Acute kidney injury Flashcards
List the functions of the kidneys
- Body fluid homeostasis – urine production
- Regulation of vascular tone – controls BP
- Excretory function – physiological waste e.g. urea, creatinine, drugs
- Electrolyte homeostasis -Na, K, Cl, Ca, Phos
- Acid-base balance –H+ and bicarbonate
- Endocrine function – production of erythropoietin; vitamin D metabolism and activation; renin
- Drug metabolism and disposal
What % of hospital admission patients develop AKI?
1 in 7 (some say 1 in 5)
Describe the traditional definition of AKI
• Rapid loss of glomerular filtration and tubular function over hours to days
• Retention of urea/creatinine
– Failure of homeostasis; even small increases in C are dangerous
What are some problems with the traditional definition of AKI?
– Lack of standardisation
– Absolute creatinine, changes in creatinine, urine output, need for dialysis
– Creatinine is insensitive and a late marker
– RRT hard endpoint but very late marker
– Wide spectrum of renal injury
Describe the current definition of AKI
• Increase in SCreatinine
– By ≥ 26.5 μmol/l (0.3 mg/dl ) within 48 hours; or
– To ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
• Urine volume <0.5 ml/kg/h for 6 hours
Describe some immediately dangerous consequences of AKI
Acidosis – can cause cardiac arrest
Electrolyte imbalance - Hyperkalaemia can cause cardiac arrest
Intoxication - e.g. opiates can cause respiratory (and then cardiac) arrest
Overload - overload with fluid and pulmonary oedema can cause cardiac arrest
Uraemic complications
What are the 3 classes of aetiology for AKI?
- Pre-renal - Blood flow to kidney
- Renal (intrinsic) - Damage to renal parenchyma
- Post-renal - Obstruction to urine exit
List some pre-renal causes of AKI
Reduce effective circulation volume
– Volume depletion (haemorrhage/dehydration) - D&V
– Hypotension / shock – Sepsis is a major contributor in up to 50% cases of AKI
– Congestive cardiac failure / Liver failure
Arterial occlusion
Vasomotor
– NSAIDs/ACE inhibitors
List some intrinsic renal causes of AKI
Acute tubular necrosis (ATN) - Ischaemic
Toxin-related – Drugs (aminoglycosides / amphotericin / NSAID) – Radiocontrast – Rhabdomyolysis (Haem pigments – Snake venom / Heavy metals - Pb, Hg – Mushrooms etc
Acute interstitial nephritis (many causes including drugs (PPIs))
Acute Glomerulonephritis
Myeloma
Intra renal vascular obstruction
– Vasculitis
– Thrombotic microangiopathy
What type of cause is myeloma?
intrinsic renal
List some post-renal causes of AKI
Obstruction
– Intraluminal (calculus, clot, sloughed papilla)
– Intramural – within wall (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
– Extramural – outside urinary system, compression (RPF, malignancy)
Why is the kidney susceptible to hypoperfusion?
Intrarenal heterogeneity of:
o Blood supply
o Oxygenation
o Metabolic demand
The cortex is richly perfused, whereas the medulla receives around 10-15% of renal blood flow
Medulla is hypoxic, yet metabolically active
Describe the course of acute ischaemic renal injury
Initiation
• Exposure to toxic/ischaemic insult
• Renal parenchymal injury evolving
• AKI potentially preventable
Maintenance
• Established parenchymal injury
• Usually maximally oliguric now
• Typical duration 1-2 weeks (up to several months)
Recovery
• Gradual increase in urine output
• Fall in serum creatinine (may lag behind diuresis)
If GFR recovers quicker than tubule resorptive capacity, excessive diuresis may result (eg post-obstructive natriuresis)
List an iatrogenic cause of AKI
Radiocontrast nephropathy (RCN)
- AKI following administration of iodinated contrast agent for imaging purposes
- Common contributor to hospital acquired AKI
- Usually transient renal dysfunction resolving after 72h
- May lead to permanent loss of function
List some risk factors for radiocontrast nephropathy
- Diabetes mellitus
- Renovascular disease
- Impaired renal function
- Paraprotein
- High volume of radiocontrast
- All of the above
What are the clinical features of myeloma
o Anaemia o Back pain o Weight loss o Fractures o Infections o Cord compression o Markedly elevated ESR o Hypercalcaemia
How is multiple myeloma diagnosed?
