Renal function, AKI and CKD

Question 1

What is clearance?

Answer 1

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

Question 2

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

Answer 2

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

Question 3

What factors affect creatinine

Answer 3

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

Question 4

What is an alternative endogenous marker used to measure GFR

Answer 4

CYSTACIN C

Question 5

What is PCR and how is it collected

Answer 5

• 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

Question 6

What is investigated in a urine dipstick

Answer 6

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)

Question 7

What to look for in urine microscopy

Answer 7

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

Question 8

Difference between AKI and CKD

Answer 8

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

Question 9

Stages of AKi

Answer 9

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

Question 10

Why ACEi are contraindicated in RAS or AKI

Answer 10

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

Question 11

Causes of Pre renal AKI

Answer 11

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

Question 12

Pre renal AKI va ATN

Answer 12

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

Question 13

Cause of post renal AKI

Answer 13

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

Question 14

Cause of intrinsic AKI

Answer 14

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)

Question 15

Stages of CKD

Answer 15

1- damage with normal GFR

2- GFR 60-89

3- 30-59

4- 15-29

5- <15 or dialysis

Question 16

Causes of CKD

Answer 16

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

Question 17

Consequences of CKD

Answer 17

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

Question 18

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

Answer 18

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

Question 19

Medications that cause hyperkalaemia

Answer 19

 ACE inhibitor

 Spironolactone (potassium-sparing diuretics)

Question 20

How CKD causes anaemia and its treatment

Answer 20

Stops producing EPO
Usually when GFR <30

Treat With erythropoietin alfa or beta

Question 21

How CKD causes bone disease and its treatment

Answer 21

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

Question 22

What complication of CKD is most likely to kill them

Answer 22

Cardiovascular disease (vascular calcification, uraemic cardiomyopathy)

Question 23

Different treatments of CKD

Answer 23

•	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

Question 24

Indications for dialysis

Answer 24

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)