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{{WBRQuestion
{{WBRQuestion
|QuestionAuthor={{Rim}}, {{AJL}} {{Alison}}
|QuestionAuthor={{YD}} (Reviewed by {{YD}} and {{AJL}})
|ExamType=USMLE Step 1
|ExamType=USMLE Step 1
|MainCategory=Pathology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|MainCategory=Pathology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|MainCategory=Pathology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|MainCategory=Pathology
|MainCategory=Pathophysiology
|MainCategory=Pathology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|MainCategory=Pathology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|MainCategory=Pathology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|MainCategory=Pathology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|MainCategory=Pathology
|MainCategory=Pathophysiology
|MainCategory=Pathology
|MainCategory=Pathophysiology
|SubCategory=Renal
|SubCategory=Renal
|Prompt=A 38-year-old male patient is brought to the ER in a state of sepsis. The patient does not smoke, drink alcohol, nor take any medications. You promptly initiate initial management. Several days later, the patient’s urine output becomes low and he is diagnosed with acute tubular necrosis (ATN). Which of the following statements provides the most accurate comparison between ATN and pre-renal azotemia?
|Prompt=A 38-year-old man is brought to the emergency department in septic shock. His past medical history is insignificant. He does not smoke, drink alcohol, or take any medications. The patient is managed promptly and is admitted to the intensive care unit. The next day, the patient’s urine output is low and his serum creatinine is 2.2 mg/dL. Following appropriate work-up, the patient is consequently diagnosed with acute tubular necrosis (ATN). Which of the following statements provides the most accurate comparison between ATN and pre-renal azotemia?
 
|Explanation=Acute kidney injury is a common complication of severe sepsis and septic shock characterized by injuries associated with ischemia, reperfusion, and direct inflammation. [[Pre-renal azotemia]] is a subtype of acute kidney injury (AKI) characterized by renal [[hypoperfusion]]. [[Pre-renal azotemia]] is frequently reversed upon appropriate fluid intake. A prompt response to fluid challenge is characteristic of [[pre-renal azotemia]]. Since [[pre-renal azotemia]] is not a disorder of the kidney itself, the kidney’s ability to retain sodium is retained. In [[pre-renal azotemia]], urine specific gravity is elevated. In contrast, [[acute tubular necrosis]] (ATN) is an intrinsic injury to the kidney itself and may be classified as toxic ATN (e.g. drug-induced) or ischemic ATN (complication of prolonged pre-renal AKI). ATN does not usually demonstrate a prompt resolution of [[oliguria]] and follows characteristic phases: inciting phase (oliguria and decline in kidney function), maintenance phase (GFR at its nadir and possible hyperkalemia), and recovery phase (polyuria and possible hypokalemia with resolution of oliguria and restoration of kidney function when managed early). ATN is in the differential diagnosis of [[pre-renal azotemia]], and distinguishing between the two is essential for appropriate management.
|Explanation=[[Pre-renal azotemia]], a type of AKI characterized by renal [[hypoperfusion]], causes impaired renal function. [[Pre-renal azotemia]] is frequently reversed upon appropriate fluid intake. A prompt response to fluid challenge is characteristic of [[pre-renal azotemia]]. Since [[pre-renal azotemia]] is not a disorder of the kidney itself, the kidney’s ability to retain sodium is retained. In [[pre-renal azotemia]], urine specific gravity is elevated.  
 
In contrast, [[acute tubular necrosis]] (ATN), an intrinsic injury to the kidney, may be a complication of prolonged [[pre-renal azotemia]]. ATN is the differential diagnosis of [[pre-renal azotemia]] and distinguishing between the two is essential for appropriate management.  ATN frequently does not demonstrate a prompt resolution of [[oliguria]], as seen in [[pre-renal azotemia]], and follows characteristic phases: inciting phase, maintenance phase, where GFR is at its nadir, and recovery phase, where [[oliguria]] is resolved and kidney function is restored (if it is not prolonged to cause permanent damage).
 
