Acute Kidney Injury

Question 1

Acute kidney injury (AKI) divided into what 3 types?

Answer 1

Prerenal, intrinsic renal, and postrenal azotemia

Question 2

Oliguria = < X mL urine per 24 hours

Answer 2

< 400 mL urine per 24 hours

Question 3

Are AKI’s reversible?

Answer 3

Most are if underlying disease is treated

Question 4

Prerenal, intrinsic renal, and postrenal AKI numbers. Which is most common?

Answer 4

Prerenal - 55% Intrinsic renal - 40% Postrenal - 5%

Question 5

Most common cause of prerenal AKI?

Answer 5

Volume depletion (decreased blood flow to kidneys)

Question 6

Pre renal AKI: GFR, BUN:Cr ratio, FENa %, urine Osm

Answer 6

GFR decreased

BUN:Cr ratio > 15 (normal = 15)

FENa < 1%

Urine Osm > 500 mOsm/kg

Question 7

Most indicative diagnostic clue of prerenal AKI?

Answer 7

FeNa < 1%

Question 8

Explain why BUN:Cr ratio increases with pre renal AKI?

Answer 8

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

Question 9

3 specific types of prerenal AKI

Answer 9

1. Hepatorenal syndrome
2. Renal artery stenosis and Angiotensin II blockers/ ACE inhibitors
3. Use of other drugs that impair renal auto regulation (NSAIDS)

Question 10

Hepatorenal syndrome occurs most commonly in what type of patients?

Answer 10

patients with cirrhosis

Question 11

SBP in 90s but with edema. What likely diagnosis?

Answer 11

Hepatorenal syndrome secondary to cirrhosis

Question 12

What clinical test is used to rule out hepatorenal syndrome?

Answer 12

Trial of volume infusion. If patient improves with volume infusion, you know it is not hepatorenal syndrome

Question 13

Ang II blockers/ ACE Inhibitors can cause pre renal AKI in what subset of patients? What is the MOA?

Answer 13

Patients with renal artery stenosis. Ang II blockers impair renal auto regulation, prevent efferent arteriole constriction to increase GFR

Question 14

NSAIDs can lead to AKI in patients with what conditions?

Answer 14

Patients with true volume depletion, CHF, & Cirrhosis

Question 15

Most common cause of postrenal AKI? Other causes?

Answer 15

Prostate disease

Other causes: pelvic or retroperitoneal malignancies, neurogenic bladder, blockage of the ureters by stones

Question 16

U/A in post renal AKI patients?

Answer 16

Unremarkable

Question 17

Best diagnostic method for postrenal AKI?

Answer 17

Ultrasound

Question 18

Most common cause of acute renal failure?

Answer 18

Acute tubular necrosis

Question 19

Postrenal AKI BUN:Cr ratio

Answer 19

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

Question 20

Most common cause of intrarenal AKI? Other causes?

Answer 20

Acute tubular necrosis Other causes: Acute interstitial nephritis, renal papillary necrosis, CHF, medication toxicity

Question 21

2 etiologic mechanisms of acute tubular necrosis?

Answer 21

Ischemic injury, nephrotoxic injury

Question 22

Ischemic acute tubular necrosis most commonly occurs in what part of the nephron? Why?

Answer 22

Proximal tubule and medullary segment of thick ascending limb of LOH, increased number of transporters here (requiring increased O2 for ATP)

Question 23

U/A finding in acute tubular necrosis (HIGH YIELD)

Answer 23

Muddy brown granular casts

Question 24

Acute tubular necrosis: GFR, BUN:Cr ratio, FENa %, urine Osm

Answer 24

GFR decreased

BUN:Cr 10-15:1

FENa > 2%

Urine Osm = 300-350 mOsm/kg (inability to concentrate urine)

Question 25

Drugs that cause acute tubular necrosis?

Answer 25

Aminoglycosides, amphotericin B

Question 26

Drugs that cause acute interstitial nephritis?

Answer 26

Penicillins, cephalosporins, sulfonamides, NSAIDS

Question 27

Aminoglycoside toxicity and creatinine levels? location of effect?

Answer 27

10-20% receiving aminoglycosides will have INCREASE in creatinine, accumulates in proximal tubule cells

Question 28

Aminoglycosides inhibit what function in the nephron?

Answer 28

Inhibit normal lysosomal function, causing acute tubular necrosis

Question 29

How do you prevent aminoglycoside toxicity?

Answer 29

Prevent with once daily dosing, results in high urinary concentrations which exceed the reabsorptive capacity of the proximal tubule.

Question 30

Common causes of nephrotoxicity leading to acute tubular necrosis?

Answer 30

IV contrast and medications

Question 31

Which subset of patients are more likely to have nephropathy with IV contrast? MOA of IV contrast nephropathy?

Answer 31

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.

Question 32

Most common cause of acute interstitial nephritis?

Answer 32

antibiotics (penicillins, cephalosporins, sulfa drugs), NSAIDS

Question 33

Patient has oliguria, fever, and rash days to weeks after starting a drug. Likely diagnosis? What common CBC and U/A finding is present?

Answer 33

acute interstitial nephritis, CBC with increased eosinophils. UA +/- eosinophils

Question 34

Granulocytes all up in the kidney interstitum? Diagnosis STAT

Answer 34

Acute interstitial nephritis

Question 35

Hypovolemic patient needs IV contrast study. What precaution should you take?

Answer 35

Give patient IV fluids BEFORE giving IV contrast