Renal: Acute Kidney Injury Flashcards
Define the term ‘acute kidney injury’ [3]
- Rise in serum creatinine of > or equal to 26 μmol/L within 48 hours
- or 1.5x increase in serum creatinine known or presumed to have occurred in the last 7 days
- or 6 hours oliguria (urine output < 0.5ml/kg/hour)
Which populations are at risk of AKI? [6]
- · Elderly
- · CKD patients (eGFR < 60ml/min/1.73m2)
- · Cardiac failure
- · Liver disease
- · Vascular disease
- · Taking potentially nephrotoxic medications (ARBS, ACEIs, NSAIDs)
What are the three ways to think about AKI? [3]
Pre-renal (most common; decreased renal perfusion)
Renal (intrinsic disease of the kidneys)
Post-renal (obstruction to the outflow of urine; creating back pressure; obstructive uropathy
What is diabetic kidney disease? [1]
How does it present:
urine findings? [2]
US? [1]
This typically presents with:
- proteinuria and albuminuria
- reduced estimated glomerular filtration rate (eGFR) in the absence of signs or symptoms of other primary causes of kidney damage.
On ultrasound, the kidneys may be enlarged if diabetes is poorly controlled
Describe the pre-renal causes of AKI [8]
Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood. This may be due to:
- Dehydration (vomiting / diarrhoea)
- Shock (e.g., sepsis or acute blood loss)
- Heart failure
- Haemorrhage
- ACE inhibitors
- Severe burns
- NSAIDs
- Congestive heart failure (can’t pump blood)
Describe intra-renal causes of AKI:
Glomerular [2]
Interstitial [3]
Vessels [2]
Intrinsic causes of renal damage
Glomerular::
* Glomerulonephritis
* Acute tubular necrosis (prolonged renal hypofusion causing intrisinsic renal damage)
Interstitial:
* Drug reaction (metformin / thiazide like diuretics / radiocontrast / NSAIDs / penicillin / PPIs)
- Infection
- Infiltration (sarcoid)
- Rhabdomyolysis
Vessels:
- Vasculitis
- Haemolytic uraemic syndrome ( infection with certain strains of E. coli bacteria)
Describe the post-renal causes of AKI [6]
Caused by obstruction to the outflow: obstructive uropathy.
- Kidney stones
- Tumours (e.g., retroperitoneal, bladder or prostate)
- Strictures of the ureters or urethra
- UTIs
- Benign prostatic hyperplasia (benign enlarged prostate)
- Neurogenic bladder
Describe how you manage AKIs
IV fluids for dehydration and hypovolaemia
- If hypovolameic: give bolus fluids (250-500mls)
- (Assess BP (lying/standard), JVP, HR, Cap. refill, Conscious level, Lactate, Weight (important if on dialysis))
- If >2 L given & remains hypoperfused: give further circulatory support (+ve inotropes)
- If euvolaemic & passing urine: give maintenence fluids (est. daily output + 500ml)
Withhold medications that may worsen the condition
- NSAIDs
- ACE inhibitors
Withhold/adjust medications that may accumulate with reduced renal function:
- metformin
- opiates
Relieve the obstruction in a post-renal AKI:
- insert a catheter in a patient with prostatic hyperplasia
Dialysis may be required in severe cases
Which fluids can you prescribe someone with AKI? [2]
Isotonic fluids (Plasmalyte, Hartmann’s); but given that contains 5 mmo/L If you are giving a low [potassium] to someone with a high [potassium] you are going to reduce plasma potassium, and the risk of hypokalaemia is very low.
0.9% saline: safe but can worsen metabolic acidosis if large volumes rapid infused (NaCl + H2O –> HCl & NaOH)
(Colloids; now out of favour as worsen AKI)
How do you monitor patients with AKI? [5]
- Urine catheter: monitor hourly input/output
- U&Es, bone profile, venous bicarbonate at least once a day whilst creatitine rising
- Blood gases & lactate: if septic & underperfused
- Daily weights (measurement of daily body weight change can provide a more accurate method of monitoring body fluid status)
- Regular fluid management
Describe how you would investigate AKI [3]
Urine dipstick:
- UTI (leukocytes & nitrates)
- Glomerulonephritis (haematuria & leuocytes)
- Acute interstitial nephritis (leucocytes by themselves)
- Glucose suggests diabetes
Bloods:
- U&E: important to ID hyperkalaemia
- FBC, CRP & bone profile
- ANA & ANCA: ID vasculitis
- anti-GBM (formation of anti-GBM antibodiescan be directed against collagen in the kidneys and lungs)
- complement levels (C3, C4)
- RF
- immuglobulins
- creatine kinase (evidence of rhabdomyolysis)
- LFTs
- HIV, HCV, IgG and Hep B Surface antigen
Ultrasound (within 24hrs; within 6hrs if due to sepsis obstruction)
- should be performed in new cases of AKI
Which therapeutic drug classes may worsen AKI? [3]
ACE inhibitors;
NSAIDs;
Aminoglycoside antibiotics
Explain why each of the following may worsen AKIs: [3]
ACE inhibitors
NSAIDs;
Aminoglycoside antibiotics
ACE Inhibitors:
- depress A-II and thus inhibit A-II-mediated vasoconstriction of the efferent arteriole (efferent arteriole dilates)
- This lowers glomerular filtration pressure and decreases the glomerular filtration rate
NSAIDS:
- Reduced renal plasma flow caused by a decrease in prostaglandins, which regulate vasodilation at the glomerular level.
Aminoglycosides:
- have a preferential accumulation in the kidney cortex
Why should metformin treatment be witheld in patients of AKI? [1]
Not nephrotoxic itself, but if have AKI can build up in kidney and cause lactic acidosis
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Why should spironolactone treatment be stopped if patient has AKI? [1]
Spironolactone: a long half-life so need to be stopped earlier to prevent a dangerous hyperkalaemia
Describe the differences between stage 1, 2 & 3 AKI [3]
Describe a common complication of AKI [1]
Why is this clinically significant? [1]
Hyperkalaemia: can lead to deadly arrythmias
How can you manage hyperkalamia (if have AKI), if:
ECG changes [1]
If K > 6.5mmol/L [1]
ECG changes:
* Calcium gluconate (stabilises cardiac membrane)
If K > 6.5mmol/L:
* Insulin dextrose (causes intracellular movement of AKI)
What are features of acute interstitial nephritis? [5]
Features:
* fever, rash, arthralgia
* eosinophilia
* mild renal impairment
* hypertension
* sterile pyuria
* white cell casts
Given the likely diagnosis of haemolytic uraemic syndrome, what are likely expected investigational findings? [3]
acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia
What type of casts does acute tubular necrosis present with? [1]
Muddy brown casts
Think of them as dead cells
Which form of GN has an overlap with IgA nephropathy? [1]
How does this commonly present? [3]
Henoch-Schonlein purpura: IgA mediated samlled vessel vasculitis
- palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
- abdominal pain
- polyarthritis
Which drugs should be stopped in cases of AKI? [5]
DIANA:
D: diuretics
I: Ionated contrasts
A: ace inhibitors / ARBs
N: NSAIDs
A: aminoglycosides
