Acute Kidney Injury Flashcards
What is AKI and how is it defined
AKI is a clinical syndrome of an acute decline in actual GFR. Have an upset of ECF volume, electrolyte and acid-base homeostasis with accumulation of nitrogenous waste
Defined as:
Increase in serum creatinine by ≥26.5μmol/L within 48hr or increase in serum creatine >1.5x baseline within 7days
Urine volume <0.5ml/kg/h for 6hrs
What are causes of AKI split into and name some for each type of AKI
Pre-renal - hypovolaemia, decreased CO, decreased effective circulating volume, imparied renal autoregulation
Intrinsic - acute glomerulonephritis, ischaemia, sepsis, infection, vasculitis, nephrotoxins
Post-renal - bladder outlet obstruction, bilateral pelvoureteral obstruction or unilateral obstruction of a solitary functioning kidney
What is oliguria and what is anuria
Oliguria - where patient produces a small amount of urine, <600ml per day
Anuria - where patient produces little to no urine per day, <100ml per day
What are the symptoms of kidney failure
Reduced urinary output
Fluid retention and oedema
Fatigue
Loss of appetite
Nausea
Vomiting
Shortness of breath
Confusion
Describe pre-renal failure
Where actual GFR is reduced due decreased renal perfusion
Kidneys are not yet imparied but are unable to maintain blood flow -> cannot maintain GFR. No cell damage
Kidneys work to restore blood flow - can result in increased reabsorption of salt and water through activation of RAAS and ADH release
How do ACEi and NSAIDs affect renal perfusion and what pathology can they cause and why
ACEi/ARBs prevent vasoconstriction of efferent arteriole
NSAIDs prevent vasodilation of afferent arteriole
This can result in renal failure as it can prevent the kidney from being able to increase glomerular pressure if it drops -> decreased GRP and causes AKI
What is ATI, what causes it and what are the risk factors
Acute tubular injury - where kidney cells become irreversibly damaged but not necrotic
Damaged cells cannot reabsorb water or salt efficiently so at risk of fluid overload and oedema
Caused by ischaemia, nephrotoxins, sepsis
Risk factors: nephrotoxins, ischaemia, hypotension, haemorrhage, cardiac failure
How do you distinguish a patient with ATI from a patient with pre-renal AKI
Pre-renal urine will have high osmolality while ATI will have low osmolality
Pre-renal will have low urine Na as body trie to retain Na but ATI will have high urine Na as cells cannot reabsorb Na
Not always the case as elderly patient on diuretics will have lost ability to concentrate urine -> pre-renal urine may not have high urine osmolality
Name some nephrotoxins
Endogenous - myoglobin, urate, bilirubin
Exogenous - exotoxins, X-ray contrast, drugs
What is rhabdomyolysis, how does it cause kidney injury and how is it treated
Rhabdomyolysis - muscle damage and necrosis
Results in myoglobin release which is then filtered by glomerulus
Myoglobin is toxic to tubule cells -> causes damage to kidney
Treat with lots of IV fluids
Name some causes of post-renal failure
Tumour
Benign prostate hyperplasia
Kidney stone
What investigations can be done to diagnose a patient with AKI
Urine testing - urinalysis for protein, blood and leucocytes. Urine microscopy/culture if dipstick +ve
Imaging - USS to look for obstruction or if cause of AKI unclear. CXR - look for fluid overload +/- infection
Serum biochemistry - look for increased urea and creatinine
How is AKI managed
Dietary Na restriction and water restriction
Treat hyperkalaemia - dextrose and insulin, stop K-sparing diuretics, calcium gluconate, beta-2 agonists
Dialysis
Restore renal perfusion is pre-renal cause of AKI
Re-establish urine flow if post-renal cause of AKI
What reasons might a patient require dialysis
If not responding to treatment
If patient cannot excrete water, salt, K and waste products
If acid-base balance cannot be maintained
High K refractory to treatment
Fluid overload refractory to treatment
Signs of ureamia
Presence of dialyzable nephrotoxin
