WBR0389
| 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). |
| 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:: |