AKI Flashcards
Briefly outline the function of the bowmans capsule and the other part of the nephron
Bowmans capsule produces 100% of filtrate
PT- 80% reabsorption back into capillary by active and passive absorption
LoH- 6% absorption of H20 and salt
DT- 9% filtrate absorbed: active secretion, variable reabsorption
CT- 4% filtrate absorption: variable salt and H2O reabsorption
Describe the criteria for the three stages of AKI
Stage 1
- Serum creatinine: 1.5-2x increase from baseline
Or 26micromol/L increase in <48hrs
- Urinary output: <0.5ml/kg/hr for 6 hours (8 hours in kids)
Stage 2
- Serum creatinine: 2-3x increase from baseline
- Urinary output: <0.5ml/kg/hr for 12 hours
Stage 3
- Serum creatinine: >3x increase from baseline
OR SC>354micromol/L with an acute increase ≥44
- Urinary output: <0.3ml/kg/hr for 24 hours
What is creatinine and how is it used to calculate eGFR?
Describe some natural variations in serum creatinine
- it is a product of muscle turnover
- its transported in the blood and excreted via the kidneys
- creatinine clearance, therefore, gives us an indication. of filtration rate (if serumCr rises, the filtration rate is falling)
- People with lower muscle mass have lower (range of normal) creatinine e.g. elderly, double amputee
- Higher muscle mass in athletes
- Dilution effect in pregnancy
What is oliguria?
What is anuria?
- Oliguria: <0.5ml/kg/hr (equates to about 500ml in 24 hours in adults)
- Anuria: no urine production but a soft definition is <100ml in a day
Consider the natural course of the development of AKI
Describe the onset phase
- triggers
- what happens
- how long does it last
- Triggers: significant blood loss, burns, diabetes insipidus, fluid losses
- renal blood flow and tissue perfusion drop to 25% of normal
- Urine output drops <0.5ml/kg/hr
- Lasts hours -days
Consider the natural course of the development of AKI
Describe the oliguric/anuric phase
- what happens
- how long does it last
- UO<400ml per day
- Theres an increase in BUN (blood urea nitrogen) and SC
- Electrolyte disturbances, acidosis, fluid overload (kidneys cant excrete)
- Lasts 8-14 days (longer depending on when dialysis treatment is started)
Consider the natural course of the development of AKI
Describe the diuretic phase
- what happens
- how long does it last
- Occurs as AKI is corrected
- Cells in tubules die as a result of injury –>oedema and scar formation
- Eventually, produce transport proteins
- Patient passes urine >400ml/day as GFR increases
- Lasts 7-14 days
Consider the natural course of the development of AKI
Describe the recovery phase
- what happens
- how long does it last
- reduction in oedema
- the normalisation of fluid balance and electrolytes
- GFR returns to 70/80%
- lasts months- 1 year
State the 7 functions of the kidney
- excretes toxins e.g. urea
- electrolyte balance
- acid and base balance
- fluid balance
- BP control
- Control of bone metabolism: Vitamin d activation and phosphate excretion
- Erythropoiten production
Dysfunction of the kidney can kill.
Describe two ways in which this will happen the fastest and how it may present
- Hyperkalaemia (>6 = bad, >6.5 medical emergency)
ECG changes: flatten of P wave and widening of QRS, tented T waves, sinus wave pattern (precardiac arrest)
Changes occur as K+ increase —-> - Fluid Overload (Shortness of breath, Orthopnoea, Limb swelling)
- the danger is pulmonary oedema which leads to severe tissue hypoxia
- Remember that patients that are oliguric/anuric cannot get rid of excess water
When is haemodialysis indicated for AKI?
- Refractory hyperkalaemia*
- Pulmonary oedema**
- Refractory acid-base disturbance
- Uraemic complications (Coma, pericarditis)
State 5 prerenal causes of AKI (the really likely ones)
- Haemorrhage
- Renal artery stenosis
- Dehydration
- MI/ PE
- Iatrogenic
- Septic shock
- Systemic vasodilation as with antihypertensive or in anaphylaxis
State 3 intrinsic causes of AKI
- Nephrotoxicity (e.g. from calcium and other metals, drugs - particularly cisplatin)
- Overproduction which leads to block tubules e.g. Rhabdomyolysis, myeloma
- Inflammation of the kidney: GN, Interstitial arthritis, Acute tubular necrosis
State 5 postrenal causes of AKI
- Renal stones
- Ureteric or Urethral stricture
- Benign prostatic hypertrophy
- Prostate cancer (or cervical and bladder cancer)
- Unary retention (neurogenic, constipation)
What is the prognosis for patients with AKI
- 50% require ITU admission
- May require haemofiltration
- Independent risk factor of mortality
What are the acute risk factors?
What are the chronic risk factors?
ACUTE S- sepsis and hypoperfusion T- toxins O- obstruction P- parenchyma
CHRONIC
- elderly, CKD, DM, nephrotoxic medication, HF, liver disease, vascular disease
How do we protect and promote AKI?
4 Ms
Monitor: Observations/news, Regular bloods, fluid chart, pathology alerts
Maintain circulation: hydration, resuscitation, oxygenation
Minimise kidney insult: remove nephrotoxic drugs, surgery, contrast, hospital acquired infections
Manage acute illness: sepsis, HF, LF
Get five categories of nephrotoxic drugs
- ACEi
- ARBs
- Diuretics
- Chemotherapy agents: cisplatin
- NSAIDs: ibuprofen, diclofenac
- Naproxen
- Metformin
- Aminoglycosides
Outline the management of AKI
Is the patient safe
- A-E approach; [K+]; volume status
- if volume deplete give 250-500ml bolus of saline
Consider catheter for monitoring
- patient needs strict fluid input/output
- check VBG for acid base status
Investigate the cause once stable:
- Urine stick, bladder scan, ultrasound kidneys, ureter and bladder (KUB)
- Take detailed Hx + exam + medication review
- FBC, U&E, VBG
What are the red flag features When taking a history family patient presenting with an AKI?
- haemoptysis
- rashes
- joint swelling/pain
- jaundice
- ENT: crusting of nose/acute hearing impairment
- significant limb swelling acutely
- noticeable urine frothiness
Draw a table outlining what you might expect to find in a urine dip of a patient with:
a) pre renal AKI
b) renal AKI
c) post renal AKI
d) UTI
a) Prerenal: -/+ for blood, - for proteins, nitrates and leukocytes
b) Renal: + for blood, protein, leukocytes; - for nitrites
c) Post renal: + for blood and protein; - for nitrites and leukocytes
d) UTI: + for all
Polyuria is a known common phase of AKI (the diuretic phase).
Name four other causes of polyuria
- DM
- Psychogenic polyuria
- Beer potomania
- Rare endocrine causes e.g. diabetes insipidus
How do you manage polyuria
- encourage drinking
- IV fluids if dry to match output (once renal function improves, reduce input to 75% of output)
