Acute Kidney Injury Flashcards
What are the stages of AKI?
KDIGO staging
Stage 1
- Creatinine 1.5-1.9x baseline (relative to the individual) within 7days
- Urine output <0.5ml/kg/hr for 6-12hrs
Stage 2
- Creatinine 2-2.9x baseline,
- <0.5ml/kg/hr >12hrs
Stage 3
- Creatinine 3x baseline
- <0.3/kg/hr >24hrs OR anuria >12hrs
What are the prerenal causes of AKI?
Anything affecting renal blood flow and leading to a reduced GFR: (60% of cases)
- Volume depletion: dehydration, diuretics, haemorrhage, severe vomiting/diarrhoea, acute pancreatitis, burns
- Oedematous states: heart failure (cardiorenal syndrome), liver cirrhosis, nephrotic syndrome
- Problems with local vasculature e.g. renal artery stenosis, renal vein thrombosis
- Hypotension: hypovolaemic, septic and cardiogenic shock
- Drugs affecting glomerular perfusion e.g.,cyclosporine,tacrolimus,NSAIDs, ACE inhibitors (especially avoid administering last two to patients with already reduced renal blood flow)
What are the renal causes of AKI?
Anything affecting renal parenchyma + subsequent function:
- Acute tubular necrosis* (can also be caused by prerenal i.e. sepsis/infection, ischaemia, nephrotoxins as low perfusion leads to necrosis; 85% of renal AKI)
- Glomerulonephritis
- Rhabdomyolysis
s - Vascular: haemolytic uraemic syndrome, TTP, vasculitis, malignant HTN
- Acute interstitial nephritis: renally excreted/toxic drugs e.g. calcineurin inhibitors e.g. tacrolimus; infection
What are the postrenal causes of AKI?
Anything leading to urinary tract obstruction: (5% of cases) - Caliculi - BPH - Cancers of bladder, ureters, prostate - Bleeding with clot formation - Congenial malformation e.g. posterior urethral valves - Catheter or catheter injury - MS, spinal lesions
As long as the contralateral kidney remains intact, patients with a unilateral obstruction typically maintain normal serum creatinine levels
What is the mnemonic for remembering some key causes of AKI?
STOP =
- Sepsis/Shock
- Toxins - contrast, aminoglycosides, cisplatin, ethlene glyol, lead etc
- Obstruction
- Pressure optimisation
What is the epidemiology of AKI?
20% of acutely presenting patients will have an AKI of some sorts so V important – as its simple to test and is associated with an increased mortality = worth knowing well
What is creatinine and why is it useful to measure it?
Creatinine is a breakdown product of the creatinine phosphate found in muscles, used for delivering energy
It is removed by glomerular filtration, but also proximal tubular secretion
It is produced at a base rate and its renal excretion rate is relatively physiologically constant; it is not absorbed or modified by the kidneys
Therefore is a good proxy for renal function
What is urea and why is it useful to measure it?
Urea is produced in the liver as a waste product of protein digestion
- Unlike creatinine, it can be reabsorbed in the kidneys and this can be regulated to help increase or decrease water reabsorption
Measured on its own, it can indicate a decrease in GFR (from any cause e.g. hypovolaemia, CCF, rapid cell destruction from infection, athletic activity etc - but clearly this is not specific
Measured in conjunction with creatinine and we get the urea-creatine ratio:
- This can be useful in the diagnosis of AKI i.e. if the urea:creatinine is high, this indicates pre-renal injury as urea levels are disproportionately higher due to an attempt to enhance water resorption and maintain intravascular volume
- May also be raised in bleeds e.g. covert GI bleeds
What is the pathophysiology of pre-renal AKI?
Decreased blood flow to kidneys (from any cause) - failure of renal vascular autoregulation to maintain renal perfusion - decreased GFR - activation of RAAS - increased aldosterone release - increase Na/H20 reabsorption - increased urine osmolality - secretion of ADH - increased reabsorption of H20 + urea
As creatinine is still excreted + blood urea rises - Ur:Cr ratio increases
What is the pathophysiology of intrinsic renal AKI?
Damage to tubules in nephron - necrosis/apoptosis of tubular cells - decreased reabsorption capacity of electrolytes, water and/or urea (depending on location of injury) - increased Na/H20 in urine - decreased urine osmolality
What is the pathophysiology of post renal AKI?
Bilateral urinary outflow obstruction (or unilateral + another pre/intrarenal cause = mixed) - increased retrograde hydrostatic pressure within renal tubules - decreased GFR and compression of renal vasculature - acidosis (from increased retention of H+) + fluid overload + increase in urea, Na, K
Again, normal GFR can be maintained` with one normally functioning kidney
What are the clinical features of AKI?
May be asymptomatic
Oliguria or anuria
Signs of uraemia:
- Anorexia, nausea
- Encephalopathy, asterixis
- Pericarditis
- Platelet dysfunction
Fatigue, confusion and lethargy
Signs of volume depletion: (pre-renal AKI)
- Orthostatic or frank hypotension
- Tachycardia
- Reduced skin turgor
Signs of fluid overload: (Na/H20 retention)
- Peripheral + pulmonary oedema
- HTN
- Heart failure
- SOB
Signs of renal obstruction: (post-renal AKI)
- Distended bladder
- Incompetent voiding
- Pain over bladder/flanks
In severe cases = seizures or coma
Increased risk of secondary infection
What is acute tubular necrosis? (aetiology, types, mechanism)
Location:
- Straight segment of the proximal tubule and thick ascending limb = particularly susceptible to ischaemic damage
- Convoluted segment of proximal tubule = particularly susceptible to damage from toxins
Types:
- Ischaemic = injury secondary severe HoTN/embolism - to
perfusion to cells containing transport proteins – necrosis – production of large volumes of poor quality urine
- Toxic = injury secondary to nephrotoxic substances (e.g. contrast, aminoglycosides etc), pigment nephropathy = myoglobinuria from rhabdomyolysis, haemoglobinuria from haemolysis; uric acid nephropathy
Mechanism:
- Necrotic proximal cells fall into tubular lumen and debris obstructs tubules = decrease GFR - pathology progresses like pre-renal AKI i.e. RAAS activation
How do you investigate ATN?
Bloods:
- Raised urea and creatinine
- Hyperkalaemia
- Metabolic acidosis
Urine:
- Possible myoglobin/haemoglobinuria
- Microscopy = Muddy brown granular casts, epithelial cell casts, free renal tubular epithelial cells
What is the prognosis for ATN?
1-3wks = most people make a full recovery; but can be lethal if AKI is severe and not managed properly
Dialysis may be required in oliguric patients with volume overload or severe hyperkalaemia
