Cardio-renal syndrome US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Cardio-renal syndrome. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Cardio-renal syndrome US Medical PG Question 1: A 62-year-old man presents to the emergency room with an acute myocardial infarction. Twenty-four hours after admission to the cardiac intensive care unit, he develops oliguria. Laboratory tests show that his serum BUN is 59 mg/dL and his serum creatinine is 6.2 mg/dL. Renal biopsy reveals necrosis of the proximal tubules and thick ascending limb of Henle's loop. Which of the following would you most likely observe on a microscopic examination of this patient's urine?
- A. White blood cell casts
- B. Broad waxy casts
- C. Fatty casts
- D. Hyaline casts
- E. Muddy brown casts (Correct Answer)
Cardio-renal syndrome Explanation: ***Muddy brown casts***
- The patient's presentation of **acute myocardial infarction** followed by **oliguria**, elevated **BUN** and **creatinine**, and necrosis of the **proximal tubules** and **thick ascending limb** of Henle's loop is characteristic of **acute tubular necrosis (ATN)**.
- **Muddy brown casts** composed of **granular material** and **renal tubular epithelial cells** are the classic finding in the urine sediment of patients with ATN.
*White blood cell casts*
- **White blood cell casts** are typically associated with **pyelonephritis** or **interstitial nephritis**, indicating renal inflammation or infection.
- While infection can exacerbate kidney injury, the primary pathology described here is **ischemic ATN**, not an infectious process.
*Broad waxy casts*
- **Broad waxy casts** indicate severe, **chronic kidney disease** with significant **tubular dilation** and **stasis**, often end-stage renal disease.
- The patient's clinical picture depicts **acute kidney injury**, not chronic kidney failure.
*Fatty casts*
- **Fatty casts** are characteristic of **nephrotic syndrome**, which involves significant proteinuria and hyperlipidemia.
- This patient's presentation does not describe the features of **nephrotic syndrome**, such as **massive proteinuria** or **edema**.
*Hyaline casts*
- **Hyaline casts** are composed of **Tamm-Horsfall protein** and can be found in healthy individuals, especially after exercise or dehydration.
- While they can be present in various kidney conditions, they are **non-specific** and not indicative of the specific **tubular epithelial cell injury** seen in ATN.
Cardio-renal syndrome US Medical PG Question 2: A 55-year-old man presents with a bilateral lower leg edema. The patient reports it developed gradually over the past 4 months. The edema is worse in the evening and improves after sleeping at night or napping during the day. There are no associated pain or sensitivity changes. The patient also notes dyspnea on usual exertion such as working at his garden. The patient has a history of a STEMI myocardial infarction 9 months ago treated with thrombolysis with an unremarkable postprocedural course. His current medications include atorvastatin 10 mg, aspirin 81 mg, and metoprolol 50 mg daily. He works as a barber at a barbershop, has a 16-pack-year history of smoking, and consumes alcohol in moderation. The vital signs include: blood pressure 130/80 mm Hg, heart rate 63/min, respiratory rate 14/min, and temperature 36.8℃ (98.2℉). The lungs are clear to auscultation. Cardiac examination shows dubious S3 and a soft grade 1/6 systolic murmur best heard at the apex of the heart. Abdominal examination reveals hepatic margin 1 cm below the costal margin. There is a 2+ bilateral pitting lower leg edema. The skin over the edema is pale with no signs of any lesions. There is no facial or flank edema. The thyroid gland is not enlarged. Which of the following tests is most likely to reveal the cause of the patient’s symptoms?
- A. D-dimer measurement
- B. Doppler color ultrasound of the lower extremity
- C. Echocardiography (Correct Answer)
- D. Soft tissue ultrasound of the lower extremities
- E. T4 and thyroid-stimulating hormone assessment
Cardio-renal syndrome Explanation: ***Correct: Echocardiography***
- The patient's history of **STEMI 9 months ago**, **dyspnea on exertion**, **bilateral pitting lower extremity edema** that worsens in the evening, **dubious S3 gallop**, and **hepatomegaly** are classic findings of **heart failure post-myocardial infarction**.
