Acute Kidney Injury Flashcards
Define “acute kidney injury”
A decline in kidney function during 48hrs as demonstrated by increase in serum Cr of more than 50%, or the development of oligouria
Outline the KDIGO AKI stages of severity
Stage 1:
Serum creatinine 1.5-1.9 times baseline OR >_ 0.3 mg/dL (>_26.5 umol/L) increase in serum creatinine.
Urine output <0.5 mL/kg/h for 6-12 hours.
Stage 2:
Serum creatinine 2.0-2.9 times baseline.
Urine output <0.5 mL/kg/h for >_12 hours.
Stage 3:
Serum creatinine 3 times baseline OR serum creatinine increased to >_ 4 mg/dL (>353.6 umol/L) OR initiation of renal replacement therapy OR in patients <18 years, decreased eGFR to <35mL/min per 1.73m^2.
Urine output <0.3 mL/kg/h for > 24 hours OR anuria for >_ 12 hours.
In-hospital mortality associated with AKI in critically ill patients is…
50%
Long-term effects of AKI (stats)
Only 50% of survivors are alive at 10 years.
Of survivors, 15% have clinically apparent residual CKD.
In survivors,
– 60% increased risk of heart failure
– 40% increased risk of MI
– 20% increased risk of stroke
Organs affected by AKI
Brain
Lungs
Liver
GIT
Bone marrow
Heart
(through IL-6)
Relationship between AKI and CKD
AKI is a risk factor for CKD
(Repeated episodes of AKI and the
severity of the AKI will ↑ ↑ ↑ the risk of CKD)
Conventional markers (urea + creat) indicate AKI too late. What other markers may be linked to damage caused by AKI?
NGAL, KIM-1, IL-18
4 common misconceptions regarding renal function
1) ‘normal creatinine = normal renal function’
2) Rising creatinine = worsening renal function
3) Improving creatinine in patients on dialysis
4) Use of eGFR in patients with AKI/non steady-state
NB risk factors for AKI (5)
Sepsis
Critical illness
Circulatory shock
Trauma
Nephrotoxic drugs
Causes of pre-renal failure (3)
(not filtering enough blood to make urine)
1) Prerenal azotemia (hypovolaemia/cardiac failure/hepatorenal syndrome)
2) Renal artery (occlusion/vasculitis)
3) Renal vein (thrombosis)
Causes of intra-renal failure (5)
(not able to make urine)
1) Small-vessel disease (thrombotic microangiopathy/atheroembolism/ vasculitis)
2) Glomerular disease (anti-GBM disease/lupus nephritis/post-infectious glomerulonephritis/infective endocarditis/membranoproliferative glomerulonephritis/cryoglobulinaemia/IgA nephropathy/Henoch-Schonlein purpura)
3) Acute tubular necrosis (ischaemia/nephrotoxins/ rhabdomyolysis/radiocontrast agents)
4) Acute interstitial nephritis (drugs/infection/systemic disease)
5) Intratubular obstruction (casts/drugs/crystalluria)
Causes of post-renal failure (1)
(blockage, urine can’t come out)
Post-renal obstruction (bladder outlet obstruction, tumours, renal calculi, papillary necrosis, retroperitoneal fibrosis)
Definition of pre-renal failure
There is a impaired perfusion of the
kidney with blood. This results from either Hypotension, Hypovolaemia, Impaired cardiac pump efficiency, Vascular disease limiting renal blood flow, Drugs (NSAID and ACEi)
How do NSAIDs affect the glomerulus?
Cause vasodilation of of afferent arteriole (promotes blood flow into glomerulus)
How do ACE inhibitors affect the glomerulus?
Cause vasoconstriction of the efferent arteriole (help maintain intra-glomerular pressure)
Signs that indicate fluid status (6)
Thirst
Dry mucous membranes (Tongue)
No sweat
Decreased skin turgor
Sunken eyes
Decreased urine output
Biochemical evaluation of pre-renal failure
Urea:creatinine ratio: 20:1
Urine specific gravity: >1.020
Urine Osmolality (mOsm/kg): >500
Urinary Na+ : <20
Fractional excretion of Na+ : low
Biochemical evaluation of intra-renal failure
Urea:creatinine ratio: may return to normal but creatine continues to rise
Urine specific gravity: <1.010
Urine Osmolality (mOsm/kg): <350
Urinary Na+ : >40
Fractional excretion of Na+ : higher
Why is urine osmolality high in pre-renal failure?
Concentrated urine because you are reabsorbing water
Why is urinary Na+ low in pre-renal failure?
Wherever sodium goes,
water goes. Urea gets reabsorbed
with sodium as well… so low sodium in urine pulling water and urea back into blood
Why can the tubules not do their job in Intra-renal failure?
Hypoperfusion/blood loss causing hypoxia/ATP loss/metabolic changes –> epithelial cells die –> slough off into tubular lumen where the casts create an obstruction to urine
Pathogenesis of Rhabdomyolysis
Muscle injury –> myoglobin breaks down.
Sequestration of fluid as it is pulled into injured muscle (activates RAAS and CNS) .
Dying muscle releases K+ , uric acid and PO4- (all elevated in blood).
Calcium moves into muscle causing hypocalcaemia.
Generation of oxygen free radicals.
Renal vasoconstriction due to increased ET, TXA2, TNF-alpha, F2IP, and decreased NO.
Filtered myoglobin causes damage to tubules – leaves behind pigmented granular myoglobin casts (obstruction distally if injury is proximal).
What colour is urine in rhabdomyolysis, and why is this not caused by RBCs?
Coke-coloured/reddish-brown.
The colour is caused by myoglobinuria (Dipstix will show haematuria, but this is because of haemoglobin in the urine, not RBCs)
Things to rule out in post-renal failure (4)
Enlarged prostate
Cervical CA
Percuss bladder – also blocked catheter
Ultrasound to rule out hydronephrosis (only 85% sensitive!)
