Acute kidney injury Flashcards
(33 cards)
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
