, reversible decline in GFR, with treatment targeted to precise cause of AKI

CKD- long, irreversible decline of GFR, with treatment targeted to prevent complications of CKD

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9
Q

Stages of AKi

A

1- 1.5-1.9x serum creatinine 0r <0.5ml/kg/hr 6-12hrs

2- 2-2.9x or >12hrs

3- >3x or <3 >24hrs

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10
Q

Why ACEi are contraindicated in RAS or AKI

A

Angiotensin II causes increased constriction of the efferent compared to other vessels to maintain GFR

However since ACEi and ARB inhibit this- it will reduce efferent constriction reducing GFR

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11
Q

Causes of Pre renal AKI

A

o True volume depletion (e.g. haemorrhage) Hypotension
o Oedematous state Selective renal ischaemia (e.g. renal artery stenosis)
o Drugs affecting renal blood flow
 ACE inhibitors or ARBs – reduce efferent constriction
• ACEi are very contraindicated in RAS
 NSAIDs or Calcineurin inhibitors – decrease afferent dilatation
 Diuretics – affect tubular function, decrease preload

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12
Q

Pre renal AKI va ATN

A

o Pre-Renal AKI is NOT associated with structural renal damage
o ATN does NOT respond to restoration of circulating volume
o Epithelial cell casts would be seen in the urine on microscopy

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13
Q

Cause of post renal AKI

A

o (Intra-renal obstruction) Ureteric obstruction (bilateral)
o Prostatic / urethral obstruction Blocked urinary catheter
o Retroperitoneal fibrosis / Ormond’s disease

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14
Q

Cause of intrinsic AKI

A

o Vascular disease (e.g. vasculitis)
o Glomerular disease (e.g. glomerulonephritis)
o Tubular disease (e.g. ATN) = MOST COMMON, myoglobin- DTI
o Interstitial disease (e.g. analgesic nephropathy – long-term excessive use of analgesics)

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15
Q

Stages of CKD

A

1- damage with normal GFR

2- GFR 60-89

3- 30-59

4- 15-29

5- <15 or dialysis

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16
Q

Causes of CKD

A
o	Diabetes
o	Hypertension (atherosclerotic renal disease)
o	Chronic Glomerulonephritis
o	Infective or obstructive uropathy
o	Polycystic kidney disease
17
Q

Consequences of CKD

A

o (1) Progressive failure of homeostatic function
 (1a) Acidosis
 (1b) Hyperkalaemia

o (2) Progressive failure of hormonal function
 (2a) Anaemia
 (2b) Renal bone disease

o (3) Cardiovascular disease
 Vascular calcification (renal osteodystrophy)

 Uraemic cardiomyopathy
o (4) Uraemia and death

18
Q

Why CKD causes acidosis, what problems that causes and its treatment

A

o Metabolic acidosis (failure of renal excretion of protons) 

 Muscle and protein degradation
 Osteopaenia due to mobilisation of bone calcium (because protons can be stored in bone)
 Cardiac dysfunction

o TREATMENT: oral sodium bicarbonate

19
Q

Medications that cause hyperkalaemia

A

 ACE inhibitor

 Spironolactone (potassium-sparing diuretics)

20
Q

How CKD causes anaemia and its treatment

A

Stops producing EPO
Usually when GFR <30

Treat With erythropoietin alfa or beta

21
Q

How CKD causes bone disease and its treatment

A

High phosphate and less Vit D is activated in the kidneys- insufficient mineralisation

Treat with vit d receptor activators- 1 alpha calcidol and phosphate binders

22
Q

What complication of CKD is most likely to kill them

A

Cardiovascular disease (vascular calcification, uraemic cardiomyopathy)

23
Q

Different treatments of CKD

A
•	Transplantation
•	Haemodialysis- 3x wk for 6 hrs
•	Peritoneal Dialysis- can be done at home- o	Peritoneal cavity is filled with fluid and the peritoneal membrane is used as the dialysing membrane
o	Increased risk of:
	Beta-2 macroglobulin amyloidosis 
	Papillary renal cell carcinoma
24
Q

Indications for dialysis

A
o	Refractory hyperkalaemia 
o	Refractory fluid overload
o	Metabolic acidosis
o	Uraemic symptoms (encephalopathy, nausea, pruritis, malaise, pericarditis)
o	CKD stage 5 (GFR <15mL/min)