|EducationalObjective= ATN is a differential diagnosis of [[pre-renal azotemia]].  [[Pre-renal azotemia]] usually corrects promptly with adequate fluid challenge, while a prompt response does not typically occur in ATN.
|References=Andreucci VE, Fuiano G, Russo D, et al.  Vasomotor nephropathy in the elderly.  Nephrol Dial Transplant. 1998;13(Suppl 7):17-24
 
|AnswerA=There is a prompt response to fluid challenge in [[pre-renal azotemia]]; response to fluid challenge is not rapid in ATN
|AnswerA=There is a prompt response to fluid challenge in [[pre-renal azotemia]]; response to fluid challenge is not rapid in ATN
|AnswerAExp=Prompt response to fluid challenge is characteristic of [[pre-renal azotemia]], while ATN usually does not show prompt resolution of oliguria.
|AnswerAExp=Prompt response to fluid challenge is characteristic of [[pre-renal azotemia]], while ATN usually does not demonstrate prompt resolution of oliguria.
|AnswerB=The ability to retain sodium in [[pre-renal azotemia]] is lost; whereas it is conserved in ATN
|AnswerB=The ability to retain sodium in [[pre-renal azotemia]] is lost; whereas it is conserved in ATN
|AnswerBExp=The ability to retain sodium is lost in ATN, while it is conversed in [[pre-renal azotemia]].
|AnswerBExp=The ability to retain sodium is lost in ATN, while it is conversed in [[pre-renal azotemia]].
|AnswerC=Urine specific gravity in [[pre-renal azotemia]] is lower than urine specific gravity in ATN
|AnswerC=Urine specific gravity in [[pre-renal azotemia]] is lower than urine specific gravity in ATN
|AnswerCExp= Patients with [[pre-renal azotemia]] characteristically have a higher urine specific gravity than patients with ATN.
|AnswerCExp=Patients with [[pre-renal azotemia]] characteristically have high urine specific gravity.
|AnswerD=In contrast to ATN, [[pre-renal azotemia]] is not a complication of medication intake
|AnswerD=ATN may be an adverse effect of drug intake whiel [[pre-renal azotemia]] is not a drug adverse effect
|AnswerDExp=[[Pre-renal azotemia]] can occur as a complication of medication intake. ACE-inhibitor-induced [[pre-renal azotemia]] is an example of medication-induced [[pre-renal azotemia]].  This occurs in patients with renal artery stenosis, a solitary kidney, or bilateral renal artery stenosis.
|AnswerDExp=[[Pre-renal azotemia]] may be an adver effect of drug intake. ACE-inhibitor-induced [[pre-renal azotemia]] is an example of drug-induced [[pre-renal azotemia]], which is common among patients with bilateral renal artery stenosis or a solitary kidney.
|AnswerE=Advanced age carries a worse prognosis in [[pre-renal azotemia]], but not in ATN
|AnswerE=Advanced age is associated with a worse prognosis in [[pre-renal azotemia]] but is not associated with a worse prognosis in ATN
|AnswerEExp=Due to impaired renal physiology with age, advanced age generally carries a worse prognosis for both ATN and [[pre-renal azotemia]].
|AnswerEExp=Due to impaired renal physiology with age, advanced age is generally associated with a worse prognosis for both ATN and [[pre-renal azotemia]].
|EducationalObjectives=Prompt response to fluid challenge is characteristic of [[pre-renal azotemia]], while ATN usually does not demonstrate prompt resolution of oliguria.
|References=Andreucci VE, Fuiano G, Russo D, et al. Vasomotor nephropathy in the elderly. Nephrol Dial Transplant. 1998;13(Suppl 7):17-24
|RightAnswer=A
|RightAnswer=A
|WBRKeyword= kidney, renal, Pre-renal azotemia, fluid challenge, ATN, acute tubular necrosis, excretory system
|WBRKeyword=Pre-renal azotemia, Acute kidney injury, Acute renal failure, Pre-renal injury, Fluid challenge, ATN, Acute tubular necrosis, Sepsis
|Approved=Yes
|Approved=Yes
|EducationalObjective=ATN is a differential diagnosis of [[pre-renal azotemia]].  [[Pre-renal azotemia]] usually corrects promptly with adequate fluid challenge, while a prompt response does not typically occur in ATN.
}}
}}

