GU/Nephrology - Acute Kidney Injury
1. What occurs during an acute kidney injury (AKI)?: 1. Rapid decrease in renal function
(decrease in GFR)
2. Azotemia (nitrogenous products in the blood accumulate with rising BUN)
3. Build up of Creatinine in blood
4. Reduction in URINE OUTPUT (oliguria or anuria)
2. What are the possible definitions of an AKI?: - ABSOLUTE increase in serum creatinine by 0.3
mg/dL or MORE within 48 hours
- Relative INCREASE in serum creatinine of at least 1.5 times baseline that is known or presumed to have occurred within
7 DAYS
- Reduction in urine output to <0.5 mL/kg/H for longer than 6 hours
- OLIGURIC (urine production <400 mL/day)
3. What is the serum creatinine level and urine output for a stage 2 AKI?: Serum
creatinine = 2-2.9 times baseline
Urine output = <0.5 mL/kg per hour for 12 or more hours
4. What is the serum creatinine level and urine output for a stage 1 AKI?: Serum
creatinine = 1.5-1.9 times baseline
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,Urine output = <0.5 mL/kg per hour for 6-12 hours
5. Which fluid and electrolyte disorders can occur with an AKI over time?: -
INCREASED K+
- INCREASE phosphate
- DECREASED Ca
- may or may not have fluid overload
6. How can metabolic acidosis occur with an AKI?: - hydrogen ions can not be excreted by the
kidneys, as the kidneys are not making bicarbonate
7. What can occur due to the buildup of BUN with an AKI?: UREMIA, which can cause
impaired cogaulation
8. How do absent functioning kidneys affect serum creatinine?: - increases serum
creatinine concentration by 1-1.5 mg/dL daily
9. Why have AKI rates been rising?: - more antibiotics
- more contrast studies
- aging population
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, 10. What are the 3 types of AKIs?: - Prerenal
- Renal (intrinsic)
- Postrenal
11. What is the MC etiology of AKI?: MC is prerenal
12. What are the types of intrinsic AKI?: - ATN
- acute glomerulonephritis
- acute interstitial nephritis
13. Which cause of AKI must always be ruled out?: POSTRENAL (make sure the patient has NO
obstruction)
14. What is the influence of ACEI/ARB and NSAIDs on the kidneys?: 1. With combined
NSAID and ACEI therapy, there is NSAID-mediated vasoCONSTRICTION of AFFERENT arteriole & ACEI mediated vasoDI-
LATION of EFFERENT arteriole
2. Causes reduced glomerular pressure, which causes a reduced GFR and increased BUN and Creatinine
15. If a prerenal AKI is not treated promptly, what can occur?: Severe or prolonged
hypoperfusion can lead ischemia and intrinsic AKI, such as acute tubular necrosis
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1. What occurs during an acute kidney injury (AKI)?: 1. Rapid decrease in renal function
(decrease in GFR)
2. Azotemia (nitrogenous products in the blood accumulate with rising BUN)
3. Build up of Creatinine in blood
4. Reduction in URINE OUTPUT (oliguria or anuria)
2. What are the possible definitions of an AKI?: - ABSOLUTE increase in serum creatinine by 0.3
mg/dL or MORE within 48 hours
- Relative INCREASE in serum creatinine of at least 1.5 times baseline that is known or presumed to have occurred within
7 DAYS
- Reduction in urine output to <0.5 mL/kg/H for longer than 6 hours
- OLIGURIC (urine production <400 mL/day)
3. What is the serum creatinine level and urine output for a stage 2 AKI?: Serum
creatinine = 2-2.9 times baseline
Urine output = <0.5 mL/kg per hour for 12 or more hours
4. What is the serum creatinine level and urine output for a stage 1 AKI?: Serum
creatinine = 1.5-1.9 times baseline
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,Urine output = <0.5 mL/kg per hour for 6-12 hours
5. Which fluid and electrolyte disorders can occur with an AKI over time?: -
INCREASED K+
- INCREASE phosphate
- DECREASED Ca
- may or may not have fluid overload
6. How can metabolic acidosis occur with an AKI?: - hydrogen ions can not be excreted by the
kidneys, as the kidneys are not making bicarbonate
7. What can occur due to the buildup of BUN with an AKI?: UREMIA, which can cause
impaired cogaulation
8. How do absent functioning kidneys affect serum creatinine?: - increases serum
creatinine concentration by 1-1.5 mg/dL daily
9. Why have AKI rates been rising?: - more antibiotics
- more contrast studies
- aging population
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, 10. What are the 3 types of AKIs?: - Prerenal
- Renal (intrinsic)
- Postrenal
11. What is the MC etiology of AKI?: MC is prerenal
12. What are the types of intrinsic AKI?: - ATN
- acute glomerulonephritis
- acute interstitial nephritis
13. Which cause of AKI must always be ruled out?: POSTRENAL (make sure the patient has NO
obstruction)
14. What is the influence of ACEI/ARB and NSAIDs on the kidneys?: 1. With combined
NSAID and ACEI therapy, there is NSAID-mediated vasoCONSTRICTION of AFFERENT arteriole & ACEI mediated vasoDI-
LATION of EFFERENT arteriole
2. Causes reduced glomerular pressure, which causes a reduced GFR and increased BUN and Creatinine
15. If a prerenal AKI is not treated promptly, what can occur?: Severe or prolonged
hypoperfusion can lead ischemia and intrinsic AKI, such as acute tubular necrosis
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