Acute Kidney Injury Flashcards
define uraemia and state some common signs/symptoms
the term given to the clinical symptoms which arise when nitrogenous metabolic waste products accumulate in the blood (i.e. urea and creatinine), as a result of decreased filtration of these products by the kidneys
- nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritus, or changes in mental status.
define AKI
- sudden deterioration of renal function over hours or days
- urea and creatinine rise rapidly
- usually but not always associated with oliguria or anuria
- usually but not always reversible
how is AKI staged
- if 2 tests show different stages, always stage according to the most severe outcome
what are the 3 categories that causes of AKI fall under
pre-renal
intrinsic renal
post-renal
what are causes of pre-renal AKI
- hypovolaemia: e.g. haemorrhage, dehydration, burns
- sepsis
- shock
- renal artery stenosis
- NSAIDs or ACEi: impair the mechanisms of renal autoregulation so can predispose to prerenal AKI
Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood
what are causes of intrinsic renal AKI
- acute tubular necrosis: ischaemia, drug toxicity, toxins
- acute intersitial nephritis: due to drugs, infections, hypercalcaemia, multiple myeloma
- glomerular disease: acute glomerulonephritis,
- vascular disease: vasculitis, malignant hypertension
what are some post-renal causes of AKI
- calculus: bilateral
- bladder outflow obstruction: BPH or urethral/ureteric strictures
- tumours
- retroperitoneal fibrosis
obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function
what are complications of AKI (4)
- metabolic acidosis
- hyperkalaemia
- uraemia –> encephalopathy and pericarditis
- volume overload
what bedside tests would be carried out in suspected AKI
- bladder scan
- urinalysis, microscopy, culture & specimen
- ECG (K+)
what blood tests would be carried out in suspcted AKI (5)
- daily FBC, U&Es, LFTs, CRP
- CK if rhabdo suspected
- anti-streptolysin O titres - post-strep GN
- haemolysis screen w blood films, LDH, bilirubin - associated thrombocytopenia
- cryoglobulins - unexplained rash, peripheral neuropathy, hep C
what imaging would be carried out in investigation of AKI
- USS KUB (kidney, ureter, bladder)
- CT
- CXR
Ultrasound of the urinary tract assesses for obstruction when a post-renal cause is suspected
what procedures would be carried out in investigating AKI
- nephrostomy
- cytoscopy
how would you treat pre-renal AKI
- IV fluids to correct hypovolaemia
- stop potentially nephrotoxic medication e.g. NSAIDs, ACEi
- diuretics if clinically indicated
how would you treat intrinsic renal AKI
- correct electrolytes
- renal replacement therapy
how would you treat post-renal AKI
- urinary or supra-pubic catheter
- ureteric stents
- nephrostomy
what would you look for peripherally in fluid assessment
HR
BP
postural BP
skin turgor
what would you look for on the face and neck in fluid assessment
sunken eyes
JVP
what would you look for in the chest and back on a fluid assessment
dull percussion
crepitations at lung bases
sacral oedema
would would be signs to look out for in the abdoman and limbs in fluid assessment
ascites
ballotable kidneys
palpable bladder
urine output
oedema
what are life-threatening complications of AKI
- hyperkalaemia
- pulmonary oedema
- bleeding
what are the NICE guidelines criteria for diagnosing an AKI
- Rise in creatinine of more than 25 micromol/L in 48 hours
- Rise in creatinine of more than 50% in 7 days
- Urine output of less than 0.5 ml/kg/hour over at least 6 hours
what are risk factors for developing an AKI
- elderly
- sepsis
- CKD
- IHD/CCF/CVD
- diabetes
- meds: NSAIDs, gentamicin, diuretics
- radiocontrast agent
what investigation finding confirms ATN
- muddy brown casts on urinalysis
- renal tubular epithelial cells may also be seen
is ATN reversible?
yes as the epithelial cells can regenerate
- recovery usually takes 1-3 weeks
what is acute intersitial nephritis caused by
an immune reaction associated with:
* drugs: NSAIDs, abx
* infections: E.Coli, HIV
* autoimmune: sarcoidosis, SLE
what are you assessing for in urinalysis for AKI
- leucocytes/nitrites: infection
- protein/blood: acute nephritis but can also be positive in infection
- glucose: diabetes
how is AKI preventable
- Avoiding nephrotoxic medications where appropriate
- Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)
- Additional fluids before and after radiocontrast agents
if blood and protein is positive on a urine dipstick for AKI, what further investigation should be ordered and why
- c-ANCA + p-ANCA: vasculitis
- anti-GBM, ANA, C3/C4: lupus nephritis
- serum immunogloblulins and electrophoresis: myeloma
what are indications for RRT in AKI (AEIOU)
- hyperK refractory to medical therapy
- metabolic acidosis “ “
- fluid overload refractory to diuretics
- uraemic pericarditis
- uraemic encephalopathy - vomiting, confusion, drowsiness
- intoxications - ethylene glycol, methanol, salicylates
what is the best way to differentiate between AKI and CKD
renal USS
- most pt w CKD will have small bilateral kidneys
- hypocalcaemia is often present in CKD due to a lack of vitamin D
what common drugs should be stopped in patients with AKI due to them worsening renal function
- NSAIDs
- aminoglycosides
- ACEi
- ARB
- diuretics
what is the triad of haemolytic uraemic syndrome
- acute kidney injury
- microangiopathic haemolytic anaemia (MAHA)
- thrombocytopenia
what are the causes of typical/secondary HUS
- STEC!
- pneumococcal
- HIV
what are the causes of atypical/primary HUS
complement dysregulation
what is the most useful initial diagnostic test in HUS
blood film
what will blood film of HUS show
- MAHA –> schistocytes
- anemia
- thrombocytopenia
what is the management of HUS
- fluids
- blood transfusion
- dialysis