- **Echocardiography** is the **gold standard test** to assess **left ventricular function**, **ejection fraction**, **regional wall motion abnormalities**, and **valve function**, which are crucial for diagnosing and determining the severity of heart failure post-MI.
- This test will directly reveal the cardiac cause of the patient's symptoms and guide management decisions.
*Incorrect: D-dimer measurement*
- This test is primarily used to rule out **deep vein thrombosis (DVT)** or **pulmonary embolism (PE)**, neither of which is strongly suggested by the patient's bilateral, gradual-onset edema and cardiac symptoms.
- A negative D-dimer is useful to exclude DVT/PE, but a positive result is non-specific and would not explain the other cardiac findings like dyspnea on exertion, S3 gallop, and hepatomegaly.
*Incorrect: Doppler color ultrasound of the lower extremity*
- This imaging is used to evaluate for **venous insufficiency** or **deep vein thrombosis**, which typically cause unilateral or acute edema with skin changes.
- While chronic venous insufficiency could cause bilateral edema, the presence of **dyspnea on exertion**, **S3 gallop**, and **hepatomegaly** strongly points to a **cardiac origin** rather than venous disease.
*Incorrect: Soft tissue ultrasound of the lower extremities*
- This test is used to evaluate for **localized soft tissue infection (cellulitis)**, **abscesses**, or other **structural abnormalities** in the subcutaneous tissue.
- The patient's edema is described as **pale with no signs of lesions**, non-tender, and bilateral, making soft tissue pathology unlikely. Additionally, there are no signs of inflammation or infection.
*Incorrect: T4 and thyroid-stimulating hormone assessment*
- While **hypothyroidism** can cause edema (myxedema), it typically presents as **non-pitting edema** and is usually accompanied by other symptoms like fatigue, weight gain, cold intolerance, and bradycardia beyond what beta-blockers would cause.
- The patient's symptoms with **pitting edema**, **post-MI history**, **dyspnea on exertion**, and **S3 gallop** are pathognomonic for cardiac causes, and there are no specific signs pointing to thyroid dysfunction.
Cardio-renal syndrome US Medical PG Question 3: A 59-year-old man with a history of congestive heart failure presents to his cardiologist for a follow-up visit. His past medical history is notable for diabetes mellitus, hypertension, and obesity. He takes metformin, glyburide, aspirin, lisinopril, and metoprolol. He has a 40 pack-year smoking history and drinks alcohol socially. His temperature is 99.1°F (37.2°C), blood pressure is 150/65 mmHg, pulse is 75/min, and respirations are 20/min. Physical examination reveals bilateral rales at the lung bases and 1+ edema in the bilateral legs. The physician decides to start the patient on an additional diuretic but warns the patient about an increased risk of breast enlargement. Which of the following is the most immediate physiologic effect of the medication in question?
- A. Decreased sodium reabsorption in the distal convoluted tubule
- B. Decreased bicarbonate reabsorption in the proximal convoluted tubule
- C. Decreased sodium reabsorption in the thick ascending limb
- D. Decreased renin enzyme activity
- E. Decreased sodium reabsorption in the collecting duct (Correct Answer)
Cardio-renal syndrome Explanation: ***Decreased sodium reabsorption in the collecting duct***
- The physician is initiating **spironolactone**, an **aldosterone antagonist**, due to its known side effect of **gynecomastia** (breast enlargement).
- Spironolactone acts on the **collecting duct** to inhibit aldosterone's effects, leading to decreased sodium reabsorption and **decreased potassium excretion** (potassium-sparing effect).
- This makes it useful in heart failure but requires monitoring for **hyperkalemia**, especially in patients on ACE inhibitors like lisinopril.
*Decreased sodium reabsorption in the distal convoluted tubule*
- This is the primary site of action for **thiazide diuretics**, such as **hydrochlorothiazide** or **chlorthalidone**.
- While effective for heart failure, thiazides are not associated with breast enlargement.
*Decreased bicarbonate reabsorption in the proximal convoluted tubule*
- This is the main action of **carbonic anhydrase inhibitors**, such as **acetazolamide**.
- These diuretics are typically used for conditions like glaucoma or metabolic alkalosis, not first-line for heart failure and do not cause breast enlargement.
