Nephro: Acute Kidney Injury Flashcards
definition of an AKI
rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine, leading to failure to maintain fluid, electrolyte and acid-base homeostasis. this can be reversible over days or weeks
criteria for diagnosing AKI
- rise in creatinine >26umol/L in 48hrs
- rise in creatinine >1.5x
- urine output <0.5mL/kg/h for >6 consecutive hours
what is the best biomarker to monitor AKIs currently?
creatinine
what are life threatening complications of AKI
- hyperkalaemia
- metabolic acidosis
risk factors
- diabetes
- high BP
- old age
- CKD
- heart failure
- liver disease
- PVD
- nephrotoxic drug
- sepsis
- hypovolaemia
- contrast use
- obstruction
define oligouria
- urine output which is not enough to eliminate all the end-products
- <400ml/24hr for 6 consecutive hours
define anuria
- no urine output
- <100ml/24hrs
define polyuria
- when you piss an abnormally high amount of pee
- >3L/24hrs
how do you classify causes of an AKI
- pre-renal
- renal
- post-renal
how do you classify AKI?
RIFLE classification (risk, injury, failure, loss, ESRF)
what is the AKIN classification?
- classifies renal failure
- considers a milder version of AKI
- depends on the creatinine rise
most common causes of an AKI
- ischaemia
- sepsis
- nephrotoxins
- prostatic disease
pre-renal causes of an AKI
- renal hypoperfusion
- hypotension
- renal artery stenosis
- cirrhosis
- drugs: ACEi, CCF, NSAIDs
renal causes of an AKI
- injury to the glomerulus, tubule or vessels
- classified into tubular, glomerular, interstitial and vascular
tubular causes of AKI
- ATN (result of pre-renal causes like nephrotoxic drugs)
- crystal damage
- myeloma
- hypercalcaemia
glomerular causes of AKI
- autoimmune conditions like SLE, HSP,
- drugs
- infections
- primary GN
interstitial causes of AKI
- drugs
- infiltration from lymphoma, infection, tumour lysis syndrome
vascular causes of AKI
- vasculitis
- malignant HTN
- thrombus
- cholesterol emboli
- HUS/TTP
- large vessel occlusion
post-renal causes of AKI
- luminal (stones, clots, sloughed papilae)
- mural (malignancy, BPH, strictures)
- external compression (malignancy, retroperitoneal fibrosis)
pathophysiology of pre-renal AKI
- impaired renal perfusion
- fall in glomerular capillary filtration pressure
- increased renal absorption of Na and water
what are the sick day rules for AKI
- stop drugs which are contraindicated in renal disease
- use a few other drugs with caution
- monitor the use of radiological contrast
which are the drugs that you should stop?
- diuretics
- ACEi
- antihypertensives (with B-blockers, consider lowering the dose rather than withholding them)
- metformin (risk of lactic acidosis)
- NSAIDs
- nephrotoxic antibiotics
which drug should you use with caution?
opiates
management for contrast
- imp cause for AKI
- keep the patient hydrated both before and after the procedure
aetiology of AKI
- volume depletion
- hypotension
- oedematous states
- selective renal ischaemia
- nephrotoxic drugs
from where can fluid be lost and cause AKI
- GI tract
- renal tract
- skin or respiratory losses
- third space sequestration
criteria to differentiate between pre-renal and renal causes of uraemia
- urine gravity/osmolality
- urine sodium
- fractional excretion of Na
what are the 2 main classifications of post-renal causes?
- intrarenal
- extrarenal (renal pelvis, ureters, bladder, urethra)
what is obstructive nephropathy?
renal disease caused by impaired flow of urine or tubular fluid
how can you check for post-renal causes?
- catheterise
- CTKUB
causes of small vessel disease
- small vessel vasculitis
- thrombotic microangiopathy
- renal atheroembolism
causes of acute glomerulonephritis
- anti-GBM
- MPGN
- post-infectious GN
- IgA nephropathy
- lupus nephritis
- cryoglobunaemia
causes of acute tubular necrosis
- ischaemia
- nephrotoxins
- rhabdomyalsis
- radiocontrast agents
- haemorrhage
- burns
- diarrhoea and vomiting
- pancreatitis
causes of acute interstitial nephritis
- drugs
- infections
- systemic disease
which are the drugs associated with renal AKI
- gold
- aminoglycosides
- radiocontrast dye
- penicillins
- rifampicin
which are the drugs associated with postrenal AKI
- indinavir
- acyclovir
- sulfonamide
pathogenesis of ATN
- intrarenal microvascular vasoconstriction due to reduced sensitivity to vasodilatory substances
- tubular cell injury (ischaemic injury causing cell death by apoptosis or necrosis)
- tubular cell recovery (quickly reversible and thus, can recover quickly from ATN)
4Ms for prevention of AKI
- monitor patient
- minimise kidney insults
- maintain circulation
- manage acute illnesses
presentation of AKI
- can be asymptomatic
- malaise, confusion, seizures or coma
- D, N, V
- anorexia
- joint pains, rashes
- oliguria or abnormal urine colour
- haematuria
- haemoptysis
what should you ask about in the history?
