AKI Flashcards
Definition of AKI.
Rise in creatinine > 26 mcmol/L within 48h
Rise in creatinine > 1.5 base line within 7 days
Urine output < 0.5 ml/kg/h for > 6 hours.
Explain AKI.
Life-threatening biochemical disturbances with oliguria, fallling urine output and rising serum urea as well as creatinine.
In some cases urea and creatinine cannot be relied upon.
When?
Low protein intake, liver failure and sodium valproate treatment will decrease the concentration of serum Urea.
Corticosteroid treatment, tetracycline and GI bleed will increase the concentration of Urea.
Low muscle mass = low creatinine
High muscles mass, red meat ingestion, muscle damage and decreased tubular secretion = high creatinine
AKI classifications.
Pre-renal
Renal parenchymal
Post-renal
Give examples of risk factors for AKI.
Diabetes/Metformin
CKD
IHD/CCF
Liver disease
Elderly >75
Sepsis
Cognitive impairment
Medications like ACEi, ARBs, NSAIDs and antibiotics.
Contrast medium during CT scans
KDIGO stages of AKI.
1 - > 26.5 micromol/l increase or 1.5 - 1.9 times the baseline of creatinine. Also < 0.5 ml/kg/h for 6-12 hours urine output.
2 - 2.0 - 2.9 times baseline creatinine. < 0.5 ml/kg/h for > 12 hours urine output.
3 - 3.0 time the baseline of creatinine, or > 353.6 micromol/l or initiation of renal replacement therapy. < 0.3 ml/kg/h > 24 hours or Anuria for > 12 hours urine output.
Pre-renal causes of AKI.
Hypovolaemia
Decreased cardiac output
Decreased effective circulating volume (CHF and Liver failure)
Impaired renal autoregulation (NSAIDs, ACEi and calcineurin inhibitors)
Causes of hypovolaemia.
Dehydration
Reduced intake
Gut losses by vomiting, nasogastric tube lossess and diarrhoea.
Burns, sweating
Haemorrhage
Third space losses from pancreatitis, peritonitis and bower obstruction.
Systemic vasodilation
Cardiac failure or shock
Causes of renal parenchymal/intrinsic AKI.
Glomerulonephritis
Ischaemia
Sepsis/infection
Nephrotoxins such as iodinated contrast, aminoglycosides, cisplating and amphotericin B. Also haemolysis, rhabdomyolysis, myeloma and intratubular crystals.
Vasculitis
Malignant hypertension
TTP
HUS
Pre-eclampsia
Give post-renal causes of AKI.
Bladder outlet obstruction
Bilateral pelvoureteral obstruction
Give causes of bladder outlet obstruction.
Intraluminal - Calculi, blood clot, sloughed papilla and tumour.
Luminal - pelviureteric neuromuscular dysfunction, ureteric stricture, ureterovesical stricture, neuropathic bladder.
Extraluminal - Tumours, Diverticulitis, Aortic aneurysm, retroperitoneal fibrosis.
How can you distinguish between pre-renal and intrinsic AKI?
By clinical examination and by urine specfic gravity, urine osmolality, urine sodium and FEna.
Distinguishing causes of shock on clinical examination.
Hypotension, peripheries and JVP in;
Hypovolaemia, low cardiac output and vasodilation.
Hypovolaemia has postural hypotension, cool peripheries and low JVP.
Low cardiac output has hypotension, cool peripheries and raised JVP.
Vasodilation has hypotension, warm peripheries and low JVP.
Urine specific gravity, urine osmolality, urine sodium and FEna in pre-renal vs. intrinsic AKI.
investigations in AKI.
Urine dipstick always.
This checks for blood and abnormal protein.
Daily FBC, U&Es, LFTs, Bone profile, CRP and serum bicarb.
Urine PCR, Urine MC+S, USS KUB to rule out obstruction.
Perform c-ANCA (PR3) + p-ANCA (MPO) to look for vasculitis, anti-GBM, ANA C3 and C4 to look for SLE, serum immunoglobulins and electrophoresis to look for myeloma.
Anti-streptolysin if post-streptococcal.
