GFR in pathophysiological states US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for GFR in pathophysiological states. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
GFR in pathophysiological states US Medical PG Question 1: A 55-year-old woman presents to a physician’s clinic for a diabetes follow-up. She recently lost weight and believes the diabetes is ‘winding down’ because the urinary frequency has slowed down compared to when her diabetes was "at its worst". She had been poorly compliant with medications, but she is now asking if she can decrease her medications as she feels like her diabetes is improving. Due to the decrease in urinary frequency, the physician is interested in interrogating her renal function. Which substance can be used to most accurately assess the glomerular filtration rate (GFR) in this patient?
- A. Para-aminohippurate (PAH)
- B. Glucose
- C. Inulin (Correct Answer)
- D. Urea
- E. Creatinine
GFR in pathophysiological states Explanation: ***Correct Answer: Inulin***
- **Inulin** is freely filtered by the glomeruli and is neither reabsorbed nor secreted by the renal tubules, making its clearance rate an **accurate measure of GFR**.
- It is considered the **gold standard** for GFR measurement, although it is not routinely used in clinical practice due to its exogenous nature and the need for continuous infusion.
*Incorrect: Para-aminohippurate (PAH)*
- **PAH** is both filtered and actively secreted by the renal tubules, meaning its clearance reflects **renal plasma flow**, not GFR.
- Due to its high extraction fraction, it is used to measure **effective renal plasma flow (ERPF)**.
*Incorrect: Glucose*
- **Glucose** is freely filtered by the glomeruli but is almost completely reabsorbed in the proximal convoluted tubule in healthy individuals, especially at normal blood glucose levels.
- Therefore, glucose clearance is typically **zero** and does not measure GFR.
*Incorrect: Urea*
- **Urea** is filtered by the glomeruli, but a significant portion is **reabsorbed** by the renal tubules, particularly in states of lower urine flow.
- Its clearance **underestimates GFR** and varies with hydration status and protein intake, making it an unreliable sole measure of GFR.
*Incorrect: Creatinine*
- **Creatinine** is freely filtered by the glomeruli, but a small amount is also **secreted** by the renal tubules, leading to an overestimation of GFR, especially in advanced kidney disease.
- Although commonly used as an **estimate of GFR** in clinical practice due to its endogenous production, it is not as accurate as inulin.
GFR in pathophysiological states US Medical PG Question 2: A 52-year-old man comes to the physician for a routine health maintenance examination. He feels well. His blood pressure is 125/70 mm Hg. His glomerular filtration rate is calculated to be 105 mL/min/1.73 m2 and glucose clearance is calculated to be 103 mL/min. This patient is most likely being treated with which of the following agents?
- A. Ifosfamide
- B. Acarbose
- C. Canagliflozin (Correct Answer)
- D. Glipizide
- E. Metformin
GFR in pathophysiological states Explanation: ***Canagliflozin***
- The key finding is that **glucose clearance (103 mL/min) approximately equals GFR (105 mL/min)**, indicating nearly complete failure of glucose reabsorption.
- **Canagliflozin** is an **SGLT2 inhibitor** that blocks the sodium-glucose cotransporter 2 in the proximal tubule, preventing glucose reabsorption.
- This causes filtered glucose to be excreted in urine, resulting in **glucose clearance approaching GFR** - exactly what is seen in this patient.
- SGLT2 inhibitors are increasingly used as first-line agents in Type 2 Diabetes, especially with cardiovascular or renal benefits.
*Metformin*
- **Metformin** is a biguanide that decreases hepatic gluconeogenesis and increases peripheral insulin sensitivity.
- It does **NOT affect renal glucose handling** or glucose clearance, which would remain near zero in patients on metformin.
- The elevated glucose clearance in this patient rules out metformin monotherapy.
*Ifosfamide*
- **Ifosfamide** is an alkylating chemotherapy agent used for cancer treatment, not diabetes management.
- It can cause **Fanconi syndrome** (proximal tubule dysfunction) leading to glycosuria, but this would also cause decreased GFR, proteinuria, and electrolyte abnormalities.
- This patient's normal GFR and otherwise normal presentation makes ifosfamide-induced toxicity unlikely.
*Acarbose*
- **Acarbose** is an alpha-glucosidase inhibitor that slows carbohydrate absorption in the intestine.
- It works in the **GI tract**, not the kidneys, and does not affect glucose clearance.
- It would not explain the elevated renal glucose excretion seen here.
*Glipizide*
- **Glipizide** is a sulfonylurea that stimulates pancreatic insulin release.
- It does **NOT affect renal glucose handling** and would not cause elevated glucose clearance.
