Acute Kidney Injury Flashcards
Function of kidneys
Body fluid homeostasis - urine production Regulation of vascular tone - BP Excretory function - urea - creatinine - drugs Electrolyte homeostasis - Na, K, Cl, Ca, P Acid base homeostasis - H+ - bicarbonate Endocrine function - Erythropoietin - Vit D metabolism - Renin
Traditional definition of acute renal failure
Rapid loss of glomerular filtration and tubular function over hours to days
What does retention or urea/creatinine show?
Failure of homeostasis
What is urea and creatinine excreted by?
The kidneys
What can small rises in creatinine cause?
Increased odds of death
Definition of acute kidney injury
Increase in serum creatinine
- By >26.5 umol/l (0.3mg/dl) within 48 hours OR
- to 1.5x baseline, which is known or presumed to have occurred within the prior 6 days
Urine volume <0.5ml/kg/h for 6 hours
Stages of AKI
AKI 1
AKI 2
AKI 3
What is AKI 1?
Serum creatinine - 1.5-1.9x baseline OR - 26.5 umol/l increase Urine output - < 0.5ml/kg/h for 6-12 hours
What is AKI 2?
Serum creatinine
- 2.0-2.9 x baseline
Urine output
- <0.5 ml/kg/h for >12 hours
What is AKI 3?
Serum creatinine - 3x baseline OR - Increase to >354 umol/l (and above) OR - initiation of RRT Urine output - < 0.3ml/kg/h > 24 hours OR - Anuria for > 12 hours
Stages of AKI
Antecedents - normal - increased risk Intermediate stage - Damage AKI - Decreased GFR - kidney failure Outcomes - death - complications
What are the stages of AKI defined as?
Creatinine
Urine output
How many hospital admissions are complicated by AKI?
1 in 7
What are the immediately dangerous consequences of AKI?
AEIOU A - acidosis E - Electrolyte imbalance I - Intoxication TOXINS O - overload U - uraemic complications
Mortality of dialysis requiring-AKI in hospital
45-75%
Mortality of non dialysis AKI stages
AKIN 1 - 8%
AKIN 2 - 25%
AKIN 3 - 33%
What is the blood values where you would act on AKI?
Rise in serum creatinine >50% baseline
Baseline creatinine of 80umol/L
Rises to 120umol/L (may still be in normal range)
Significant kidney injury
Pathological causes of AKI
Pre renal - blood flow to kidney
Renal (intrinsic) - damage to renal parenchyma
Post renal - obstruction to urine exit
Causes of intrinsic AKI
Acute tubular injury - prolonged pre renal AKI - rhabdomyosis - haemoglobuineria - nephrotoxins (Iodinated contrast, NSAIDs, gentamicin) snake venom, heavy metals Mushrooms Acute tubular necrosis (ATN) Tubulointestinal injury Acute Glomerulonephritis Myeloma Vasculitis - Lupus - ANCA associated Thrombotic microangiopathy
Causes of pre renal AKI
Sepsis Hypovolaemia - haemorrhage - burns - vomiting/diarrhoea - diuretics Hepatorenal syndrome Cardiac failure Liver failure Hypotension - medications
Causes of post renal AKI
Kidney stones Clot Sloughed papilla Prostatic hypertrophy Tumours Ureteric stricture Retroperitoneal / radiation fibrosis RPF
Commonest cause of AKI
Poor perfusion leading to established tubular damage
Pathology of pre renal AKI
Failure of the circulation (loss of volume and/or pressure) to provide sufficient plasma flow to maintain blood chemistry and fluid balance
Outcomes of pre renal AKI
If promptly treated, can resolve
If sustained, may lead to acute tubular necrosis
Why are the kidneys susceptible to hypoperfusion?
Blood supply
Oxygenation
Metabolic demand
Perfusion of kidneys
Cortex richly perfused
Medulla receives around 10-15% of renal blood flow
Does the kidney have the potential to regenerate following an acute kidney injury?
Yes
Pathology of initiation of AKI
Exposure to toxic/ischaemic insult
Renal parenchymal injury evolving
AKI potentially preventable
Pathology of maintenance of AKI
Established parenchymal injury
Usually maximally oliguric now
Typical duration 1 - 2 weeks (up to several months)
Pathology of recovery of AKI
Gradual increase in urine output
Fall in serum creatinine (may lag behind diuresis)
If GFR recovers quicker than tubule resorptive capacity, excess diuresis may result (e.g. post obstructive natriuresis)
What is radiocontrast nephropathy (RCN)?
AKI following administration of iodinated contrast agent
Presentation of RCN
Transient renal dysfunction
Resolving after 72 hours
What may RCN lead to?
Permanent loss of function
Risk factors for RCN
DM Renovascular disease Impaired renal function Paraprotein High volume of radiocontrast
What is myeloma?
A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
Who is myeloma common in?
