Introduction to kidney tests - acid-base metabolism Flashcards
Significance of K and PO4 in kidney function tests
K and PO4 retained with decreased GFR
Urea and GFR
- Urea is the end product of protein metabolism and is retained with decreased GFR
Creatinine and GFR
- Creatinine is the end product of creatine breakdown and is retained with decreased GFR
Kidney blood flow
- 1500mL/min
GFR
- Most frequent test of kidney function
Based on serum creatinine:
- Starts to rise - 50% glomeruli lost
- Marker of progressive kidney damage
- Poor sensitivity - minor kidney damage
Hierarchy of kidney function tests - inaccurate to accurate
- s-Urea
- 24h creatinine clearance
- s-Creatinine
- eGFR is best index of glomerular function, estimated from s-Creatinine(EPI, MDRD, cockcroft-gault)
- Direct GFR measurement
What is creatinine dependent on
- Muscle mass
Changes in creatinine levels with age
With age muscle mass decreases
- Elderly lower muscle mass than younger
With age, kidney function decreases
With age, glomeruli decrease
- Elderly less glomeruli than younger
Blacks from Africa, USA, West Indies have greater muscle mass - than other ethnic groups
Formula for estimating GFR
- CKD-EPI (based on the largest population of any calculator, best for ‘normal sized’ people)
- Account for outliers in muscle mass
- Creatinine clearance = ( Urine Cr * urine volume)/ (plasma Cr* time)
Creatinine origin
Muscle mass proportional to creatine proportional to creatinine
- Creatine + ATP - creatine-P + ADP
- There is a constant decay of creatine to creatinine
- CK - creatine kinase is the enzyme that carries out the above reaction
- Creatine-p - high energy phosphate
Urea origin
- Protein proportional to amino acids proportional to urea
- Alanine –ALT–> urea + pyruvate
Aspartate –AST–> Urea + oxalo-acetate –> glucose
- Enhanced by stress: cortisol (glucocorticoid)
Ureamia
- Condition having ‘urea in the blood’
- Denotes a very high serum urea that is the result of kidney failure
- Describes the pathological and symptomatic manifestations of severe loss of GFR
AKI
- GFR compromised - low BP, shock
- Decreased blood flow to kidneys
Which waste products accumulate in AKI
- Urea, creatinine, acid, PO4
What should be considered in AKI
Review urgently
Consider drugs: ACEI/ARB, NSAID, diuretics (most important drugs of relevance)
- Also obstruction, hydration, infection
Complications of AKI
- Volume overload, raised K+, H+, PO4
- Initial assessment - volume status(possible dehydration, CHF)
- s-K, HCO3, PO4, calcium, albumin
- s-uric acid, magnesium
- FBC
ACEI pathophysiology in AKI
- Reduce systemic vascular resistance
- Renoprotective - diabetic and renal disease
- Kidney adverse effects (intrarenal efferent vasodilation, fall in filtration pressure and GFR)
- Fall in filtration pressure (antiproteinuric and long term renoprotection)
- GFR dependency on angiotensin II- mediated efferent vascular tone is lost
Most common cause of lactic acidosis in hospitalised patients
- Sepsis
- Usual cause is tissue hypoperfusion
- Impaired tissue oxygenation, leading to increased anaerobic metabolism
- Hypovolemia
- Cardiac failure
- Sepsis
- Cardiopulmonary arrest
Sepsis 6
- Deliver O2 to target 94-98% or 88-92% in COPD
- Take blood culture
- Give IV (intravenous) antibiotics
- Start IV resuscitation
- Measure serum lactate
- Monitor urine output
Maintenance of acid base balance
- Lungs remove CO2 (fast)
- Kidneys reabsorb HCO3- and secrete H+
H+ + HCO3- –> H2CO3 –> H2O + CO2 - Lungs - CO2 removal shifts equation to right with loss of H+ and HCO3=
- Kidneys - PCT - HCO3- reabsorption
- DCT - H+ secretion, urine acidified
What happens in a patient with metabolic acidosis
- The fall in pCO2 will mitigate the fall in pH caused by reduced HCO3
- In all simple acid-base disorders, the primary abnormality will cause a compensatory response such that the HCO3 concentration and pCO2 will move in the same direction
- Both will decrease or both will increase
- These directional changes will act to return the pH toward normal
- The compensatory responses are mediated by alterations in pH within the respiratory center
- Respiratory compensation for metabolic acidosis generates a linear relationship between arterial pCO2 and bicarbonate
Main cation in extracellular fluid
Sodium
Main cation in intracellular fluid
Potassium
How are electrolytes usually measured
- Usually measured with creatinine, urea
- Also chloride, bicarbonate required with acid/base disturbance to determine anion gap
What is anion gap due to
- Albumin- phosphate- sulphate-
Formula for anion gap
Measured cations - measured anions
What is the increased AG in acidosis due to
- Ketone- , lactate- ,salicylate- ,ethylene, glycol-
DKA - acid added
- Na+ + HCO3- exist in serum
- Addition of H+
- Combines with HCO3-
- Leaving Na+ salt of the acid
- Na+ ketone-
To maintain pH or H+
- H+ combines with HCO3- forming H2CO3
- CO2 blown off
- Resulting loss HCO3- and H+
- In serum ketone- exists instead of HCO3-