*Decreased sodium reabsorption in the thick ascending limb*
- This is the mechanism of action for **loop diuretics**, such as **furosemide** or **bumetanide**.
- Loop diuretics are potent and frequently used in heart failure, but they do not cause breast enlargement.
*Decreased renin enzyme activity*
- This effect is primarily seen with **beta-blockers** or **direct renin inhibitors**.
- While beta-blockers (like metoprolol, which the patient is already taking) are used in heart failure, they do not cause breast enlargement.
Cardio-renal syndrome US Medical PG Question 4: On cardiology service rounds, your team sees a patient admitted with an acute congestive heart failure exacerbation. In congestive heart failure, decreased cardiac function leads to decreased renal perfusion, which eventually leads to excess volume retention. To test your knowledge of physiology, your attending asks you which segment of the nephron is responsible for the majority of water absorption. Which of the following is a correct pairing of the segment of the nephron that reabsorbs the majority of all filtered water with the means by which that segment absorbs water?
- A. Distal convoluted tubule via passive diffusion following ion reabsorption
- B. Distal convoluted tubule via aquaporin channels
- C. Thick ascending loop of Henle via passive diffusion following ion reabsorption
- D. Proximal convoluted tubule via passive diffusion following ion reabsorption (Correct Answer)
- E. Collecting duct via aquaporin channels
Cardio-renal syndrome Explanation: ***Proximal convoluted tubule via passive diffusion following ion reabsorption***
- The **proximal convoluted tubule (PCT)** is responsible for reabsorbing approximately **65-70% of filtered water**, making it the primary site of water reabsorption in the nephron.
- This water reabsorption primarily occurs **passively**, following the active reabsorption of solutes (especially **sodium ions**), which creates an osmotic gradient.
*Distal convoluted tubule via passive diffusion following ion reabsorption*
- The **distal convoluted tubule (DCT)** reabsorbs a much smaller percentage of filtered water (around 5-10%) and its water reabsorption is largely **regulated by ADH**, not primarily simple passive diffusion following bulk ion reabsorption.
- While some passive water movement occurs, it is not the main mechanism or location for the majority of water reabsorption.
*Distal convoluted tubule via aquaporin channels*
- While aquaporin channels do play a role in water reabsorption in the DCT, particularly under the influence of **ADH**, the DCT is not the segment responsible for the **majority of all filtered water absorption**.
- The bulk of water reabsorption occurs earlier in the nephron, independently of ADH for the most part.
*Thick ascending loop of Henle via passive diffusion following ion reabsorption*
- The **thick ascending loop of Henle** is primarily involved in reabsorbing ions like Na+, K+, and Cl- but is largely **impermeable to water**.
- Its impermeability to water is crucial for creating the **osmotic gradient** in the renal medulla, which is necessary for later water reabsorption.
*Collecting duct via aquaporin channels*
- The **collecting duct** is critically important for **regulated water reabsorption** via **aquaporin-2 channels** under the influence of **ADH**, allowing for fine-tuning of urine concentration.
- However, it reabsorbs only a variable portion (typically 5-19%) of the remaining filtered water, not the **majority of all filtered water**.
Cardio-renal syndrome US Medical PG Question 5: A 66-year-old man with congestive heart failure presents to the emergency department complaining of worsening shortness of breath. These symptoms have worsened over the last 3 days. He has a blood pressure of 126/85 mm Hg and heart rate of 82/min. Physical examination is notable for bibasilar crackles. A chest X-ray reveals bilateral pulmonary edema. His current medications include metoprolol succinate and captopril. You wish to add an additional medication targeted towards his symptoms. Of the following, which statement is correct regarding loop diuretics?
- A. Loop diuretics can cause metabolic acidosis
- B. Loop diuretics can cause ammonia toxicity
- C. Loop diuretics can cause hyperlipidemia
- D. Loop diuretics decrease sodium, magnesium, and chloride but increase calcium
- E. Loop diuretics inhibit the action of the Na+/K+/Cl- cotransporter (Correct Answer)
Cardio-renal syndrome Explanation: ***Loop diuretics inhibit the action of the Na+/K+/Cl- cotransporter***
- Loop diuretics, like furosemide, directly block the **Na+/K+/2Cl- cotransporter** in the **thick ascending limb of the loop of Henle**, preventing the reabsorption of these ions.
