WBR0389
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| 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.
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| 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:: |
