L1: AKI Flashcards
Def of AKI
Epidemeology of AKI
Dx Criteria of AKI
S. Cr in AKI
Urine Output in AKI
Staging Cr in AKI
Stage I AKI
Stage II AKI
Stage III AKI
Urinary obstruction must be excluded as a cause of low urine output.
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The most abnormal parameter is used for classifications.
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Etiology of AKI
Pre-Renal Causes of AKI
Pre-Renal Causes of AKI
- Hypovolemia
Pre-Renal Causes of AKI
- ## Shock
Septic, Cardiogenic or Anaphylactic
Pre-Renal Causes of AKI
- Drugs
Renal Causes of AKI
- Glomerular
- Tubulo-interstitial
- Vascular
Renal Causes of AKI
- Glomerular
Glomerulonephritis (Especially rapidly progressive glomerulonephritis) → Discussed separately.
Renal Causes of AKI
- Interstitial
AIN = Acute Interstitial Nephritis
Renal Causes of AKI
- Tubular
- Ischemic ATN
- Toxic ATN
- Sepsis
Causes of ATN
- Ischemic ATN
- Toxic ATN
- Sepsis
Ischemic ATN
- ALL CAUSES OF PRERENAL DISEASE particularly if SEVERE, PROLONGED & accompanied by hypotension, surgery, and/or sepsis can cause ATN.
Types of Toxic ATN
- Endogenous & Exogenous
Types of Endogenous Nephrotoxins
Protein Endogenous Nephrotoxins
Crystals as endogenous nephrotoxins
Uric acid → in Tumor lysis syndrome.
Types of Exogenous Nephrotoxins
- Drugs
- Toxic Manifestations
- Heavy Metals
- Contrast Agents
Exogenous Nephrotoxins
- Drugs
â–ª Antibiotics: Aminoglycosides.
â–ª Antifungal: Amphotericin B.
▪ Antiviral: Acyclovir – Cidofovir.
â–ª Chemotherapeutic agents: Cisplatin, Methotrexate.
Exogenous Nephrotoxins
- Toxic Ingestions
Ethylene glycol
Exogenous Nephrotoxins
- Heavy Metals
Mercury – Lead – Arsenic
Renal Causes of AKI
- Vascular
Intrinsic renal vascular diseases directly affect both SMALL & LARGE sized blood vessels
within the kidneys.
Vascular Causes of AKI
- Small Blood Vessels
Vascular Causes of AKI
- Large Blood Vessels
â‘ Renal infarction from aortic dissection or renal artery abnormality (such as aneurysm).
â‘¡ Acute renal vein thrombosis.
Post-Renal Causes of AKI
Pathophysiology Stages of AKI
- Initiating Event (Kidney Injury)
- Oliguric / Anuric (Maintenance)
- Polyuric (Diuretic)
- Recovery
Pathophysiology Stages of AKI
- Initiating Injury
Pathophysiology Stages of AKI
- Oliguric / anuric (Maintainence) Phase
Decreased GFR Mehcanisms in Oliguric / anuric (Maintainence) Phase
◈ Toxins + Ischemia → Necrosis & Sloughing of tubular epithelial cells into tubular lumen → obstruction of tubules → Increased intraluminal pressure.
â—ˆ Back-leak of tubular fluid to renal interstitium.
◈ Excess renin activation → Afferent vasoconstriction.
Complications of Oliguric / anuric (Maintainence) Phase
①Fluid retention → Dilutional hyponatremia.
② Electrolyte retention → Hyperkalemia & Hyperphosphatemia.
â‘¢ Ca++: Decreased (May still normal).
â‘£ Increases S. Creatinine, Urea & H+ (Metabolic acidosis).
Duration of Oliguric / anuric (Maintainence) Phase
1–3 weeks
Pathophysiology Stages of AKI
- Polyuric (Diuretic) Phase
Mechanism of Polyuric (Diuretic) Phase
Complications of Polyuric (Diuretic) Phase
â‘ Loss of water (dehydration).
② Loss of electrolytes (hyponatremia, hypokalemia etc…).
Duration of Polyuric (Diuretic) Phase
∼ 2 weeks