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)
Causes of acute tubular necrosis (ATN) intrinsic type of injury. (4)
- Progression from pre-renal injury
- increased risk in elderly, DM, pre-existing renal disease - Specific renal disease
- glomerulonephritis
- interstitial nephritis (allergic reaction to drugs, e.g. penicillins, sulphonamides) - Nephrotoxins
- aminoglycosides (MC)
- IV contrast
- cisplastin (chemo)
- heavy metal (lead, mercury) - Sepsis
Which of the following about acute tubular necrosis is incorrect?
A. Oliguric phase: UOP <400ml/2h
B. Diuretic phase: UOP >400ml/24h
C. Recovery phase: return of GFR to 70-80% of normal
D. Each phase ~ 1 week, recovery phase can be up to a year
E. All phases can be seen
E
- few patients maintain a normal urine output through the course of illness
Suggest causes for post-renal azotaemia: obstructive nephropathy? (at least 6)
- Luminal
- stones, clots, sloughed papillae - Mural
- structures, BPH, malignancy (ureteric, bladder, prostate) - Extraluminal
- pelvic malignancy, retroperitoneal fibrosis
Name all the urine tests. Briefly describe their functions.
- Urine dipstick
- infection (leukocytes, nitrites)
- glomerular disease (haematuria, proteinuria, red cell casts) - Urine microscopy:
- casts, crystals, cells - Urine culture
- infection - Urine electrolytes
- to differentiate pre-renal CS intrinsic injury
Autoantibodies can be investigated if systemic cause of renal injury is suspected. Give examples. (3)
- ANCA (Antineutrophil cytoplasmic antibody)
- ANA (Antinuclear antibody)
- Anti-GBM esp if haemoptysis
What are the differences between Pre-renal injury and ATN (acute tubular necrosis)?
** MUST EXAMINE HE SAID
(6)
* Main principle is by whether the kidney still preserves concentrating ability by looking at the listed parameters.
- Mechanism of action
- Prerenal: salt/water reabsorption secondary to reduced blood filtered
- ATN: failed tubular reabsorption and secretion - FENa (fraction excretion of Na)
- Prerenal: <1%
- ATN: >2% - Urine Na (mmol/L)
- Prerenal: <20
- ATN: >40 - Urine osmolality (mmol/kg)
- Prerenal: >500 -dehydration
- ATN: <350 - no concentrating ability - Urine/Plasma urea ratio
- Prerenal: >20
- ATN: <10 - Urine/plasma creatinine ratio
- Prerenal: >40
- ATN: <20
How is FENa calculated?
Fraction excretion of Na
[Una x Pcr]
————— x 100%
[Pna x Ucr]
What to expect in CBC when suspected (a) myeloma ?
(b) vasculitis
(a) look for light chains;
(b) high ESR, anaemia
Renal USG is for distinguishing? also for look at?
Distinguish obstruction VS hydronephrosis ;
Cysts, small kidneys, masses
If renal USG is inconclusive, what further investigations?
CT without contrast
If there is signs of fluid overload, what to order?
CXR
