Acute Kidney Injury Flashcards
Acute kidney injury (AKI) divided into what 3 types?
Prerenal, intrinsic renal, and postrenal azotemia
Oliguria = < X mL urine per 24 hours
< 400 mL urine per 24 hours
Are AKI’s reversible?
Most are if underlying disease is treated
Prerenal, intrinsic renal, and postrenal AKI numbers. Which is most common?
Prerenal - 55% Intrinsic renal - 40% Postrenal - 5%
Most common cause of prerenal AKI?
Volume depletion (decreased blood flow to kidneys)
Pre renal AKI: GFR, BUN:Cr ratio, FENa %, urine Osm
GFR decreased
BUN:Cr ratio > 15 (normal = 15)
FENa < 1%
Urine Osm > 500 mOsm/kg
Most indicative diagnostic clue of prerenal AKI?
FeNa < 1%
Explain why BUN:Cr ratio increases with pre renal AKI?
Decreased blood flow to kidney triggers RAAS, increased aldosterone causes increased Na+ reabsorption. H20 follows. Urea reabsorption increases but creatinine is not reabsorbed. Therefore, BUN:Cr ratio > 15
3 specific types of prerenal AKI
- Hepatorenal syndrome
- Renal artery stenosis and Angiotensin II blockers/ ACE inhibitors
- Use of other drugs that impair renal auto regulation (NSAIDS)
Hepatorenal syndrome occurs most commonly in what type of patients?
patients with cirrhosis
SBP in 90s but with edema. What likely diagnosis?
Hepatorenal syndrome secondary to cirrhosis
What clinical test is used to rule out hepatorenal syndrome?
Trial of volume infusion. If patient improves with volume infusion, you know it is not hepatorenal syndrome
Ang II blockers/ ACE Inhibitors can cause pre renal AKI in what subset of patients? What is the MOA?
Patients with renal artery stenosis. Ang II blockers impair renal auto regulation, prevent efferent arteriole constriction to increase GFR
NSAIDs can lead to AKI in patients with what conditions?
Patients with true volume depletion, CHF, & Cirrhosis
Most common cause of postrenal AKI? Other causes?
Prostate disease
Other causes: pelvic or retroperitoneal malignancies, neurogenic bladder, blockage of the ureters by stones
U/A in post renal AKI patients?
Unremarkable
Best diagnostic method for postrenal AKI?
Ultrasound
Most common cause of acute renal failure?
Acute tubular necrosis
Postrenal AKI BUN:Cr ratio
Initially, BUN:Cr > 15 due to increased tubular pressure causing urea (not creatinine) to diffuse back in blood. However, persistent obstruction damages tubular epithelium causing renal azotemia with BUN:Cr < 15
Most common cause of intrarenal AKI? Other causes?
Acute tubular necrosis Other causes: Acute interstitial nephritis, renal papillary necrosis, CHF, medication toxicity
2 etiologic mechanisms of acute tubular necrosis?
Ischemic injury, nephrotoxic injury
Ischemic acute tubular necrosis most commonly occurs in what part of the nephron? Why?
Proximal tubule and medullary segment of thick ascending limb of LOH, increased number of transporters here (requiring increased O2 for ATP)
U/A finding in acute tubular necrosis (HIGH YIELD)
Muddy brown granular casts
Acute tubular necrosis: GFR, BUN:Cr ratio, FENa %, urine Osm
GFR decreased
BUN:Cr 10-15:1
FENa > 2%
Urine Osm = 300-350 mOsm/kg (inability to concentrate urine)
Drugs that cause acute tubular necrosis?
Aminoglycosides, amphotericin B
Drugs that cause acute interstitial nephritis?
Penicillins, cephalosporins, sulfonamides, NSAIDS
Aminoglycoside toxicity and creatinine levels? location of effect?
10-20% receiving aminoglycosides will have INCREASE in creatinine, accumulates in proximal tubule cells
Aminoglycosides inhibit what function in the nephron?
Inhibit normal lysosomal function, causing acute tubular necrosis
How do you prevent aminoglycoside toxicity?
Prevent with once daily dosing, results in high urinary concentrations which exceed the reabsorptive capacity of the proximal tubule.
Common causes of nephrotoxicity leading to acute tubular necrosis?
IV contrast and medications
Which subset of patients are more likely to have nephropathy with IV contrast? MOA of IV contrast nephropathy?
Patients with pre-existing renal disease, heart failure, or hypovolemia. Also patients who receive high dose of contrast or multiple closely spaced studies. MOA: Direct vasoconstrictive effects on arterioles and tubular toxicity.
Most common cause of acute interstitial nephritis?
antibiotics (penicillins, cephalosporins, sulfa drugs), NSAIDS
Patient has oliguria, fever, and rash days to weeks after starting a drug. Likely diagnosis? What common CBC and U/A finding is present?
acute interstitial nephritis, CBC with increased eosinophils. UA +/- eosinophils
Granulocytes all up in the kidney interstitum? Diagnosis STAT
Acute interstitial nephritis
Hypovolemic patient needs IV contrast study. What precaution should you take?
Give patient IV fluids BEFORE giving IV contrast