- The patient's glucose clearance pattern is inconsistent with sulfonylurea therapy.
GFR in pathophysiological states US Medical PG Question 3: A 64-year-old African American female comes to the physician's office for a routine check-up. The patient's past medical history is significant for hypertension, diabetes, and osteoarthritis in her right knee. Her medications include metformin, glimepiride, lisinopril, metoprolol, hydrochlorothiazide, and ibuprofen as needed. Her only complaint is an unremitting cough that started about 3 weeks ago and she has noticed some swelling around her mouth. The drug most likely responsible for her recent symptoms causes its primary renal hemodynamic effect on which part of the kidney?
- A. Collecting duct
- B. Distal convoluted tubule
- C. Juxtaglomerular cells
- D. Efferent arteriole (Correct Answer)
- E. Afferent arteriole
GFR in pathophysiological states Explanation: ***Efferent arteriole***
- The patient's symptoms of an **unremitting cough** and **angioedema** (swelling around her mouth) are classic side effects of **ACE inhibitors**, such as **lisinopril**.
- ACE inhibitors primarily exert their renal hemodynamic effects by **dilating the efferent arteriole**, leading to a decrease in intraglomerular pressure and glomerular filtration rate.
*Collecting duct*
- The collecting duct is the primary site of action for **vasopressin (ADH)** and **aldosterone**, regulating water and sodium reabsorption, respectively.
- While other medications like **thiazides** (used by the patient) affect distal tubules and collecting ducts indirectly, their direct impact on the collecting duct is not the cause of angioedema or cough.
*Distal convoluted tubule*
- The distal convoluted tubule is the main site of action for **thiazide diuretics** (e.g., hydrochlorothiazide), which inhibit the Na-Cl cotransporter.
- This tubule segment is not directly involved in the mechanism leading to angioedema or cough caused by ACE inhibitors.
*Juxtaglomerular cells*
- Juxtaglomerular cells are responsible for producing **renin**, which is the initial step in the **renin-angiotensin-aldosterone system (RAAS)**.
- While ACE inhibitors block the conversion of angiotensin I to angiotensin II, they do not directly act on the juxtaglomerular cells themselves to cause their side effects.
*Afferent arteriole*
- The afferent arteriole is primarily regulated by **sympathetic tone** and local factors, and is the main site of action for medications like **NSAIDs** (e.g., ibuprofen, which the patient takes as needed).
- While NSAIDs cause **afferent arteriole constriction** and can impair renal function, they do not cause angioedema or a chronic cough.
GFR in pathophysiological states US Medical PG Question 4: 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)
GFR in pathophysiological states 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.
GFR in pathophysiological states US Medical PG Question 5: 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
GFR in pathophysiological states 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.
GFR in pathophysiological states US Medical PG Question 6: A 72-year-old male is brought from his nursing home to the emergency department for fever, chills, dyspnea, productive cough, and oliguria over the past 72 hours. He was in his normal state of health and slowly developed breathing problems and fever. His past medical history is significant for hepatitis C, hypertension, and hypercholesterolemia. His medications include bisoprolol, hydrochlorothiazide, and atorvastatin. Upon arrival to the ED, his blood pressure is 80/48 mm Hg, pulse is 120/min, a respiratory rate of 28/min, and body temperature of 39.0°C (102.2°F). Physical examination reveals decreased breathing sounds in the base of the left lung, along with increased vocal resonance, and pan-inspiratory crackles. The abdomen is mildly distended with a positive fluid wave. The patient's level of consciousness ranges from disoriented to drowsiness. He is transferred immediately to the ICU where vasoactive support is initiated. Laboratory tests show leukocytosis, neutrophilia with bands. Since admission 6 hours ago, the patient has remained anuric. Which of the following additional findings would you expect in this patient?
- A. Urine sodium > 40 mEq/L
- B. Urinary osmolality > 500 mOsmol/kg
- C. Urinary osmolality < 350 mOsmol/kg
- D. Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio <15:1
- E. Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio > 20:1 (Correct Answer)
GFR in pathophysiological states Explanation: ***Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio > 20:1***
- This patient is presenting with signs of **septic shock** (fever, hypotension, altered mental status, oliguria, leukocytosis) likely due to **pneumonia**. The prolonged hypotension and poor perfusion lead to **prerenal acute kidney injury (AKI)** that may be progressing to **acute tubular necrosis (ATN)**.
- In **prerenal AKI**, reduced renal perfusion leads to increased reabsorption of urea and water in the renal tubules, resulting in a **BUN:creatinine ratio greater than 20:1**. This elevated ratio persists even as the patient transitions to ATN.