Revision as of 15:36, 17 February 2015
Author [[PageAuthor::Yazan Daaboul, M.D. (Reviewed by Yazan Daaboul, M.D. and Alison Leibowitz [1])]]
Exam Type ExamType::USMLE Step 1
Main Category MainCategory::Pathophysiology
Sub Category SubCategory::Renal
Prompt [[Prompt::A 38-year-old man is brought to the emergency department in septic shock. His past medical history is insignificant. He does not smoke, drink alcohol, or take any medications. The patient is managed promptly and is admitted to the intensive care unit. The next day, the patient’s urine output is low and his serum creatinine is 2.2 mg/dL. Following appropriate work-up, the patient is consequently diagnosed with acute tubular necrosis (ATN). Which of the following statements provides the most accurate comparison between ATN and pre-renal azotemia?]]
Answer A [[AnswerA::There is a prompt response to fluid challenge in pre-renal azotemia; response to fluid challenge is not rapid in ATN]]
Answer A Explanation [[AnswerAExp::Prompt response to fluid challenge is characteristic of pre-renal azotemia, while ATN usually does not demonstrate prompt resolution of oliguria.]]
Answer B [[AnswerB::The ability to retain sodium in pre-renal azotemia is lost; whereas it is conserved in ATN]]
Answer B Explanation [[AnswerBExp::The ability to retain sodium is lost in ATN, while it is conversed in pre-renal azotemia.]]
Answer C [[AnswerC::Urine specific gravity in pre-renal azotemia is lower than urine specific gravity in ATN]]
Answer C Explanation [[AnswerCExp::Patients with pre-renal azotemia characteristically have high urine specific gravity.]]
Answer D [[AnswerD::ATN may be an adverse effect of drug intake whiel pre-renal azotemia is not a drug adverse effect]]
Answer D Explanation [[AnswerDExp::Pre-renal azotemia may be an adver effect of drug intake. ACE-inhibitor-induced pre-renal azotemia is an example of drug-induced pre-renal azotemia, which is common among patients with bilateral renal artery stenosis or a solitary kidney.]]
Answer E [[AnswerE::Advanced age is associated with a worse prognosis in pre-renal azotemia but is not associated with a worse prognosis in ATN]]
Answer E Explanation [[AnswerEExp::Due to impaired renal physiology with age, advanced age is generally associated with a worse prognosis for both ATN and pre-renal azotemia.]]
Right Answer RightAnswer::A
Explanation [[Explanation::Acute kidney injury is a common complication of severe sepsis and septic shock characterized by injuries associated with ischemia, reperfusion, and direct inflammation. Pre-renal azotemia is a subtype of acute kidney injury (AKI) characterized by renal hypoperfusion. Pre-renal azotemia is frequently reversed upon appropriate fluid intake. A prompt response to fluid challenge is characteristic of pre-renal azotemia. Since pre-renal azotemia is not a disorder of the kidney itself, the kidney’s ability to retain sodium is retained. In pre-renal azotemia, urine specific gravity is elevated. In contrast, acute tubular necrosis (ATN) is an intrinsic injury to the kidney itself and may be classified as toxic ATN (e.g. drug-induced) or ischemic ATN (complication of prolonged pre-renal AKI). ATN does not usually demonstrate a prompt resolution of oliguria and follows characteristic phases: inciting phase (oliguria and decline in kidney function), maintenance phase (GFR at its nadir and possible hyperkalemia), and recovery phase (polyuria and possible hypokalemia with resolution of oliguria and restoration of kidney function when managed early). ATN is in the differential diagnosis of pre-renal azotemia, and distinguishing between the two is essential for appropriate management.

Educational Objective: Prompt response to fluid challenge is characteristic of pre-renal azotemia, while ATN usually does not demonstrate prompt resolution of oliguria.
References: Andreucci VE, Fuiano G, Russo D, et al. Vasomotor nephropathy in the elderly. Nephrol Dial Transplant. 1998;13(Suppl 7):17-24]]

Approved Approved::Yes
Keyword WBRKeyword::Pre-renal azotemia, WBRKeyword::Acute kidney injury, WBRKeyword::Acute renal failure, WBRKeyword::Pre-renal injury, WBRKeyword::Fluid challenge, WBRKeyword::ATN, WBRKeyword::Acute tubular necrosis, WBRKeyword::Sepsis
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