Acute Kidney Injury Flashcards
Acute kidney injury (AKI) is defined as abnormal kidney __ and/or __, duration: within __ up to __
Complex syndrome of __, __ and __
Characterised by: (4)
Abnormal kidney function and/or structure
Within 7 days up to 3 months
Complex syndrome of injury, regeneration and repair
Characterised by:
1. Rapid decline in GFR
2. Impaired excretion of urea and waste products
3. Loss of water and electrolyte regulation
4. Loss of acid-base regulation
KDIGO 2012 Criteria for Staging of AKI
- Creatinine and urine output levels
What happens if baseline serum creatinine is unknown?
Stage 1
- Creatinine 1.5 - 1.9 times (50% more from baseline), or > 26.5 mcgmol/L
- Urine output < 0.5 mL/kg/hr for 6-12 hours
Stage 2
- Creatinine 2.0 - 2.9 times baseline
- Urine output < 0.5 mL/kg/hr for > 12 hours
Stage 3
- Creatinine 3.0 times baseline, or Cr > 353.6mcgmol/L
- Initiation of RRT
- Reduced eGFR < 35 in patients < 18 years old
- Urine output < 0.3 mL/kg/hr for > 24 hours, or anuria > 12 hours
If baseline Cr is unknown
- Assume baseline of 120 mL/min/1.73 m2,
- Or published minimum/maximum normal serum creatinine for age and gender
Formal and complete diagnosis and labelling of acute kidney injury
(KDIGO) (community/hospital) (urine output) (location) AKI secondary to (cause)
KDIGO: 1 /2 / 3
Community/hospital acquired
Urine output: anuric / oliguric / non-oliguric / polyuric
Location: pre-renal / renal / post-renal
Eg: KGIDO 2 community acquired non-oliguric pre-renal AKI secondary to gastrointestinal losses
Classification of AKI - based on anatomical location
A. Pre-renal
B. Renal
C. Post-renal
A. Pre-renal
1. Volume depletion - GI losses, haemorrhage, burns, renal salt wasting
2. Renal hypoperfusion
- Reduced arterial pressuer: cardiac failure
- Systemic vasodilatation: septic shock, neurogenic shock, cirrhosis
- Intestinal obstruction
3. Intrarenal vasoconstriction
- Hepatorenal syndrome, cardiorenal syndrome
- Meds: CNI, NSAIDs, ACEi, ARBs
B. Renal
1. Glomerulonephritis (GN) - post-infectious, SLE, IgA vasculitis, MPGN, ANCA, Anti-GBM (Goodpasture), RPGN, malignant hypertension, diabetes mellitus
2. Vascular - HUS, renal artery stenosis/thrombosis, renal vein thrombosis, thrombotic microangiopathy
3. AIN - infection (EBV, CMV, HIV, leptospirosis), drugs
4. Acute pyelonephritis
5. Tumour infiltration
6. Tubular nephrotoxins
- Aminoglycosides, furosemide, vancomycin, acyclovir, wasp sting, toxins, snack bite
- Pigments: haemolysis (G6PDD, malaria), myoglobin (rhabdomyolysis)
- Radiocontrast
C. Post-renal
1. Structural - posterior urethral valve, ureteric obstruction, neurogenic bladder, retroperitoneal fibrosis, BPH/prostate cancer
2. Crystalluria - tumour lysis syndrome, melamine poisoning
3. Renal calculi
4. Urinary retention - antihistamines, anticholinergic, epidural
What are the key differences between community vs hospital acquired AKI?
Community - often single insult, frequently reversible
Hosopital - multifactorial, multiorgan involvement
Define urine output
- Anuria
- Oliguria
- Normouria / non-oliguria
- Polyuria
Anuria: no urine output
Oliguria: < 0.5 mL/kg/hr for > 6 hours
Non-oliguria: 0.5 - 1 mL/kg/hr for > 5 hours
Polyuria: > 3mL/kg/hr
Clinical presentation of AKI
- Severe hypovolaemia
- Vomiting / diarrhoea, reduced oral intake - gastroenteritis, food posioning
- Polyuria - DKA, RTA, chronic tubulopathies
- Tachycardia, CRT > 2s, reduced skin turgor, dry mucous membrane, sunken eyes, hypotension - Oliguria and oedema - fluid retention
- Gross haematuria - post-infectious GN
- Bloody diarrhoea or pneumonia with oliguria +/- bicytopenia - HUS
- Purpuric or malar rashes, joint pain/swelling, haemoptysis - vasculitis, RPGN
- Incidental abnormal laboratory parameters
- Routine: look for acute causes
- Critically ill: septic shock/hypotensive nephropathy, septic ATN
- Post-CABG - Post-chemotherapy or bone marrow transplantation
Corrected creatinine in fluid overlaod
cCr = measured Cr x (1 + net balance / TBW)
TBW = 0.6 x weight (kg)
Early AKI detection investigation for aged 2 months - 21 years
Urinary/plasma neutrophil gelatinase-associated lipocalin (NGAL)
< 50 ng/mL - rules out structural AKI
> 150 ng/mL - predicts structural AKI
Tested in patients at high risk and of YOUNG age:
1. Criticall ill
2. Cardiac surgery
3. Fluid overload
3. Nephrotoxin exposure
4. Solid organ transplant
Laboratory Evaluation of AKI
Labs
1. RP, urine sodium and urine creatinine
1A. Includes anion gap - HAGMA - ehylene glycol poisoning
2. UFEME
3. FBC - anaemia, thrombocytopenia, reticulocytosis
4. PBF - schistocytes (HUS), spherocytes (SLE)
5. Urine haemoglobin, serum CK or aldolase - pigment nephropathy
6. C3, C4, ANA, ANCA, anti-GBM
- C3 is low in post-infectious GN, lupus, MPGN, familial HUS
7. Elevated LDH - HUS, haemolysis
8. Hypocalcaemia, hyperphosphataemia, hyperuricaemia - TLS
9. Factors H, I, B, CD46, anti-factor H, ADAMTS13 - HUS
Imaging
1. US KUB and prostate - kidney size and echogenicity, hydronephrosis, obstruction, BPH
2. MAG3 radionuclide imaging in children < 5 years, or post-kidney transplant
3. Comuted tomography without contrast
4. MR urography for obstructive uropathy
Biopsy
1. Unclear etiology
2. Clinical suspicion of RPGN or AIN
3. Prolonged AKI - assess extnt of damage, ATN vs cortical necrosis
UFEME results in AKI
- Haematuria and red cell morphology
- Casts and EC
- Pyuria
- Eosinophils
- Crystals
- Fat globules
- Haematuria and dysmorphic red cells - glomerulonephritis
- Casts and EC - ATN
- Pyuria - pyelonephritis, tubulointerstitial disorder (sterile pyuria)
- Eosinophils - acute allergic interstitial nephritis
- Uric acid crystals - tumour lysis syndrome
- Calcium oxalate crystals - ethylene glycol poisoning
- Fat globules - fat embolism
Fractional sodium excretion FENA
Fractional urea excertion FEurea
How do you differentiaet pre-renal vs intrarenal AKI based on these serum and urine indices?
FENA = (urine sodium / plasma sodium) x (plasma creatinine / urine creatinine) x100%
FEurea = (urine urea / plasma urea) x (plasma creatinine / urine creatinine) x100%