- Given **6 hours of anuria** despite vasoactive support, this suggests significant renal injury, but the BUN:Cr ratio remains the most reliable finding at this stage.
*Urine sodium > 40 mEq/L*
- A urine sodium concentration greater than 40 mEq/L is typically seen in **intrinsic AKI** (e.g., acute tubular necrosis), where tubular damage impairs sodium reabsorption.
- While this patient may be developing ATN given the prolonged anuria, in the **early phase** of septic AKI with recent hypotension, the kidneys initially attempt to conserve sodium, resulting in **low urine sodium (<20 mEq/L)**.
*Urinary osmolality > 500 mOsmol/kg*
- A urinary osmolality above 500 mOsmol/kg indicates appropriately concentrated urine, which is a compensatory mechanism in **early prerenal AKI** as the kidneys try to conserve water.
- However, given this patient has been **anuric for 6 hours** despite ICU-level vasoactive support, the kidney injury has likely progressed beyond pure prerenal state. In established ATN, the concentrating ability is impaired, and urinary osmolality would be **closer to isotonic (<350 mOsmol/kg)** rather than highly concentrated.
- The **elevated BUN:Cr ratio** is more reliable in this mixed clinical picture.
*Urinary osmolality < 350 mOsmol/kg*
- A urinary osmolality less than 350 mOsmol/kg indicates inappropriately diluted urine, which is characteristic of **established intrinsic AKI (acute tubular necrosis)**, where the kidney's concentrating ability is impaired.
- While the patient may be progressing toward ATN, the **BUN:Cr ratio elevation** develops earlier and is the most expected finding at this presentation stage.
*Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio <15:1*
- A BUN:creatinine ratio less than 15:1 is typically seen in **intrinsic AKI after several days**, **normal renal function**, or conditions with decreased urea production.
- In this patient with septic shock and acute hypoperfusion leading to AKI, the ratio would be **elevated (>20:1)** due to enhanced urea reabsorption in the setting of decreased renal blood flow.
GFR in pathophysiological states US Medical PG Question 7: A new drug X is being tested for its effect on renal function. During the experiments, the researchers found that in patients taking substance X, the urinary concentration of sodium decreases while urine potassium concentration increase. Which of the following affects the kidneys in the same way as does substance X?
- A. Aldosterone (Correct Answer)
- B. Furosemide
- C. Spironolactone
- D. Atrial natriuretic peptide
- E. Hydrochlorothiazide
GFR in pathophysiological states Explanation: ***Aldosterone***
- **Aldosterone** acts on the **principal cells** of the **collecting duct** to increase sodium reabsorption and potassium secretion.
- This action leads to a decrease in urinary sodium concentration and an increase in urinary potassium concentration, matching the effects of drug X.
*Furosemide*
- **Furosemide** is a **loop diuretic** that inhibits the **Na-K-2Cl cotransporter** in the **thick ascending limb** of the loop of Henle.
- This inhibition leads to increased excretion of sodium, potassium, and water, resulting in higher urinary sodium concentration.
*Spironolactone*
- **Spironolactone** is an **aldosterone antagonist** that blocks aldosterone's effects on the collecting duct.
- This leads to increased sodium excretion and decreased potassium excretion (potassium-sparing effect), which is the opposite of drug X.
*Atrial natriuretic peptide*
- **Atrial natriuretic peptide (ANP)** is released in response to atrial stretch and causes **natriuresis** (increased sodium excretion) and **diuresis**.
- It works by dilating afferent arterioles and constricting efferent arterioles, increasing GFR, and inhibiting sodium reabsorption, thus increasing urinary sodium concentration.
*Hydrochlorothiazide*
- **Hydrochlorothiazide** is a **thiazide diuretic** that inhibits the **Na-Cl cotransporter** in the **distal convoluted tubule**.
- This leads to increased sodium and chloride excretion but typically causes potassium wasting (hypokalemia), which differs from the increased urinary potassium concentration seen with drug X.
GFR in pathophysiological states US Medical PG Question 8: A 58-year-old man presents to the Emergency Department after 3 hours of intense suprapubic pain associated with inability to urinate for the past day or two. His medical history is relevant for benign prostatic hyperplasia (BPH) that has been under treatment with prazosin and tadalafil. Upon admission, he is found to have a blood pressure of 180/100 mm Hg, a pulse of 80/min, a respiratory rate of 23/min, and a temperature of 36.5°C (97.7°F). He weighs 84 kg (185.1 lb) and is 175 cm (5 ft 7 in) tall. Physical exam, he has suprapubic tenderness. A bladder scan reveals 700 ml of urine. A Foley catheter is inserted and the urine is drained. Initial laboratory tests and their follow up 8 hours after admission are shown below.