- symptoms of fluid loss
- symptoms of infections
- backache
- drug history
- past medical history
- risk factors
physical signs to look out for
- vital parameters
- signs of jaundice
- rashes
- fluid status
- abdominal masses
- renal punch
- catheters
how can you check for fluid overload?
elevated JVP, crackles on auscultation of lungs, lower limb oedema
signs of dehydration
hypotension, postural BP drop, tachycardia, decreased skin turgor
renal signs to look out for in an examination
- palpable bladder
- palpable kidneys
- abdominal/pelvic masses
- renal bruits
- rashes
what should you assess in severe situations?
- ABCDE
- fluid status
- urine output
- hyperkalaemia
- acidosis (ABG)
investigations for AKI
- creatinine
- urea and electrolytes
- CBC
- ESR, CRP
- glucose
- ABG
- urinalysis and microscopy
- uPCR and/or uACR
- MSU for C&S
- US kidneys
- CXR
- HepB, HepC, HIV
- coagulation screen
what type of urine output is unusual in AKI?
anuria (suggests obstructive cause)
distinguish AKI or CKD
persistently high creatinine levels in the past (CKD); small kidneys (CKD)
causes of red cells or red cell casts
- GN
- vasculitis
- malignant HTN
- thrombotic microangiopathy
causes of white cells or white cell casts
- interstitial nephritis
- GN
- pyelonephritis
- allograft rejection
- malignant infiltration of the kidneys
what are RTE cells
renal tubular epithelial cells
causes of RTE cells or RTE/pigmented cell casts?
- ATN
- tubulo-interstitial nephritis
- acute cellular allograft rejection
- myoglobinuria
- haemoglobinuria
causes of granular casts
- ATN
- GN
- vasculitis
- tubulo-interstitial nephritis
causes of eosinophiluria
- allergic interstitial nephritis
- atheroembolic disease
causes of crystalluria
- acute uric acid nephropathy
- calcium oxalate
- drugs or toxins (antivirals, amoxicillin, sulfadiazine)
specific investigations of AKI
- LFT
- serum protein electrophoresis
- serum free light chains
- immunoglobulins
- creatinine kinase
- blood film, LDH
- ANCA, anti-GBM, ANA, ENA, anti-dsDNA, C3, C4, RF
- ASOT
- cryoglobulins
- anti-phospholipid, anti-cardiolipin
- blood cultures
- consider renal biopsy if indicated
what type of anaesthetic is used for renal biopsies?
local anaesthetic
3 types of rapidly progressive GN
- immune complex disease
- pauci-immune disease
- anti-GBM disease
how would RPGN present?
AKI and systemic symptoms like fever, myalgia, weight loss, haemoptysis
how would you treat RPGN?
aggressive immunosuppression with high dose IV steroids and cyclophosphamide +/- plasma exchange
histology in AIN
- mononuclear inflammatory infiltrate
- no glomerular changes
- tubules are separated by inflammation and oedema
management of AKI
- treat the underlying cause
- assess circulating volume and fluid administration if required
- prevent and treat hyperkalaemia
- prevent and treat metabolic acidosis
- discontinue nephrotoxic drugs
- adjust dose of drugs, where necessary
ECG changes in mild hyperkalaemia
- peaked T waves
- prolonged PR segments
ECG changes in moderate hyperkalaemia
- loss of P wave
- prolonged QRS complex
- ST segment elevation
- ectopic beats and escape rhythms
ECG changes in severe hyperkalaemia
- progressive widening of QRS complex
- sine wave
- ventricular fibrillation
- asystole
- axial deviation
- bundle branch blocks
- fascicular blocks
management of pulmonary oedema
- sit up
- high flow O2
- venous vasodilator
- furosemide 80-250mg IV/IVI
- if that does not work, urgent haemodialysis or haemofiltration is needed
- consider CPAP
- IV nitrates
medical treatment of AKI
- overload: loop diuretics
- hyperkalaemia: calcium gluconate, dextrose, salbutamol, calcium resonium
- acidosis: sodium bicarbonate
- RPGN: immunosuppression
red flags in AKI
- intractable hyperkalaemia
- pulmonary oedema and hypoxia
- severe acidosis
- uraemic encephalopathy/pericarditis