- This inhibition leads to increased excretion of water, sodium, potassium, and chloride, which is beneficial in conditions like **pulmonary edema** due to **congestive heart failure**.
*Loop diuretics can cause metabolic acidosis*
- Loop diuretics typically cause **metabolic alkalosis**, not acidosis, because they increase the excretion of hydrogen ions and potassium, leading to a compensatory increase in bicarbonate.
- The increased delivery of sodium to the collecting duct can also stimulate potassium and hydrogen secretion, contributing to alkalosis.
*Loop diuretics can cause ammonia toxicity*
- Loop diuretics do not directly cause **ammonia toxicity**; this is more commonly associated with conditions like **hepatic encephalopathy** or certain other medications.
- Their primary mechanism of action is on renal ion transport, not ammonia metabolism.
*Loop diuretics can cause hyperlipidemia*
- While some diuretics like **thiazide diuretics** can cause mild increases in **lipid levels**, loop diuretics are not typically associated with significant **hyperlipidemia**.
- The most common metabolic side effects of loop diuretics include electrolyte imbalances.
*Loop diuretics decrease sodium, magnesium, and chloride but increase calcium*
- Loop diuretics decrease the reabsorption of **sodium**, **magnesium**, and **chloride**, leading to their increased excretion.
- They also increase **calcium excretion** (cause hypocalcemia), rather than increasing serum calcium levels, by inhibiting its reabsorption in the thick ascending limb of the loop of Henle.
Cardio-renal syndrome US Medical PG Question 6: A 53-year-old woman presents to her physician for evaluation of sudden onset respiratory distress for the past few hours. The past medical history includes a myocardial infarction 2 years ago. The vital signs include a blood pressure 70/40 mm Hg, pulse 92/min, respiratory rate 28/min, and SpO2 92% on room air. The physical examination reveals bilateral basal crepitations on auscultation. The echocardiogram reveals an ejection fraction of 34%. She is admitted to the medical floor and started on furosemide. The urine output in 24 hours is 400 mL. The blood urea nitrogen is 45 mg/dL and the serum creatinine is 1.85 mg/dL. The fractional excretion of sodium is 2.4%. Urinalysis revealed muddy brown granular casts. Which of the following is the most likely cause of the abnormal urinalysis?
- A. Acute interstitial nephritis
- B. Acute tubular necrosis (Correct Answer)
- C. Acute pyelonephritis
- D. Chronic kidney disease
- E. Acute glomerulonephritis
Cardio-renal syndrome Explanation: ***Acute tubular necrosis***
- The presence of **muddy brown granular casts** on urinalysis is pathognomonic for **acute tubular necrosis (ATN)**, indicating damage to the renal tubules.
- The patient's history of **cardiogenic shock** (low BP 70/40 mm Hg, respiratory distress, low SpO2, low ejection fraction of 34%) led to **renal hypoperfusion** and ischemic tubular injury.
- The **fractional excretion of sodium (FENa) of 2.4%** (>2%) is characteristic of **intrinsic renal injury** (ATN), as damaged tubules cannot effectively reabsorb sodium.
- **Oliguria** (400 mL/24 hours), elevated **BUN (45 mg/dL)** and **creatinine (1.85 mg/dL)** further support acute kidney injury from ATN.
*Acute interstitial nephritis*
- This condition is typically associated with **drug hypersensitivity** (e.g., NSAIDs, antibiotics, PPIs) or **infections** and is characterized by inflammatory infiltrate in the renal interstitium.
- Urinalysis typically shows **white blood cell casts** and **eosinophiluria**, not muddy brown granular casts.
*Acute pyelonephritis*
- This is an **infection of the kidney** parenchyma, usually caused by bacterial ascension from the urinary tract.
- Symptoms often include **fever, flank pain, dysuria**, and urinalysis reveals **leukocyturia** (white blood cells) and **bacterial casts**, not muddy brown granular casts.
