NON-PROTEIN NITROGENOUS BIOMARKERS Flashcards

1
Q

Ref: eGFR

A

<60 mL/ min/ 1.73 m2

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

Ref: Creatinine Clearance

A

1.30 - 2.30 mL/ sec/ 1.73 m2

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

Ref: ACR (albumin: creatinine ratio)

A

<3 mg/mmol

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

Ref: Ammonia (plasma)

A

<35 μmol/L

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

Critical: Ammonia (plasma)

A

> 199 μmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ref: Creatinine

A

Female: 40-100 μmol/L

Male: 50-120 μmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ref: Urea

A

2.5 - 8.0 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ref: Uric Acid (urate)

A

Female: 150 - 400 mol/L

Male: 200 - 500 mol/L

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

What is RAAS ?

A

Renin-Angiotensin-Aldosterone System ?
- responds to low blood pressure/ low [Na] = REABSORBS sodium and water
- kidney releases renin
- liver releases angiotensinogen
- renin converts angiotensinogen to angiotensin I
- angiotensin I converted to angiotensin II by ACE in lungs
- angiotensin II acts on adrenal gland to release aldosterone
- aldosterone promotes KIDNEY REABSORPTION OF SODIUM AND WATER

ACE = angiotensin-converting-enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How and where is ammonia produced ?

A
  • in the liver by deamination of proteins
  • in the intestine by bacteria and endogenous enzymes
  • in renal tubular cells (from glutamine etc.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical Significance of increased ammonia

A
  • liver and kidney disease
  • Reye’s Syndrome (CNS disorder)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Specimen type for Ammonia

A
  • lithium heparin or EDTA
  • immediately on ice (4°C)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Interferences for Ammonia Testing

A
  • HEMOLYSIS; RBCs contain ammonia = increased
  • smoking and ethanol = increased
  • prolonged venous occlusion and fist clenching = increased
  • AMMONIUM HEPARIN = increased
  • delayed handling = increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is urea ?

A

Produced in the liver from ammonia
- freely filtered but 50% is reabsorbed in PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical Significance of Increased Urea

A
  • increased protein deamination/ intake
  • increased protein catabolism from tissue breakdown and gastrointestinal bleeds
  • congestive heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical Significance of Decreased Urea

A
  • severe liver disease
  • low protein intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T or F: Urea is a good indicator of renal function

A

FALSE; urea is NOT a good indicator of renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Interferences in two-step urease reaction

A
  • HEMOLYSIS; RBCs contain ammonia = increased
  • AMMONIUM HEPARIN (forest green top) = increased
  • endogenous ammonia = increased
  • SODIUM FLOURIDE anticoagulant inhibits urease (gray top) = decreased
19
Q

What is uric acid ?

A

Formed from oxidation of purine bases
- freely filtered, some reabsorbed by PCT

20
Q

Clinical Significance of Increased Uric Acid

A

Hyperuricemia:
- chronic renal failure; decreased excretion
- chemotherapy
- thiazide diuretics
- hypertension

21
Q

Clinical Significance of Decreased Uric Acid

A

Hypouricemia = Fanconi’s Syndrome (loss of uric acid in PCT), decreased liver enzymes required for depurination

22
Q

Interferences in two-step uric acid (uricase) reaction

A
  • SODIUM FLOURIDE anticoagulant (gray top) = increased
  • salicylates = increased
  • bilirubin = decreased
  • ascorbic acid/ vit C = decreased
  • hemolysis = decreased
23
Q

What is creatinine ?

A
  • formed from creatine in skeletal muscle
  • freely filtered
  • dependant on muscle mass (higher in males)
  • little change in response to diet
24
Q

Clinical Significance of Increased vs Decreased Creatinine

A
  • used to estimate glomerular filtration rate

Increased = decreased GFR

Decreased = muscular dystrophy; inadequate conversion of creatine

25
Q

What does creatinine clearance test for ?

A

Glomerular function

26
Q

Sample Requirements for Creatinine Clearance

A
  • blood sample drawn within 72 hours of urine collection
  • 24 hour urine collection must be refrigerated
27
Q

Creatinine Clearance Formula

A

C (mL/s) = (UV/P) x (1.73/SA)

where,
U = urine creatinine concentration (μmol/L)
V = volume of urine (mL/ sec OR mL/ min)
P = plasma creatinine concentration (μmol/L)
SA = of patient, calculated using height and weight

28
Q

How many seconds in 24 hours ?

A

24 hours = 86,400 seconds

29
Q

Why does the creatinine clearance test overestimates GFR ?

A

~10% of creatinine in urine is due to tubular secretion

30
Q

Creatinine clearance is __ in renal disease.

A

Creatinine clearance is DECREASED in renal disease.

31
Q

Why is eGFR useful ?

A

estimates GFR WITHOUT a 24 URINE COLLECTION

32
Q

In what cases is eGFR not applicable ?

A
  • acute kidney injury
  • abnormal muscle mass
  • medication ie. salicylates, furosemide
33
Q

Albuminuria is a marker for __.

A

Abuminuria is a marker for CHRONIC KIDNEY DISEASE.

34
Q

Proteinuria due to low MW globulins is a marker for __.

A

Proteinuria due to low MW globulins is a marker for TUBULAR DAMAGE.

35
Q

What is ACR used for ?

A

Albumin:Creatinine Ratio is used to overcome diurnal variation of albumin/ hydration

36
Q

How many positive ACR results are required to diagnose chronic kidney disease (CKD) ? What is used to monitor CKD ?

A
  • 2 or more positive ACR results to diagnose
  • ACR is also used for monitoring
37
Q

What small peptide is a good indicator of GFR ? Why ?

A

β-microglobulin:
- freely filtered by glomerulus
- unaffected by muscle mass and diet
- increased in renal failure and malignancies

38
Q

Causes of pre-renal Acute Kidney Injury (AKI)

A
  • decreased circulating blood supply (hypovolemia)
  • cardiac failure
  • burns, hemorrhage, vomiting, diarrhea, sepsis
39
Q

Causes of renal Acute Kidney Injury (AKI) ?

A
  • vascular, glomerular, interstitial damage
  • myoglobinuria
  • heavy metal poisoning
40
Q

Causes of post-renal Acute Kidney Injury (AKI) ?

A
  • obstruction of flow of urine after kidney
  • prostatic enlargement, renal stones, fibrosis, neoplasms
41
Q

What does isosthenuria indicate in CKD ?

A
  • SG is the SAME as protein-free plasma
  • kidney’s lack of concentrating ability
42
Q

What is the primary cause of CKD ?

A

Diabetes mellitus > hypertension > glomerular nephritis

43
Q

Creatinine is measured by the __ reaction.

A

Creatinine is measured by the JAFFE KINETIC reaction.

44
Q

Interferences in the Jaffe Kinetic reaction

A
  • ketones, ascorbate, cephalosporin, glucose, proteins = increased
  • bilirubin and HEMOGLOBIN = decreased

NOTE: jaffe kinetic reaction is used to measure creatinine