Admission 8 hours after admission
Serum potassium 4.2 mmol/L Serum potassium 4.0 mmol/L
Serum sodium 140 mmol/L Serum sodium 142 mmol/L
Serum chloride 102 mmol/L Serum chloride 110 mmol/L
Serum creatinine 1.4 mg/dL Serum creatinine 1.6 mg/dL
Serum blood urea nitrogen 64 mg/dL Serum blood urea nitrogen 62 mg/dL
Urine output 250 mL Urine output 260 mL
A senior attending suggests a consultation with Nephrology. Which of the following best justifies this suggestion?
- A. Estimated glomerular filtration rate (eGFR)
- B. Urine output (Correct Answer)
- C. Serum creatinine (SCr)
- D. Serum blood urea nitrogen (BUN)
- E. Serum potassium
GFR in pathophysiological states Explanation: ***Urine output***
- The patient's **urine output is severely reduced** at 260 mL over 8 hours (approximately **32.5 mL/hour**), which constitutes **oliguria** (defined as <0.5 mL/kg/hr; this patient at 84 kg should produce ≥42 mL/hr).
- Despite **relief of the post-renal obstruction** via Foley catheterization, the persistent oliguria indicates **intrinsic kidney injury** rather than simple mechanical obstruction.
- The combination of **oliguria persisting after decompression** + **rising serum creatinine** (1.4→1.6 mg/dL) meets **KDIGO criteria for Stage 2 AKI** (urine output <0.5 mL/kg/hr for ≥12 hours).
- This requires **urgent nephrology consultation** to assess for acute tubular necrosis (ATN), guide fluid management during potential post-obstructive diuresis, and consider renal replacement therapy if oliguria worsens.
*Serum creatinine (SCr)*
- The serum creatinine **rose from 1.4 to 1.6 mg/dL** despite bladder decompression, which is concerning and suggests intrinsic renal injury.
- However, creatinine is a **lagging indicator** of kidney function - it takes 24-48 hours to reflect acute changes in GFR, whereas **urine output is a real-time indicator** of kidney function.
- While the rising creatinine supports the need for nephrology involvement, **urine output is the more immediate and actionable parameter** that prompted the attending's suggestion at this early time point.
*Estimated glomerular filtration rate (eGFR)*
- eGFR is **calculated from serum creatinine** using equations that assume steady-state conditions, which **do not apply in acute kidney injury**.
- In the **acute setting with rapidly changing kidney function**, eGFR calculations are unreliable and can significantly overestimate or underestimate true GFR.
- Clinicians rely more on **urine output and serial creatinine measurements** rather than eGFR when managing AKI.
*Serum blood urea nitrogen (BUN)*
- The BUN decreased slightly from 64 to 62 mg/dL, remaining elevated but showing minimal change after catheterization.
- Elevated BUN can reflect **pre-renal azotemia, dehydration, or upper GI bleeding** and is less specific for intrinsic kidney injury than oliguria.
- The **BUN:Cr ratio** is approximately 40:1 (64/1.6), suggesting a **pre-renal component**, but this alone doesn't justify urgent nephrology consultation as strongly as the persistent oliguria does.
*Serum potassium*
- Serum potassium levels remain **normal** (4.2→4.0 mmol/L) and do not indicate a metabolic emergency.
- While **hyperkalemia** is a common complication of AKI that would warrant nephrology involvement, this patient's potassium is well-controlled and not the driving concern at this time.
GFR in pathophysiological states US Medical PG Question 9: A 75-year-old woman is brought to a physician’s office by her son with complaints of diarrhea and vomiting for 1 day. Her stool is loose, watery, and yellow-colored, while her vomitus contains partially digested food particles. She denies having blood or mucus in her stools and vomitus. Since the onset of her symptoms, she has not had anything to eat and her son adds that she is unable to tolerate fluids. The past medical history is unremarkable and she does not take any medications regularly. The pulse is 115/min, the respiratory rate is 16/min, the blood pressure is 100/60 mm Hg, and the temperature is 37.0°C (98.6°F). The physical examination shows dry mucous membranes and slightly sunken eyes. The abdomen is soft and non-tender. Which of the following physiologic changes in glomerular filtration rate (GFR), renal plasma flow (RPF), and filtration fraction (FF) are expected?
- A. Decreased GFR, decreased RPF, decreased FF
- B. Decreased GFR, decreased RPF, no change in FF
- C. Increased GFR, increased RPF, increased FF
- D. Increased GFR, decreased RPF, increased FF
- E. Decreased GFR, decreased RPF, increased FF (Correct Answer)
GFR in pathophysiological states Explanation: ***Decreased GFR, decreased RPF, increased FF***
- Due to **dehydration** from diarrhea and vomiting, there is a decrease in blood volume leading to decreased renal blood flow and **renal plasma flow (RPF)**.
