Acute Kidney Injury Flashcards
What are the consequences of acute kidney injury (AKI)?
Acute metabolic complications - Hyperkalaemia Acute cardiovascular complications - Pulmonary oedema Prolonged hospitalisation Patient death common End-stage kidney disease (ESKD) uncommon
What is AKI?
No validated biomarker for immediate renal injury
Increased by 25 umol/L in creatinine
- Anything more than that, is more severe increase
What are the main physiological roles of the kidneys in the normal state?
Fluid balance
Excretion of waste products
Acid/base balance
Hormone production
How does kidney disease affect fluid balance?
Na/water imbalance
- Inability to excrete fluid lode OR
- Inability to conserve Na and water
How does kidney disease affect excretion of waste products?
Accumulation of solutes and waste products
How does kidney disease affect acid/base balance?
Accumulation of acids
How does kidney disease affect hormone production?
Abnormalities in function
- Anaemia
- Bone disease
Is loss of urine output in AKI invariable?
No
Why aren’t accumulation of solutes, waste products, and acids immediately abnormal in AKI?
Because time dependent
What are the three categories of causes of AKI?
Pre-renal = sudden and severe drop in blood pressure/interruption to blood flow to kidneys Intra-renal = direct damage to kidneys by inflammation, toxins, drugs, infection, or prolonged reduced blood supply Post-renal = sudden obstruction due to enlarged prostate, kidney stones, bladder tumour, or injury
What is active urine sediment?
Blood and protein in urine dipstick
Is intrinsic renal failure common?
Other than due to acute tubular necrosis (ATN), no
What is the commonest cause of post-renal AKI in women?
Cervical carcinoma
What is the commonest cause of post-renal AKI in men?
Benign prostatic hypertrophy
What structure does prostatic carcinoma tend to block, and why?
Blocks ureters rather than urethra, because tends to grow behind bladder
What stages of AKI do pre-renal causes correspond to?
Stage I-II early AKI
What maintains blood pressure in pre-renal AKI?
CNS sympathetic outflow > stimulates RAAS
What mediates salt and water retention in pre-renal AKI?
Anti-diuretic hormone (ADH) and aldosterone
What happens to the urinary concentration capacity in pre-renal AKI?
Intact
Is pre-renal AKI reversible, and if so, how?
Yes, reversible by prompt restoration of renal perfusion
But prolonged hypo-perfusion causes renal decompensation
What happens in renal decompensation as a result of prolonged hypo-perfusion?
Excessive SNS and RAAS > ischaemic injury
Dysautoregulation with concomitant NSAID and ACE inhibitor
Is intrinsic AKI reversible?
Not readily
What are the possible pathologies of intrinsic AKI?
Tubular injury - Common - Ischaemia/prolonged hypoperfusion = ATN - Toxins Interstitial nephritis - Common - Drugs - Infection - Infiltration Glomeruli - Uncommon - Inflammation = glomerulonephritis - Thrombosis Vascular disease - Uncommon - Inflammation = vasculitis - Occlusion
Which part of the nephron is most susceptible to ischaemia?
Thick ascending loop of Henle
What finding tends to indicate a glomerular problem?
Proteinuria
What drug classes can possibly cause interstitial nephritis?
Anti-inflammatories
Protein pump inhibitors
Antibiotics
What is the most common cause of intrinsic AKI?
ATN
What is ATN?
Usually because of acute event, either
- Ischaemic
- Toxic
Oliguria not invariable > don’t rely too much on urine output
What is happening at a cellular level in ATN?
Ischaemic depletion of ATP > release of ROS and apoptosis
Cell desquamation > obstructive cast > back-leak of tubular fluid
Reversible after regeneration of tubular endothelial cells
What are the phases of ATN?
Initiation
Maintenance
Recovery
Does the serum creatinine level indicate GFR?
Not when it’s changing, especially if it’s increasing
Best to assume that GFR = 0
- Helps appreciate seriousness of AKI
What is the pathophysiology of ATN?
