WBR0389: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
m (refreshing WBR questions)
 
(6 intermediate revisions by 3 users not shown)
Line 1: Line 1:
{{WBRQuestion
{{WBRQuestion
|QuestionAuthor={{Rim}}
|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 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 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=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.  
|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.<br>


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.
[[Image:Distinguishing Prerenal Azotemia and ATN.png|500px]]
 
|AnswerA=There is a prompt response to fluid challenge in [[pre-renal azotemia]]; response to fluid challenge is not rapid in ATN
Educational Objective:
|AnswerAExp=Prompt response to fluid challenge is characteristic of [[pre-renal azotemia]], while ATN usually does not demonstrate prompt resolution of oliguria.
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.
|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]].
Reference:
|AnswerC=Urine specific gravity in [[pre-renal azotemia]] is lower than urine specific gravity in ATN
Andreucci VE, Fuiano G, Russo D, et al.  Vasomotor nephropathy in the elderly.  Nephrol Dial Transplant.  1998;13(Suppl 7):17-24
|AnswerCExp=Patients with [[pre-renal azotemia]] characteristically have high urine specific gravity.
 
|AnswerD=ATN may be an adverse effect of drug intake whiel [[pre-renal azotemia]] is not a drug adverse effect
|AnswerA=There is a prompt response to fluid challenge in pre-renal injury; response to fluid challenge is not rapid in ATN
|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.
|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.
|AnswerE=Advanced age is associated with a worse prognosis in [[pre-renal azotemia]] but is not associated with a worse prognosis in ATN
|AnswerB=The ability to retain sodium in pre-renal injury is lost; whereas it is conserved in ATN
|AnswerEExp=Due to impaired renal physiology with age, advanced age is generally associated with a worse prognosis for both ATN and [[pre-renal azotemia]].
|AnswerBExp=The ability to retain sodium is lost in ATN.  It is conversed in pre-renal injury
|EducationalObjectives=Prompt response to fluid challenge is characteristic of [[pre-renal azotemia]], while ATN usually does not demonstrate prompt resolution of oliguria.
|AnswerC=Urine specific gravity in pre-renal injury is lower than urine specific gravity 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.<br>
|AnswerCExp=Pre-renal injury has a higher urine specific gravity than that in ATN
First Aid 2014 page 543
|AnswerD=In contrast to ATN, pre-renal injury is not a complication of medication intake
|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.
|AnswerE=Advanced age carries a worse prognosis in pre-renal injury, 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 kidney injury.
|RightAnswer=A
|RightAnswer=A
|Approved=No
|WBRKeyword=Pre-renal azotemia, Acute kidney injury, Acute renal failure, Pre-renal injury, Fluid challenge, ATN, Acute tubular necrosis, Sepsis
|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.
}}
}}

Latest revision as of 00:25, 28 October 2020
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.
First Aid 2014 page 543]]

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
Linked Question Linked::
Order in Linked Questions LinkedOrder::
Retrieved from "https://www.wikidoc.org/index.php?title=WBR0389&oldid=1671644"