*Chronic kidney disease*
- While the patient has elevated creatinine and BUN, **chronic kidney disease (CKD)** develops over months to years and is characterized by persistent kidney damage or decreased function.
- Urinalysis in CKD often shows **broad waxy casts** and typically does not present with such **acute, sudden onset** of severe renal dysfunction with muddy brown granular casts.
*Acute glomerulonephritis*
- This condition involves inflammation of the glomeruli and typically presents with **hematuria, proteinuria, and red blood cell casts** (dysmorphic RBCs).
- The patient's clinical picture, including the absence of significant hematuria and the presence of **muddy brown granular casts**, does not fit acute glomerulonephritis.
Cardio-renal syndrome US Medical PG Question 7: A 70-year-old Caucasian male visits your office regularly for treatment of New York Heart association class IV congestive heart failure. Which of the following medications would you add to this man's drug regimen in order to improve his overall survival?
- A. Spironolactone (Correct Answer)
- B. Furosemide
- C. Amiloride
- D. Acetazolamide
- E. Hydrochlorothiazide
Cardio-renal syndrome Explanation: ***Spironolactone***
- **Spironolactone** is an **aldosterone antagonist** that has been shown to reduce mortality and morbidity in patients with **NYHA Class III and IV heart failure**.
- It works by blocking the harmful effects of **aldosterone** on the heart, such as **fibrosis** and remodeling, improving cardiac function and survival.
*Furosemide*
- **Furosemide** is a **loop diuretic** primarily used to relieve **symptoms of congestion** (edema, dyspnea) in heart failure by promoting fluid excretion.
- While it improves symptoms, **furosemide** alone does not significantly improve long-term survival in patients with heart failure.
*Amiloride*
- **Amiloride** is a **potassium-sparing diuretic** that works by blocking sodium channels in the collecting duct, leading to modest diuresis.
- It is often used to prevent **hypokalemia** caused by other diuretics but does not have the same proven mortality benefit in heart failure as spironolactone.
*Acetazolamide*
- **Acetazolamide** is a **carbonic anhydrase inhibitor** primarily used for glaucoma, metabolic alkalosis, and altitude sickness.
- It has a weaker diuretic effect and is not a commonly used or recommended medication for improving long-term survival in patients with heart failure.
*Hydrochlorothiazide*
- **Hydrochlorothiazide** is a **thiazide diuretic** primarily used for hypertension and mild to moderate edema.
- While it can help manage fluid retention, it does not offer the same mortality benefit in advanced heart failure as aldosterone antagonists like spironolactone.
Cardio-renal syndrome US Medical PG Question 8: Activation of the renin-angiotensin-aldosterone system yields a significant physiological effect on renal blood flow and filtration. Which of the following is most likely to occur in response to increased levels of Angiotensin-II?
- A. Decreased renal plasma flow, decreased filtration fraction
- B. Decreased renal plasma flow, increased glomerular capillary oncotic pressure
- C. Increased renal plasma flow, decreased filtration fraction
- D. Increased renal plasma flow, increased filtration fraction
- E. Decreased renal plasma flow, increased filtration fraction (Correct Answer)
Cardio-renal syndrome Explanation: ***Decreased renal plasma flow, increased filtration fraction***
- **Angiotensin II** causes **efferent arteriolar constriction**, which reduces blood flow leaving the glomerulus, thereby **decreasing renal plasma flow**.
- This efferent constriction also increases **glomerular hydrostatic pressure** and reduces plasma flow distal to the glomerulus, leading to a **higher filtration fraction** (GFR/RPF).
*Decreased renal plasma flow, decreased filtration fraction*
- While **renal plasma flow decreases**, a **decreased filtration fraction** would imply that either GFR decreases disproportionately more than RPF or GFR does not increase despite the RPF reduction, which is not the typical response to **angiotensin II** due to its predominant effect on the **efferent arteriole**.
*Decreased renal plasma flow, increased glomerular capillary oncotic pressure*
- **Increased glomerular capillary oncotic pressure** is a consequence of increased filtration fraction, as more fluid is filtered out, leaving behind a more concentrated plasma. This option includes a correct element (decreased RPF) but pairs it with a less direct and defining outcome of acute Angiotensin II action as the primary physiological effect.