Elderly
Presentation of myeloma
Anaemia Back pain Weight loss Fractures Infections Cord compression Marked elevated ESR Hypercalcaemia
Investigations of myeloma
Bone marrow aspirate > 10% clonal plasma cells
Serum paraprotein +/- immunoparesis
Urinary Bence-Jones Protein (BJP)
Skeletal survery - lytic lesions
Pathology of renal failure in myeloma
Cast nephropathy 'myeloma kidney' Light chain nephropathy Amyloidosis Hypercalcaemia Hyperuricaemia
Investigations of AKI
Fluid status Drugs Insults Renal failure Urine dipstick FBC USS Blood gas Renal biopsy Renal USS
What is better than treatment for AKI?
Prevention
At risk events for AKI occuring
Sepsis (e.g. pneumonia, cellulitis, UTI etc)
Toxins (e.g. X ray contrast, NSAIDs, gentamicin, herbal remidies)
Hypotension
Hypovolaemia
Major surgery
Causes of hypovolaemia
Haemorrhage
Vomiting
Diarrhoea
Risk factors for AKI
Age > 75 Previous AKI Heart failure Liver disease Chronic kidney disease DM Vascular disease Cognitive impairment
What is done to identify patients at risk of AKI?
In the presence of a risk event and one or more risk factors, consider activating the below STOP AKI Prevention care bundle
- STOP
- S = sepsis (if suspected screen and treat promptly - SEPSIS 6)
- T = Toxins - avoid (e.g. gentamicin, NSAIDs, iodinated contrast)
- O = optimise BP and volume status - avoid/correct hypovolaemia, review BP meds
- P = prevent harm - daily U and Es, fluid balance and medication review
Examples of nephrotoxic drugs
Gentamicin
NSAIDs
Iodinated contrast
Aminoglycosides
How should you optimise BP and volume status?
Consider IV fluids if hypovolaemic;
- resus fluids 250-500mls IV crystalloid ? bolus over 15 mins and review response
Withhold Antihypertensives
Withhold Diuretics
How is fluid balance monitored?
Input
Output
Daily weights
Treatment of AKI
Remove/treat cause if possible If pre renal - Fluid - BP support Renal - remove participant Post renal - catheter Treat sepsis Stop/avoid potential nephrotoxins Optimise BP - fluids - withhold antihypertensive drugs Treatment of complications
What are the 5Rs from IV prescribing?
Resuscitation Routine maintenance Replacement Redistribution Reassessment
When would patients need replacement fluids?
If dont need urgent IV resuscitation but do need IV additional to maintenance to correct existing deficit or ongoing abnormal External losses e.g. diarrhoea, fever
When would patients need redistribution fluids?
When the patients have abnormal internal fluid redistribution or abnormal fluid handling, particularly with sepsis, or major illness, cardiac, liver or renal disease e.g. tissue oedema, GI tract/thoracic/peritoneal collection
How many ml from water are usually on the intake in health?
2500ml
25-35ml/kg/day
How much output of water is normal? How is water excreted from the body?
Urine Insensible - skin - lungs - faeces
How much Na and K are taken in on average?
1mmol/kg/day both
What is the only electrolytes dextrose contains?
Glucose
variable K
What is the only electrolytes NaCl / glucose solution contains?
Na
Variable K
Cl
Glucose
What electrolytes does Hartmanns contain?
Na K Cl Ca Bicarb precursor (lactate)
What electrolytes does plasma contain?
Na K Cl Ca Bicarb Glucose
What electrolytes does plasma lyte contain?
Na
K
Cl
Bicarb precursor (acetate and gluconate)
ECG changes in hyperkalaemia
Peaked T waves - tall tented T waves P wave widens and flattens PR segment lengthens P waves eventually disappear Prolonged QRS interval High grade AV block with slow junctional and ventricular escape rhythms Sinus bradycardia or slow AF Development of a sine wave appearance (a pre terminal rhythm) Cardiac arrest Asystole VF
Treatment of hyperkalaemia
Stabilise myocardium - calcium gluconate Shift (K+ intracellularly) - salbutamol - insulin-dextrose Remove - diuresis - dialysis - anion exchange resins
Treatment of morphine toxicity
Naloxone
Treatment of digoxin toxicity
Digibind
Indication for dialysis in AKI
Acidosis - Decreased HCO3 - Increased lactate - increased pCO2 Electrolytes - Increased K - Increased or decreased Na - Increased Ca - Increased uric acid - Increased PO4- - Increased Mg2+ Intoxication - aspirin - theophylline - lithium - ethylene glycol - methanol - metformin Overload - nutrition - pulmonary oedema - HTN Uraemia - altered mental status - Pericarditis - unexplained bleeding
Solute removal in haemodialysis vs hemofiltration
Haemodialysis
- removal by diffusion
Haemofiltration
- removed by convection
What type of therapy is haemodyalsis?
