L23 Acute kidney injury Flashcards
Creatinine clearance =?
Creatinine clearance = volume of plasma cleared of creatinine
= UV/[P x time]
= [Urine creatinine x volume] / [Plasma creatinine x time factor]
unit: ml/min
urine creatinine is mmol/L and plasma creatinine is umol/L (requires conversion)
time factor is in 24h = 1440 minutes
Why is creatinine more reflective of GFR compared to urea? (2)
- It is excreted only by kidneys
(c. f. urea - small amount excreted via sweat and faeces) - It is not reabsorbed (although there is a small amount of Cr secreted by PCT)
- urea: varying
Urea secretion in urine varies. How about creatinine?
- It is secreted in small amount
2. increased by drugs like cotrimaxzole, cephalosporins
A substance could accurately reflect GFR if its concentrated is unaffected by factors other than GFR.
What would affect urea and creatinine concentration respectively? (5+ 2)
Urea
- hydration state
- catabolic state
- diet/fasting
- GI bleeding
- Liver disease: increases ammonium, reduced urea
Creatinine
- Diet
- Muscle mass: decreased in advanced age/ CRF (reduced serum creatinine)
Rise in creatinine is only observed after significant proportion of nephrons around _________% are destroyed.
It is also affected by interfering chromogens such as ____ and _____?
50-60%;
glucose and vitamin C
Index of acute-on-chronic failure is when plasma urea/Cr ratio >?
80
Urea is an indicator of retention of toxic metabolites.
What is the role of looking at creatinine? (3)
- Detection of acute kidney injury.
- Monitoring of chronic kidney disease:
- CrCl is inversely proportional to [Cr]p
- 24h urine connection required, as production of Cr varies with time of the day > calculate eGFR - Planning of future therapy: dialysis required in ESRF at [Cr]p 800-1000 umol/L
4 reasons that causes an increase in urea-creatinine ratio.
- Pre-renal AKI: increased urea reabsorption, but not creatinine because cannot be reabsorbed
- UGIB - as a high-protein meal
- Catabolic state: trauma, severe infection, starvation, corticosteroids
- Decreased muscle mass
Acute kidney injury is an crux and sustained deterioration in renal function over hours or days, usually (but not always) reversible over days/weeks.
What is the diagnostic definition by KDIGO 2012?
Any 1 of the followings:
1. Rise in serum Cr 26.5 umol/L in 48 hours - abrupt
- Rise in serum Cr >1.5x baseline within 7 days - sustained
- Urine output <0.5ml/kg/h (oliguria) for 6 hours (not all AKI is oliguric)
Oliguria definition?
Anuria?
<0.5 ml/kg/h
or <400ml/day
<50ml/day
Clinical staging of acute kidney injury? (Stages 1-3)
Stage 1
- Plasma Cr 1.5-2x baseline
- Oliguric for 6h
Stage 2
- Plasma Cr 2-3x baseline
- Oliguric for 12h
Stage 3
- Plasma Cr >=3x baseline
- Oliguric <0.3 ml/kg/h for 24 h/ Anuric for 12 hours
What are the 3 types of AKI? Briefly describe them. (6)
- Prerenal injury (MC)
- reduced renal blood flow due to reduced ECV - Intrinsic injury
- acute tubular necrosis (ATN) due to renal ischemia to tubular toxins - Postrenal azotaemia
- obstructive nephropathy
What are the 3 causes to Pre-renal injury type of AKI? (3) Give examples (3)
- Renal hypoperfusion
- dehydration, GI bleed, osmotic diuretics, DI, third spacing
- Drugs: NSAID, ACEI (e.g. lisinopril), ARB (angiotensin II receptor blocker e.g. losartan)
precipitated by renal artery stenosis or chronically low ECV
- Hypotension
- septic/ anaphylactic shock - Low cardiac output
- CHF, cardiogenic shock
Why NSAID and ACEI/ARB would cause renal hypoperfision respectively?
NSAID
- inhibits prostaglandins synthesis > constricts afferent arterioles (reduced GFR)
ACEI/ARB
- inhibits angiotensin II which constricts the efferent arterioles to preserve GFR
- now: no constriction > reduced GFR
What would happen if pre-renal acute kidney injury is not treated?
Normal:
renal hypoperfusion > efferent arterioles constriction + increase PCT reabsorption, decrease in urine volume > both plasma urea and creatinine increases
Now: Autoregulation fails, will progress to irreversible acute tubular necrosis (intrinsic)