*Increased renal plasma flow, decreased filtration fraction*
- **Angiotensin II** causes **vasoconstriction**, predominantly of the efferent arteriole, which by definition would **decrease renal plasma flow**, not increase it.
- A **decreased filtration fraction** would be inconsistent with efferent arteriolar constriction which typically raises GFR relative to RPF.
*Increased renal plasma flow, increased filtration fraction*
- **Angiotensin II** causes **vasoconstriction**, leading to a **decrease in renal plasma flow**, not an increase.
- While **filtration fraction is increased**, the initial premise of increased renal plasma flow is incorrect.
Cardio-renal syndrome US Medical PG Question 9: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?
- A. Lidocaine
- B. Verapamil
- C. Carvedilol (Correct Answer)
- D. Aspirin
- E. Ibutilide
Cardio-renal syndrome Explanation: ***Carvedilol***
- The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**.
- **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function.
*Lidocaine*
- **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management.
- It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias.
- It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function.
*Aspirin*
- **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease).
- It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology.
*Ibutilide*
- **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm.
- It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.
Cardio-renal syndrome US Medical PG Question 10: A 39-year-old woman is brought to the emergency department in a semi-unconscious state by her neighbor who saw her lose consciousness. There was no apparent injury on the primary survey. She is not currently taking any medications. She has had loose stools for the past 3 days and a decreased frequency of urination. No further history could be obtained. The vital signs include: blood pressure 94/62 mm Hg, temperature 36.7°C (98.0°F), pulse 105/min, and respiratory rate 10/min. The skin appears dry. Routine basic metabolic panel, urine analysis, urine osmolality, and urine electrolytes are pending. Which of the following lab abnormalities would be expected in this patient?
- A. Serum blood urea nitrogen/creatinine (BUN/Cr) > 20 (Correct Answer)
- B. Urine osmolality < 350 mOsm/kg
- C. Fractional excretion of sodium (FENa) > 2%
- D. Urine Na+ > 40 mEq/L
- E. Serum creatinine < 1 mg/dL
Cardio-renal syndrome Explanation: ***Serum blood urea nitrogen/creatinine (BUN/Cr) > 20***
- The patient presents with classic signs of **hypovolemia**, including hypotension, tachycardia, dry skin, and decreased urine output, likely due to significant fluid loss from diarrheal illness. This state leads to **prerenal azotemia**.
- In prerenal azotemia, the kidneys reabsorb more water and urea to conserve fluid, leading to a disproportionate rise in BUN compared to creatinine, resulting in a **BUN/Cr ratio typically > 20:1**.
*Urine osmolality < 350 mOsm/kg*
- This value indicates the kidney is actively excreting dilute urine, which would be expected in conditions like **diabetes insipidus** or **excessive fluid intake**.
- In response to hypovolemia, the kidneys attempt to conserve water, leading to the excretion of **highly concentrated urine**, with osmolality typically **> 500 mOsm/kg**.
*Fractional excretion of sodium (FENa) > 2%*
- An FENa > 2% suggests **intrinsic renal damage** (acute tubular necrosis) where the kidneys cannot effectively reabsorb sodium.
- In prerenal azotemia, the kidneys are structurally intact and actively conserve sodium to maintain circulating volume, leading to an **FENa < 1%**.
*Urine Na+ > 40 mEq/L*
- A urine sodium concentration above 40 mEq/L is observed in **intrinsic kidney injury** or during **diuretic use**, where sodium reabsorption is impaired.
- With hypovolemia, the kidneys avidly reabsorb sodium, striving to restore volume. This results in a **low urine sodium concentration**, typically **< 20 mEq/L**.
*Serum creatinine < 1 mg/dL*
- While a serum creatinine < 1 mg/dL *could* be normal for some individuals, in the context of significant dehydration and prerenal azotemia, one would expect a **rise in serum creatinine** alongside BUN.
- The patient's condition, characterized by hypovolemia and decreased renal perfusion, leads to **elevated serum creatinine**.
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