WBR0389: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
No edit summary
Line 1: Line 1:
{{WBRQuestion
{{WBRQuestion
|QuestionAuthor={{Rim}}
|QuestionAuthor={{Rim}}, {{AJL}} {{Alison}}
|ExamType=USMLE Step 1
|ExamType=USMLE Step 1
|MainCategory=Pathology
|MainCategory=Pathology
Line 20: Line 20:
|MainCategory=Pathology
|MainCategory=Pathology
|SubCategory=Renal
|SubCategory=Renal
|Prompt=A 38 year old male patient who is previously healthy is brought to the emergency department in sepsis.  Patient does not smoke, does not drink alcohol, and does not take any medications.  Initial management is promptly initiated.  Several days later, the patient’s urine output becomes low.  He is diagnosed with acute tubular necrosis (ATN).  Which of the following statements is generally true about the difference between ATN and pre-renal injury?
|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?
|Explanation=Pre-renal kidney injury is a type of AKI characterized by renal hypoperfusion that cause impaired renal function.  Pre-renal injury is generally reversed by appropriate fluid intake. Prompt response to fluid challenge is characteristic of pre-renal kidney injury.  Since pre-renal injury is not a disorder of the kidney itself, the kidney’s ability to retain sodium in pre-renal injury is thus retained.  As such, urine specific gravity in pre-renal injury is elevated.


In contrast, acute tubular necrosis (ATN) is an intrinsic injury to the kidney.  It may be a complication of prolonged pre-renal injury. ATN is the differential diagnosis of pre-renal injury.  Distinguishing between the two is important for appropriate management.  ATN usually does not show prompt resolution of oliguria as seen in pre-renal injury.  ATN follows characteristic phases: inciting phase, maintenance phase where GFR is at its nadir, and finally recovery phase where oliguria is resolved and kidney function is restored, if the damage is not prolonged to cause permanent damage.
|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.  


Educational Objective:
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).
ATN should always be a differential diagnosis of pre-renal kidney injury.  Pre-renal injury usually corrects promptly with adequate fluid challenge.  This prompt response is not typically seen in ATN.  


Reference:
|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.
Andreucci VE, Fuiano G, Russo D, et al.  Vasomotor nephropathy in the elderly.  Nephrol Dial Transplant.  1998;13(Suppl 7):17-24
|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 injury; response to fluid challenge is not rapid in ATN
 
|AnswerAExp=Prompt response to fluid challenge is characteristic of pre-renal kidney injury.  ATN usually does not show prompt resolution of oliguria as seen in pre-renal injury.
|AnswerA=There is a prompt response to fluid challenge in [[pre-renal azotemia]]; response to fluid challenge is not rapid in ATN
|AnswerB=The ability to retain sodium in pre-renal injury is lost; whereas it is conserved in ATN
|AnswerAExp=Prompt response to fluid challenge is characteristic of [[pre-renal azotemia]], while ATN usually does not show prompt resolution of oliguria.
|AnswerBExp=The ability to retain sodium is lost in ATN.  It is conversed in pre-renal injury.
|AnswerB=The ability to retain sodium in [[pre-renal azotemia]] is lost; whereas it is conserved in ATN
|AnswerC=Urine specific gravity in pre-renal injury is lower than urine specific gravity in ATN
|AnswerBExp=The ability to retain sodium is lost in ATN, while it is conversed in [[pre-renal azotemia]].
|AnswerCExp=Pre-renal injury has a higher urine specific gravity than that in ATN.
|AnswerC=Urine specific gravity in [[pre-renal azotemia]] is lower than urine specific gravity in ATN
|AnswerD=In contrast to ATN, pre-renal injury is not a complication of medication intake
|AnswerCExp= Patients with [[pre-renal azotemia]] characteristically have a higher urine specific gravity than patients with ATN.
|AnswerDExp=Pre-renal injury could be a complication of medication intake.  ACE-inhibitors-induced pre-renal injury is a classical case of medication-induced pre-renal injury.  This is especially true in the case  of renal artery stenosis in a solitary kidney or bilateral renal artery stenosis.
|AnswerD=In contrast to ATN, [[pre-renal azotemia]] is not a complication of medication intake
|AnswerE=Advanced age carries a worse prognosis in pre-renal injury, but not in ATN
|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.
|AnswerEExp=Due to impaired renal physiology with age, advanced age generally carries a worse prognosis for both ATN and pre-renal kidney injury.
|AnswerE=Advanced age carries a worse prognosis in [[pre-renal azotemia]], but not in ATN
|AnswerEExp=Due to impaired renal physiology with age, advanced age generally carries a worse prognosis for both ATN and [[pre-renal azotemia]].
|RightAnswer=A
|RightAnswer=A
|Approved=No
|WBRKeyword= kidney, renal, Pre-renal azotemia, fluid challenge, ATN, acute tubular necrosis, excretory system
|Approved=Yes
}}
}}

Revision as of 14:16, 17 July 2014
Author [[PageAuthor::Rim Halaby, M.D. [1], Alison Leibowitz [2] (Reviewed by Alison Leibowitz)]]
Exam Type ExamType::USMLE Step 1
Main Category MainCategory::Pathology
Sub Category SubCategory::Renal
Prompt [[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?]]
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 show 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 a higher urine specific gravity than patients with ATN.]]
Answer D [[AnswerD::In contrast to ATN, pre-renal azotemia is not a complication of medication intake]]
Answer D Explanation [[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.]]
Answer E [[AnswerE::Advanced age carries a worse prognosis in pre-renal azotemia, but not in ATN]]
Answer E Explanation [[AnswerEExp::Due to impaired renal physiology with age, advanced age generally carries a worse prognosis for both ATN and pre-renal azotemia.]]
Right Answer RightAnswer::A
Explanation [[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).
Educational Objective:
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::kidney, WBRKeyword::renal, WBRKeyword::Pre-renal azotemia, WBRKeyword::fluid challenge, WBRKeyword::ATN, WBRKeyword::acute tubular necrosis, WBRKeyword::excretory system
Linked Question Linked::
Order in Linked Questions LinkedOrder::
Retrieved from "https://www.wikidoc.org/index.php?title=WBR0389&oldid=994951"