AKI Flashcards
Define oliguria.
< 500 ml/day urine
o Obligatory solute excretion = 600 mosm/day
o Maximal concentrating ability = 1200 mosm/L
o Result: minimal volume each day = 0.5 L
Define acute kidney injury
Decline in glomerular filtration rate occurring over < 2 weeks
o Decline in GFR measured by increased serum creatinine: increase in serum creatinine by 0.5 -1.0 mg/d or by 25-50%
o Inability of output to match input (water, Na+, K+, nitrogen, phosphorus, acid)
Incidence: 7% of hospital admissions
Mortality is high; correlates with multiorgan failure
• In surgical setting: 70-100%
• In medical setting: 50-80%
o AKI patients die from infection (major cause), arrhythmias, GI hemorrhage
List the main categories of acute kidney injury
• Prerenal (60% of AKI patients)
• Intrarenal (30%)
o Glomerulonephritis
o Acute Tubular Necrosis (ischemic and toxic types)
o Acute Interstitial Necrosis
• Postrenal (10% of AKI patients)
Prerenal AKI
Decreased renal perfusion
• Kidneys not yet injured = reversible AKI
Causes: Hypovolemia (decreased ECF) • Hemorrhage • Sweating • GI losses • Burns → skin losses • Pancreatitis • Diuretics Impaired cardiac function • Cardiomyopathies • Pericardial tampanade • Pulmonary HT Peripheral vasodilation → shunts blood away from kidney • Sepsis • Medications • Autonomic neuropathy Other causes: • Medications (NSAIDs, immunosuppressive agents)
Acute Tubular Necrosis types
Intrarenal AKI
1) Ischemic
2) Toxic
Decreased GFR:
o Cells detach from basement membrane = obstruct tubules → back pressure of filtration and decreasing GFR
o Back leak of filtrate between cells
Ischemic Acute Tubular Necrosis
Initiation Phase
• Occurs in proximal tubule
• Normally = polarity established in epithelium cells:
o Tight junctions
o Adhesions (CAMs = Cellular adhesion molecules)
o Integrins
o Actin cytoskeleton
• During ischemia = decreased ATP → disrupts cellular processes → loss of cell polarity → cells unable to transport normally
• Some cells slough into urine
• With reperfusion: formation of oxygen radicals → damage cells
Extension Phase • Occurs in thick ascending limb • Endothelial activation Leads to leukocyte infiltration o Obstruction, coagulation and hypoperfusion of microcirculation o Reactive oxygen species o Cytotoxic cytokines Result: altered vasoactive balance o Increased endothelin o Decreased nitric oxide Further ischemia and extension preventing recovery
Toxic Acute Tubular Necrosis: causes
Radiocontrast • Oliguric • Within 24-48 hours of dye • Low fractional excretion of sodium • Risks: hypovolemia, CRF, DM + CRF
Aminoglycosides:
• Classic non-oliguric
• 5-7 days of antibiotics
Pigments: • Immobility (ethanol, drugs) • Seizures • Trauma • Diagnostic triad of AKI, serum creatinine phosphokinase > 1000 U/L, dipstick heme without RBCs
Cisplatinum
• Drug for squamous cell carinoma
• Risks: aminoglycosides, CRF, hypovolemia
Amphotericin B
• Antifungal drug
• Severe hypokalemia, hypomagnesemia
• Risks: CRF, hypovolemia, higher doses
Others:
• Antiretrovirals
• Bisphosphonates
• IV globulin
Acute Interstitial Necrosis
o 83% with fevers or rash on eosinophila
o Occurs while on certain classes of medications for a week or two
o Urinalysis with WBCs, WBC casts
o May have higher number of eosinophils in urine
o Improves with removal of medication, but sometimes treated with corticosteroids
Associated drugs: Antibiotics: • Penicillins • Cephalosporins • Others: rifampin, sufonamides, quinolones Others: • Proton pump inhibitors • Analgesics • Diuretics (furosemide) • Anticonvulants (dilantin) • Misc: cimetidine, allopurinol NSAIDs
Postrenal AKI
Obstruction; potentially reversible
Causes:
Bilateral ureteral obstruction
• Extraureteral: cervical cancer, uterine cancers, retroperitoneal fibrosis
• Intraureteral: stones, clots, papillary necrosis
Bladder obstruction
• Structural: bladder cancer
• Functional: anticholinergics, diabetes
Urethral obstruction
• BPH
• Prostate cancer
Distinguish the clinical courses between ischemic and toxic acute tubular necrosis
Ischemic acute tubular necrosis:
o Kidney failure phase → increased serum creatinine (days to weeks)
o Diuretic phase → serum creatinine plateaus, urine output increases in volume
o Recovery phase → serum creatinine rapidly falls, GFR is restored
Toxic acute tubular necrosis:
o 1-2 weeks of drug
o Develop rash, eosinophilia, increased serum creatinine
o Stop drug = kidney function returns to normal
o Re-exposure does not cause same problem (not a true allergy)
Determine an acute vs. chronic renal problem
o Serial creatinine levels
o Renal size (shrink with chronic disease)
o Hematocrit (decreased when chronic; normal with acute)
Compare the history of the 3 different types of AKI diseases
Prerenal
• Fluid losses: diuretics, burns, hemorrhage
• Symptoms of CHF and/or fluid gains (surgery)
• Fevers, chills, cough, dysuria
Intrarenal
• Hypotension
• Surgery
• Toxin exposure
Postrenal
• Anuria
• Wide swings in urine output
• History of pelvic malignancies or radiation
Compare the physical exam findings of the 3 different types of AKI diseases
Prerenal • Postural BP/P • Dry mucus membranes • Decreased skin turgor • Rales, S3, JVD
Intrarenal
• Nothing specific
Postrenal
• Distended bladder on percussion
• Abnormal pelvic/rectal examination
Compare the imaging studies and Lab values of the 3 different types of AKI diseases
Prerenal:
• FE Na+ < 1%
• Urine [osm] >500 mOsm/kg
Intrarenal:
• FE Na+ > 3%
• Urine [osm] < 1%
• Late: FE Na+ > 2%
• Bladder catheter or scan = measures amount of urine left in bladder after voiding (normally <100 ml elderly)
• Renal ultrasound = excellent rule-out test for ureteral obstruction
Renal Failure Index equation
RFI = U Na+ / (U Cr/ P Cr)
