Acute Kindey Injury Flashcards
Acute Kidney Injury (AKI) definition
- characterized by what?
- what do we see?
= abrupt ↓↓ in renal function
- characterized by sudden ∆ in creatinine and/or urine output
- retention of uremic toxins
- dysregulation of fluid, electrolytes, acid-base balance
- previously referred as acute renal failure…
Acute Renal Failure (ARF) =
= abrupt, sustained ↓ GFR; most severe AKI
Azotemia =
↑ blood nitrogen compounds (i.e. BUN, creatinine)
Uremia =
severe azotemia with adverse clinical manifestations
Traditional view of azotemia
- what this means for nephron loss
- what this means for timing
Traditionally …
- Azotemia = BUN + creatinine outside established reference ranges (>75% loss of nephron function) → very late diagnosis
Acute Kidney Injury = spectrum of renal injury + disease severity
- what is this spectrum
- what is the most sever form of AKI
- when is recovery possible?
Normal - Clinically non-detectable, non-azotemic injury
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Intrinsic injury - dysfunction
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structural damage - altered function
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kidney failure - most severe stage of AKI = Acute Renal Failure
- Recovery (CKD stage 1)
- CKD stage 2-4
- death
Measures of Renal Function, and what they tell us
Urine specific gravity (USG)
- tubular function
- ability to concentrate and/or dilute urine
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Serum creatinine (SCr)
- late surrogate marker of GFR
- elevation when ~75% of nephrons loss
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Symmetric dimethylarginine (SDMA)
- earlier surrogate marker of GFR
- sensitive, but less specific
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Urine output (UOP)
limitations of creatinine as a measurement
- late surrogate marker of GFR
- elevation when ~75% of nephrons loss
<><> - It is possible to have functional loss of an entire kidney, but creatinine still within normal reference range!
<><><><> - In early kidney disease, large changer in GFR relate to very small changes in creatinine.
- Only in late kidney disease do small changes in GFR relate to larger creatinine changes
creatinine measurement within a 4h period that is consistent with AKI?
- therefore, what must we do for proper interpretation?
- An increase in creatinine by 26.5 𝜇mol/L (even in the non-azotemic range) within a 48-hour period is consistent with AKI
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Therefore:
1. look at changes outside established reference range
2. evaluate for small changes in creatinine (26.5 𝜇mol/L) from baseline
Categories of Azotemia
Pre-renal (volume-responsive)
- 2° to hypoperfusion in a structurally normal kidney
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Intrinsic / renal
- 2° to intrinsic kidney dysfunction
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Post-renal
- 2° to urine flow / drainage obstruction
Pre-renal Azotemia
- causes
- lab results
- fixable? progression?
- ↓ blood flow to functional kidneys impair solutes / toxins clearance, e.g.:
- dehydration
- hypovolemia
- hypotension
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Usually ↑ BUN / creatinine with a concentrated USG
<><> - Rapidly improves when underlying condition is corrected promptly
> otherwise, may progress to intrinsic AKI
Intrinsic Renal Azotemia
- causes
- Ischemic
> Hemodynamic
instability
v Prolonged dehydration
v Shock
vAnesthesia (↓ BP)
vRenal artery thrombosis
vSepsis / SIRS
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Infectious - Leptospirosis
- Pyelonephritis
- Borreliosis (Lyme)
- Feline infectious peritonitis (FIP)
<><> - Toxins / Drugs
<><> - Neoplasia
> Renal lymphoma
Intrinsic Renal AKI - Nephrotoxic drugs
- NSAIDS
- Aminoglycoside
- Amphotericin B
- ACE inhibitors
- Furosemide
- Cisplatin
- Carboplatin
Intrinsic Renal AKI - Nephrotoxic toxins?
- Ethylene glycol
- Lilies 🐈
- Grapes/raisins 🐩
- Heavy metals (copper, lead)
- Vit D3 analogs (psoriasis cream)
- Vit D3 (cholecalciferol) rodenticide
- Myoglobinuria / hemoglobinuria
- Radiocontrast agents
- Envenomation
Post-Renal Azotemia causes, how to fix . progression
- Urine leakage (uroabdomen)
> any part of the urinary tract
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Urinary obstruction - urethral obstruction
- bilateral ureteral obstruction
- unilateral ureteral obstruction + ↓ renal function of contralateral kidney
<><> - Restoration of urine flow / drainage rapidly resolves the azotemia
> prolonged obstruction may lead to renal parenchymal injury
