227 - Acute Renal Failure Flashcards
If this marker is high it suggests a poor prognosis / high mortality in AKI
High serum creatinine
What criteria is used for rating severity of AKI?
RIFLE criteria
GFR/Cr, urine output
Affected by age, DM, high BP, CCF
What extra-renal systems does AKI affect?
Pulmonary (pul oedema, ARDS, Leukocyte invasion, heamorrhage)
CNS (inflam reaction, altered conscious level, acidosis + electrolyte imbalence - confusion, convulsions, coma)
Cardiac (electrolyte imbalance, uraemic toxins, acidosis.. sympathetic NS - increase Bp, pericarditis, arrhythmias, Mi)
The causes of AKI are split into what 3 domains?
Pre-renal
Intrinsic
Post-renal
Describe how pre-renal issues can cause AKI
GFR reduced ↓ , due to haemodynamic disterbances - so causes ↓ globerular filtration.
No cellular injury
IF you reverse haemodynamic factors - should revert to ok
List 4 pre-renal causes of AKI
Intravascular vol depletion
↓ effective blood volume (burns)
Altered intrarenal haemodynamics (dehydration, sepsis)
3rd space sequestration (bowel obstruction)
List 3 intrinsic causes of AKI
Acute tubular necrosis (85%)
Radiocontrast nephropathy
Acute tubulo-interstial nephritis
What can cause acute tubular necrosis?
50% due to ischaemia - ↓bp, sepsis, cardiopulmonary arrest, bypass
35% nephrotoxic - drugs (aminoglycosides, radiocontrast, ACEi, NSAIDS) or pigment (Rhabdomyolysis, heamolysis)
How long does acute tubular necrosis last for?
Recover in 1 week due to proliferation and differentiation
Mortality linked with number of other failed organs
When might you be at risk of radiocontrast nephropathy?
When you need IV or intra-arterially injected contrast (special CT scans)
Not oral contrast or MRI contrast
Why can contrast cause nephropathy?
Contrast is hypertonic, so can induce transient vasodilation then constriction - can cause renal ischaemia.
How can you prevent contrast nephropathy?
Give lots of fluid - before and during
Use low osmolality contrast
What are the features of acute tubulo-interstitial nephritis?
An allergic reaction (so high mast cells and eosinophils)
Drug induced or infection mediated
- Get fever, rash, arthralgia, eosinophila
What investigation can confirm acute tubulo-interstitial nephritis?
A biopsy - will show cellular infiltrates
What can cause post renal AKI?
An obstruction
- stone, necrosis, clot, TCC, stricture, fibrosis, tumour, aortic aneurysm
What are the features of urine in someone with post-renal AKI?
Dilute (can’t be concentrated as well)
Acidification is imparied - high blood acid and alkaline urine
What are 2 life threatening complications of AKI?
Metabolic acidosis
Hyperkaleamia
Describe metabolic acidosis in AKI
Can have a normal anion gap (bicarb is lost) or increased anion gap (acid is overproduced)
Get muscle weakness, altered mental state, kasmail breathing, high potassium and low BP
Describe how hyperkalemia occurs in AKI
When the pH of blood is low, H+ moves intracellularly
K+ moves out of cells to help keep the + balance
-> too much K+ in the blood
= muscle weakness, cardiac issues, big T waves (lots of pot lots of tea), wide QRS, bradycardia
How do you treat hyperkaleamia in AKI?
Treat cause
Give fluids
Correct acidosis
Protect heart - IV Ca Gluconate
Shift K+ back into cells - IV dextrose insulin
Reduce K+ absorption in GI tract - cation exchange resin
What is Rhabdomyolysis?
AKI caused by muscle necrosis releasing intracellular constituents. The AKI then causes electrolyte imbalance
How does Rhabdomyolysis cause AKI?
Haem pigment casts obstruct tubules - proximal tubular injury by heam iron
+ volume depetion due to swelling of damaged muscle
What are the signs and blood abnormalities of rhabdomyolysis?
Red/brown urine (as pigmented granular casts and supernatant in)
High serum enzymes - CK and LDH
Hifh K+, phosphate and uric acid
Low Ca (as goes to damaged muscles)
What could it mean if Ca was high in someone with known rhabdomyolysis?
They might be recovering, the excess Ca taken up by damaged muscles is released as it heals