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104-theme 3-the excretory system and renal function > the role of clinical biochemistry in renal disease > Flashcards

the role of clinical biochemistry in renal disease Flashcards

1
Q

what key analyses are available in the lab? 9

A
  • U&E request gives serum concentrations of:
  • Creatinine- reference interval is higher in males than females
  • Urea
  • Sodium
  • Potassium
  • E-GFR calculated using serum creatinine concentration
  • .
  • Urine:
  • Albumin: creatinine ratio (ACR)
  • Protein: creatinine ratio (PCR)
  • .
  • Plus, a range of supporting assays for AKI or CKD
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2
Q

describe kidney blood flow?

A

1500 mL/min

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3
Q

describe the measurement of glomerular filtration?

what does it require? 2

A
  • GFR= (U x V)/S= ml/min
  • U= urine concentration
  • V= urine flow rate
  • S= serum concentration
  • A substance that is filtered and then neither absorbed or secreted in the renal tubules
  • 24h urine collection and a blood sample
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4
Q

why do we use creatinine for GFR? 5

A
  • Derived from creatine in muscle
  • Serum concentrations are relatively stable
  • 24h urine output is also stable day to day
  • No absorption and very little secretion in renal tubules
  • Simple to measure
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5
Q

what causes variation in serum concentrations and 24 hour urine output? 5

A
  • Age
  • Sex- male> female
  • Lean body mass
  • Ethnic origin
  • Effect of diet
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6
Q

how do we overcome the variations in serum concentrations and 24 hour urine output? 5

A
  • GFR related to body surface area- so standardise to a given body surface area
  • This allows:
  • Comparison against the general standard
  • Staging of renal disease
  • Monitoring of change in renal function- individual or cohort
  • Chosen standard= 1.73m^2
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7
Q

what does very high plasma glucose cause?

A

an osmotic diuresis leading to loss of water and sodium

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8
Q

describe dehydration? 3

A
  • Very likely is the serum urea: creatinine ratio is greater than 100
  • The mechanism is the passive re-absorption of urea in the nephron at low flow rates
  • Serum protein concentrations may also be elevated
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9
Q

how can we tell someone has AKI? 4

A
  • A rise in serum creatinine of 26 or greater within 48 hours
  • A 50% of greater rise in serum creatinine known or presumed to have occurred within the last 7 days
  • A fall in urine output to less than 0.5ml/kg/hr for more than 6 hours for adults and more than 8 hours in children and young people
  • A 25% or greater fall in eGFR in children and young people
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10
Q

describe the AKI alert system? 3

A
  • Stage 1= rise of. >1.5x baseline level
  • Stage 2= rise of >2x baseline
  • Stage 3= rise of 3x baseline
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11
Q

what are the causes of AKI? 5

A

P- poor perfusion (loss of isotonic fluids)
S- sepsis (any severe infection)
T- toxins (drugs)
O- obstruction (renal calculus, prostatic enlargement)
P- parenchymal (glomerulonephritis)

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12
Q

describe body builders and liver function? 5

A
  • High serum creatinine
  • High serum creatine kinase
  • High urea albumin: creatinine ratio
  • This is because they have a high muscle mass and protein intake
  • Mild hypokalaemia is not uncommon in body builders
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13
Q

what is the origin of creatinine? 2

A
  • Muscle mass is proportional to creatine and creatinine

Creatine + ATP= creatinine

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14
Q

describe some causes of CKD? 9

A
  • Hypertension
  • Diabetes
  • Hyperlipidaemia
  • Recurrent renal infection
  • Chronic glomerulonephritis
  • Systemic disease (systemic lupus, multiple myeloma)
  • Genetic- polycystic kidney, Alport syndrome
  • Chronic obstruction prostatic hypertrophy, renal calculi, reflux
  • Medication- NSAIDS, lithium
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15
Q

describe the albumin: creatinine ratio? 4

A
  • Proteinuria is a common finding in renal disease
  • Normally large proteins are retained by the glomerulus and only small proteins such as amylase are filtered
  • A small amount of albumin is normally filtered but metabolised in the proximal tubule. At larger loads due to glomerular damage more albumin escapes into the urine
  • Measurement as a ration with creatinine allows the use of a random urine sample rather than a timed collection
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16
Q

describe the different stages of CKD and the different eGFR? 6

A 
1- normal- >90
2- mild reduction- 60-89
3a- mild-moderate reduction- 44-59
3b- moderate-severe reduction- 30-44
4-severe reduction- 15-29
5- kidney function <15
17
Q

describe the metabolic features of CKD? 4

A

2- elevated serum urea and creatinine concentrations, some increase in the serum parathyroid hormone concentration
3- calcium absorption decreased, lipoprotein lipase decreased, malnutrition, anaemia- erythropoietin decreased
4- elevated serum triglyceride concentration, elevated serum phosphate concentration, metabolic acidosis, hyperkalaemia
5- marked elevation of serum creatinine and urea concentrations

18
Q

what is the importance of lab results for the treatment of CKD? 9

A
  • Elevated urea- low protein diet
  • High potassium- diet, diuretics, treat acidosis
  • Low bicarbonate- bicarbonate supplements
  • Low haemoglobin- iron supplements and possible erythropoietin with a target Hb 100-120
  • Low ferritin and transferrin saturation- iron supplements with a target saturation of >20%
  • Low calcium- reduce serum phosphate, vitamin D supplements
  • Raised phosphate- phosphate binding drugs
  • Raised PTH- raise serum calcium, calcimimetric drugs to keep PTH within 2-9 x upper limit of RI
  • Raised TG- diet, weight reduction, statins
19
Q

what is the role of the lab in finding the cause of renal disease? 7

A
  • AKI:
  • Plasma lactate- prognostic indicator
  • Infection- serum procalcitonin, CRP, WBC, blood culture
  • Autoimmune causes
  • .
  • CKD:
    serum and urine light chains- myeloma
  • Glycated Hb- diabetic control
  • Antibody tests
  • Biopsy- histology
20
Q

how do we monitor renal dialysis? 9

A
  • Pre and post dialysis samples
  • Show the effectiveness of dialysis
  • Indicate the required frequency of dialysis
  • Determine the need for other interventions
  • Diet
  • Supplements
  • Phosphate binders
  • Lipid lowering agents
  • Iron supplements
21
Q

how do we monitor renal transplant patients? 6

A
  • Serum creatinine- transplant function
  • E-GFR
  • ACR or OCR- potential damage to transplanted kidney
  • Measuring anti-rejection drugs
  • Checking for any tubular dysfunction
  • Monitoring as for CKD 3
22
Q

when is an individuals GFR required? 2

A
  • Remember MDRD and CKD- epi are linked to a standard body surface area
  • The real GFR of an individual is required to determine the dose of renally excreted drugs that are potentially toxic, monitoring dialysis and transplant patients
23
Q

describe the Cockcroft and Gault measurement of GFR? 2

A
  • GFR= (140-age) x (weight x constant)/ serum creatinine

- Constant= 1.23 in males and 1.04 in females

24
Q

describe renal tubular disorders? 4

A
  • There are many and they may be inherited or acquired
  • Renal tubular acidosis
  • Fanconi syndrome
  • Diabetes insipidus
25
Q

what are the next tests? 3

A
  • Early morning urine pH- this will be greater than 5.5 in type 1 renal tubular acidosis with hypokalaemia
  • Treatment to reduce the risk of nephrocalcinosis/ renal stone formation:
  • Potassium citrate, sodium bicarbonate, thiazide diuretics

104-theme 3-the excretory system and renal function (14 decks)

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