Hypoperfusion > reperfusion to vascular network where there’s been micro-vessel thrombosis and occlusion > further inflammation > reperfusion injury
What happens in the initiation phase of ATN?
Acute decrease in GFR to low-very low levels
Increase in serum creatinine and urea
What happens in the maintenance phase of ATN?
Sustained reduction in GFR
Creatinine and urea continue to rise
What happens in the recovery phase of ATN?
Tubular function restores with increase in urine volume
- If oliguria present
Gradual decrease in creatinine and urea
How long can recovery take after ATN?
2-6 weeks
Risk of chronic damage
How do you determine whether renal impairment is acute or chronic?
Lab values don’t discriminate between acute and chronic disease
Oliguria supports acute renal failure
What are the clues that support a chronic disease process in the kidneys?
Pre-existing illness - Diabetes - Hypertension - Age - Vascular disease Previous serum creatinine measurements Small, echogenic kidneys by ultrasound
What suggests that the cause is an obstruction rather than AKI?
Often complete anuria
May have palpable bladder on examination
Renal ultrasound shows bilateral hydronephrosis
How do you assess a patient’s volume status?
History - Thirst - Lightheaded/dizziness - Cramping Examination - If can't see JVP lying down, probably very fluid deplete - Postural hypotension - Urinary concentration indices
How do you determine whether there’s evidence of other intrinsic renal disease apart from ATN?
Clues from history and exam
Urinalysis, including microscopy
How do you determine whether a major vascular occlusion has occurred?
History of vascular disease
Renal asymmetry on ultrasound
Loin pain with macro haematuria
Complete anuria
What is the treatment for AKI?
Facilitating renal repair
Very little available at present
What are the risk factors for developing AKI?
Elderly Chronic kidney disease Cardiac failure Liver disease Diabetes Vascular disease Background nephrotoxic medications
What acute insults over background morbidity may cause AKI?
Sepsis and hypoperfusion
Toxicity
Obstruction
Parenchymal kidney disease
How do you prevent AKI?
Monitor patient
Maintain circulation
Minimise kidney insults
Manage acute illness
How do you recognise AKI?
5x increase from most recent baseline creatinine OR
6 hours oliguria
How is AKI monitored?
Discontinue offending agents and nephrotoxins
Assessment of volume status
Measure urea, creatinine, electrolytes, and venous bicarbonate daily while creatinine rising
What is the relationship between volume status and outcomes of AKI?
Volume overload associated with poorer outcomes
What is the mnemonic for the causes of AKI?
S = sepsis and hypoperfusion T = toxicity O = obstruction P = parenchymal disease
What are the investigations for AKI?
Urine dipstick Urine PCR Renal ultrasound LFTs CRP CK Platelet count
What is oliguric renal failure?
Urine output less than required to maintain solute balance
Less than 400 mL/24 hours
What is anuric renal failure?
Less than 100 mL/24 hours
Less common
What are the possible acute metabolic complications of AKI?
Volume overload Hyperkalaemia Metabolic acidosis Hypocalcaemia Infections Nutrition
How do you treat volume overload?
Salt and water restriction
Diuretics
- Give big dose first, because if they don’t respond, escalate to dialysis
How do you treat hyperkalaemia?
Restrict K intake IV glucose and insulin Kayexalate Calcium gluconate Acute dialysis
How do you treat metabolic acidosis?
Sodium bicarbonate
Dialysis
How do you treat hypocalcaemia?
Calcium carbonate
Calcium gluconate
What is peritoneal dialysis?
Dialysate infused into peritoneal cavity
Left to dwell for equilibration of solutes and fluids
Used dialysate discarded
Describe haemodialysis
Solutes removed by diffusion Fast Not always well tolerated Small molecules removed Clearance of drugs variable Requires dialysis expertise
Describe haemofiltration
Solute removed by convection Slow Usually well tolerated Medium sized molecules removed Clearance of most drugs More expensive, in ICU
Which form of dialysis is better?
No evidence that one form better than other
What often dictates choice of the dialysis used?
Clinical status of patient
Available resources
Physician expertise
