Acute kidney injury Flashcards
Etiopathogeneis of AKI
- Sudden impairment of kidney fucntions resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys
- Heterogenus group of conditions that share comon diagnostic features
- Increase in BUN
- Increase in serum creatinine
- Associated with reduction
KDIGO 2012 Definition of AKI
- Increase in serum creatinine by >0.3 mg/dL (2.65 mmol/L) within 48 hours
OR
- Increase in serum creatinine to >1.5x the baseline, which is known or presumed to have occured within the prior 7 days
OR
- Urine volume <0.5 mL/kg/h for 6 hours
KDIGO 2012 Staging of AKI
Estimating the baseline serum creatinine
- Many aptients will present with AKI without a reliable baseline SCr - if so an estimated SCr can be use used, provided there is no evidence of CKD
- Can be estimated using the MDRD study equation, assuming that baseline eGFR is 75 mL/min/1.73
Rifle Criteria
- System for diagnosis and Classification of a broad range of acute impairment of kidney function
Pre-Renal AKI
- Due to inadequate renal plasma flow and intraglomerular hydrostatic pressure
- Involves no parenchymal damage to the kidney
- Prolonged hypoperfusion leads to ischemic injury (acute tubular necrosis)
Post Renal AKI
- Occurs when there is an obstruction to the passage of urine
- This leads to increased retrograde hydrostatic pressure and interference with GFR
Intrinsic AKI
- Sepsis
- causes generalized vasodialtion leading to endothelial damage resulting in microvascular thrombosis, activation of ROS adn leukocyte adhesion and migration
- Ischemia
- Hypoxia in the renal medulla leads to imapired autoregulation, endothelial and vascular smooth muscle damage and leukocyte-endothelial adhesion, vasuclar obstruction, and inflammation
- Categorized to major site of parenchymay damage
- Tubular damage
- Glomerular damage
- Intestitial damage
- Vascular damage
Decreased Kidney Perfusion
- Caused by
- Fluid depletion, Heart failure ,Impaired autoregulation
- Evidence of volume depletion (tachycardia, hypotension, dry mucous membrane, low JVP)
- Most diagnostic feature: Azotemia is rapidly reversed once hemodynamics are restored
- Renal indices: BCR >20, FENa <1%
- May show hyaline cast
Obstruction
- Caused by
- Bladder enck obstruction (most common), proistatic disease, neurogenic bladder, ureteral calculi, strictures
- No specific findings other than AKI
- Often needs imaing with UTZ or CT
Non-specific AKI
- Ischemia associated
- Systemic hypotension, often superimposed on sepsis and those with limited renal reserve
- Granular casts and renal tubular epithelial cell casts
- FENa>1%
- Sepsis associated AKI
- Overt hypotension
- granular and renal tubular epithelial cell casts
- FENa usually >1% (but may be low early in the course)
Glomerulonephritis
Recent skin infections or pharyngitis
Variable features of arthralgias, sinusitis, lung hemorrhage
Intestitial nephritis
Recent medication exposures (penicillins, cephalosporins, sulfonamide) or infections (leptospirosis)
Fever, rash, arthralgia
eosinophlia, steile pyuria
kidney biopsy may be helpful
Acute tubular necrosis
Recent exposure to ischemia or nephrotoxins (aminoglycosides, cisplatin, zolendronate, contrast agents, amphotericin, rhabdomyolysis
granular casts, renatl tubular epithelial cell cast on urinalysis, FENa >1%
TTP/HUS
Recent Gi infections or use of calcineurin inhibitors
Hematologic workup: schistocytes on PBS, elevated LDH, anemia, thrombocytopenia
Kidney biopsy may be helpful
Diagnostic Work up For AKI
PreRenal AKI vs ATN
Management
