NON-PROTEIN NITROGENOUS BIOMARKERS Flashcards
Ref: eGFR
<60 mL/ min/ 1.73 m2
Ref: Creatinine Clearance
1.30 - 2.30 mL/ sec/ 1.73 m2
Ref: ACR (albumin: creatinine ratio)
<3 mg/mmol
Ref: Ammonia (plasma)
<35 μmol/L
Critical: Ammonia (plasma)
> 199 μmol/L
Ref: Creatinine
Female: 40-100 μmol/L
Male: 50-120 μmol/L
Ref: Urea
2.5 - 8.0 mmol/L
Ref: Uric Acid (urate)
Female: 150 - 400 mol/L
Male: 200 - 500 mol/L
What is RAAS ?
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 and where is ammonia produced ?
- in the liver by deamination of proteins
- in the intestine by bacteria and endogenous enzymes
- in renal tubular cells (from glutamine etc.)
Clinical Significance of increased ammonia
- liver and kidney disease
- Reye’s Syndrome (CNS disorder)
Specimen type for Ammonia
- lithium heparin or EDTA
- immediately on ice (4°C)
Interferences for Ammonia Testing
- HEMOLYSIS; RBCs contain ammonia = increased
- smoking and ethanol = increased
- prolonged venous occlusion and fist clenching = increased
- AMMONIUM HEPARIN = increased
- delayed handling = increased
What is urea ?
Produced in the liver from ammonia
- freely filtered but 50% is reabsorbed in PCT
Clinical Significance of Increased Urea
- increased protein deamination/ intake
- increased protein catabolism from tissue breakdown and gastrointestinal bleeds
- congestive heart failure
Clinical Significance of Decreased Urea
- severe liver disease
- low protein intake
T or F: Urea is a good indicator of renal function
FALSE; urea is NOT a good indicator of renal function