o Bone marrow aspirate - >10% clonal plasma cells
o Serum paraprotein ± immunoparesis
o Urinary Bence-Jones protein (BJP)
o Skeletal survey - lytic lesions
List some causes of AKI
- Cardiac failure
- Haemorrhage
- Sepsis
- Vomiting and diarrhea
- Tumours
- Prostate disease
- Stones
- Drugs e.g. NSAIDs, gentamicin
- Rhabdomyolysis
- Myeloma
- Radiocontrasts
- Vasculitis
- Glomerulonephritis
How can AKI be prevented?
o Avoid dehydration
o Avoid nephrotoxic drugs
o Review clinical status in those at risk + act on findings
o ? hold medication e.g. beta blockers, ACE inhibitors
o ? Give fluids
o Treat sepsis – major risk of developing AKI
Describe briefly the management of AKI
- Remove / treat cause if possible
- Make safe!
- Pre-renal – do they need fluid? BP support
- Renal (intrinsic) - can you remove precipitant?
- Post-renal – do they need a catheter?
What acronym is used for management of AKI?
STOP-AKI
Sepsis
Toxins
Optimise BP
Prevent harm
Describe supportive management of AKI
Fluid balance – Volume resuscitation if volume deplete – Fluid restriction if volume overload – Optimise blood pressure – Give fluid /vasopressors – Stop ACE inhibitors / anti-hypertensives
Stop nephrotoxic drugs
– NSAIDs
– Aminoglycosides
What are the 5 R’s for IV prescribing of fluids?
Resuscitate Routine maintenance Replacement Redistribution Review/reassessment
Describe the ECG changes in hyperkalaemia as it increases in severity
- Peaked T waves (usually the earliest sign of hyperkalaemia)
- P wave widens and flattens (can be small and indiscernible) – represents loss of atrial contraction
- PR segment lengthens
- P waves eventually disappear
- Prolonged QRS interval with bizarre QRS morphology
- High-grade AV block with slow junctional and ventricular escape rhythms
- Any kind of conduction block (bundle branch blocks, fascicular blocks)
- Sinus bradycardia or slow AF
- Development of a sine wave appearance (a pre-terminal rhythm)
- Asystole – flatline ECG
- Ventricular fibrillation
- PEA with bizarre, wide complex rhythm
How is hyperkalaemia treated?
Stabilise the myocardium
– Calcium Gluconate
Shift the K+ intracellularly
– Salbutamol
– Insulin-Dextrose
Remove any excess potassium
– Diuresis – urinate out potassium
– Dialysis – may be needed if kidneys are functioning well
– Anion exchange resins
What is used to stabilise the myocardium in hyperkalaemia?
Calcium Gluconate
What is used to shift K+ intracellularly in hyperkalaemia?
– Salbutamol
– Insulin-Dextrose
How can excess K+ be removed in hyperkalaemia?
Diuresis – urinate out potassium
Dialysis – may be needed if kidneys are functioning well
Anion exchange resins
What antidote is available for digoxin?
Digibind
What antidote is available for morphine?
Naloxone
Describe haemodialysis and haemofiltration
Haemodialysis (HD)
– Solute removal by diffusion
– Intermittent therapy – each session lasting 3-5 hours
Haemofiltration/CRRT – used in ITU
– Solute removal by convection
– Larger pore size
– Continuous therapy
What are the advantages and disadvantages of haemodialysis?
Advantages of HD
o Rapid solute removal
o Rapid volume removal
o Rapid correction of electrolyte disturbances
o Efficient treatment for hypercatabolic patient
Disadvantages of HD
o Haemodynamic instability
o Concern if dialysis associated with hypotension, may prolong AKI
o Fluid removal only during short treatment time
What are the advantages and disadvantages of haemofiltration/continuous renal replacement therapy?
Advantages of CRRT
o Slow volume removal associated with greater haemodynamic stability
o Absence of fluctuation in volume and solute control over time
o Greater control over volume status
Disadvantages of CRRT
o Need for continuous anticoagulation
o May delay weaning/mobilisation
o May not have adequate clearance in hypercatabolic patient