Intermittent
Each session lasting 3 - 5 hours
What type of therapy is haemofitration?
Continous
When is haemofiltration used?
In an ITU setting usually to treat AKI but can be used in multiple organ dysfunction or sepsis
Advantages of haemodialysis
Rapid solute removal
Rapid volume removal
Rapid correction of electrolyte disturbances
Efficient treatment for hypercatabolic patient
Disadvantages for haemodialysis
Haemodynamic instability
Concern if dialysis associated with hypotension, may prolong AKI
Fluid removal only during short treatment time
Advantages of continuous therapy
Slow volume removal associated with greater haemodynamic stability
Absence of fluctuation in volume and solute control over time
Greater control over volume status
Disadvantages of continuous renal replacement therapy
Need for continuous anticoagulation
May delay weaning/mobilisation
May not have adequate clearance in hypercatabolic patient
What is the staging system for AKI called?
AKIN staging system
How many stages are there in AKI?
3
What is the pneumonic to remember immediate problems of AKI?
AEIOU
What are the long term problems caused by AKI?
Secondary problems / infections
- pneumonia
- sepsis
- MI
What is the most common type of cause of AKI?
Pre renal AKI
What kind of obstruction of pre renal AKI is needed to cause an AKI?
Bilateral OR
Unilateral with something else e.g. sepsis
Why in prevention of AKI are anti-hypertensives withholded?
Hypotension can cause an AKI
What medicines should be stopped on sick days? Give examples of “sick days”
ACEIs, ARBs, NSAIDs, Diuretics, Metformin
Sick days = vomiting, diarhrhoea, vomiting, fever, sweats, shakes
What happens in the body when you are unwell?
Stimulate RAAS -> conserve salt and water
Stimulate sympathetic system
Can metformin cause an AKI?
No, but it can cause lactic acidosis if unwell for another reason e.g. sepsis
Most patients with AKI will have a degree of what?
Hypovolaemia
What does ATN stand for?
Acute tubular necrosis
How can AKI cause ATN?
Insult to the kidneys so severe that they develop necrosis of the tubules
What is trimethoprim bad to use in?
CKD
What can trimethoprim cause in CKD?
Hyperkalaemia
Increased creatinine
Does not reduce GFR but inhibits the tubular secretion of creatinine and effects the K channels as well
Indications for RRT in AKI
Refractory AEIOU
What are the uraemic complications?
Uraemic encephalopathy
Uraemic pericarditis
In hyperkalaemia, what can help stabilise the myocardium and how? Then what can be done once the K > 6.5?
Calcium gluconate 10mls/10% / calcium chloride
Does not lower the K but stops an MI
Then have to push potassium back into the cells by
- nebulised salbutamol 2.5-5mg
- insulin dextrose IV 6 - 10 units in 50mls/50% dextrose over 30 mins
What do nebulised salbutamol and insulin dextrose IV do?
Lower K+
Why should you not give diuretics in AKI? (unless in fluid overload)
Can worsen AKI
When having insulin dextrose, what should be done for a few hours after?
Monitor blood glucose
What group of patients are more likely to be hyperkalaemic and why?
DM patients
Not as much insulin
What is renal papillary necrosis?
Coagulative necrosis of the renal papillae
Causes of renal papillary necrosis
Severe acute pyelonephritis Diabetic nephropathy Obstructive nephropathy Analgesic nephropathy (NSAIDs) Sickle cell anaemia
Presentation of renal papillary necrosis
Visible haematuria
Loin pain
Proteinuria
What investigation is required in the investigation of all patients presenting with an AKI of unknown etiology?
Renal USS
What is a sign of acute interstitial nephritis? What is it often due to?
Eosinophilic casts
Often due to a drug reaction
Pathology of rhabdomyolysis
The toxicity of myoglobin on the tubular cells directly causes damage and necrosis of the cells - so causing tubular cell necrosis
What does a raised anion gap suggest?
Increased production or reduced excretion of fixed / organic acids
Examples of things causing raised anion gap acidosis
Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (DKA)
Drugs / Toxins (salicylates, methanol, ethylene glycol)
What is a metabolic acidosis with a normal anion gap due to?
Loss of bicarbonate or accumulation of H+ ions
Causes of metabolic acidosis with normal anion gap
Renal tubular acidosis
Diarrhoea
Addisons disease
Pancreatic fistula
What would indicate a AKI caused by dehydration?
A urea that is proportionally higher than the rise in creatinine
What should be considered in a young female patient who develops AKI after initiation of an ACEI?
Fibromuscular dysplasia
Causes of renal vascular disease
Renal artery stenosis secondary to atherosclerosis (90%) Fibromuscular dysplasia (10%)
What % of patients with fibromuscular dysplasia are female?
90%
Presentation of fibromuscular dysplasia
HTN
CKD or acute renal failure e.g. 2ndry to ACEI initiation
‘Flash’ Pulmonary oedema