- The body responds to hypovolemia by activating the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, which cause **preferential efferent arteriolar constriction** (more than afferent constriction). This helps maintain glomerular hydrostatic pressure despite reduced renal perfusion.
- As a result, **GFR decreases** but proportionally **less than RPF decreases**, causing the **filtration fraction (FF = GFR/RPF) to increase**.
- In this patient with significant dehydration (tachycardia, hypotension, dry mucous membranes), both GFR and RPF are reduced, but FF is elevated due to compensatory mechanisms.
*Decreased GFR, decreased RPF, decreased FF*
- While GFR and RPF will decrease due to dehydration, the **filtration fraction is expected to increase**, not decrease.
- A decreased FF would imply GFR fell proportionally more than RPF, which contradicts the physiologic response where efferent arteriolar constriction helps preserve GFR relative to RPF.
*Decreased GFR, decreased RPF, no change in FF*
- With significant fluid loss and compensatory mechanisms (efferent arteriolar constriction via angiotensin II), a change in **filtration fraction** is expected.
- The body actively alters arteriolar tone to prioritize GFR maintenance, which directly increases FF.
*Increased GFR, increased RPF, increased FF*
- This pattern suggests **hypervolemia** or increased renal perfusion, which directly contradicts the patient's severe dehydration.
- Both GFR and RPF are expected to decrease in volume depletion, not increase.
*Increased GFR, decreased RPF, increased FF*
- An increase in GFR is physiologically impossible given the patient's severe volume depletion and reduced renal perfusion.
- While FF does increase in dehydration, this occurs in the context of **both GFR and RPF being decreased**, not with an increased GFR.
GFR in pathophysiological states US Medical PG Question 10: A 32-year-old man is brought to the Emergency Department after 3 consecutive days of diarrhea, fatigue and weakness. His stool has been soft and mucoid, with no blood stains. The patient just came back from a volunteer mission in Guatemala, where he remained asymptomatic. His personal medical history is unremarkable. Today his blood pressure is 98/60 mm Hg, pulse is 110/min, respiratory rate is 19/min, and his body temperature is 36.7°C (98.1°F). On physical exam, he has sunken eyes, dry mucosa, mild diffuse abdominal tenderness, and hyperactive bowel sounds. Initial laboratory tests are shown below:
Serum creatinine (SCr) 1.8 mg/dL
Blood urea nitrogen (BUN) 50 mg/dL
Serum sodium 132 mEq/L
Serum potassium 3.5 mEq/L
Serum chloride 102 mEq/L
Which of the following phenomena would you expect in this patient?
- A. Low urine osmolality, high FeNa+, high urine Na+
- B. High urine osmolality, high fractional excretion of sodium (FeNa+), high urine Na+
- C. Low urine osmolality, high FeNa+, low urine Na+
- D. High urine osmolality, low FeNa+, low urine Na+ (Correct Answer)
- E. Low urine osmolality, low FeNa+, high urine Na+
GFR in pathophysiological states Explanation: ***High urine osmolality, low FeNa+, low urine Na+***
- The patient exhibits signs of **dehydration** (hypotension, tachycardia, sunken eyes, dry mucosa) and **acute kidney injury (AKI)** with elevated BUN and creatinine, particularly a **BUN/creatinine ratio of 27.8** (50/1.8). These findings point to **prerenal AKI** due to hypovolemia from diarrhea.
- In prerenal AKI, the kidneys attempt to conserve water and sodium to restore intravascular volume. This leads to **increased ADH** secretion and **aldosterone**, resulting in **high urine osmolality** (concentrated urine), **low fractional excretion of sodium (FeNa+)** (<1%), and **low urine sodium concentration** (<20 mEq/L).
*Low urine osmolality, high FeNa+, high urine Na+*
- This pattern is typical of **acute tubular necrosis (ATN)**, an intrinsic cause of AKI, where tubular damage impairs the kidney's ability to concentrate urine and reabsorb sodium.
- The context of dehydration and prerenal state makes ATN less likely as the initial primary pathology compared to the body's compensatory mechanisms during hypovolemia.
*High urine osmolality, high fractional excretion of sodium (FeNa+), high urine Na+*
- This combination is generally contradictory. High urine osmolality suggests water conservation, while high FeNa+ and urine Na+ indicate sodium wasting, which would typically be seen in diuretic use or specific renal tubular disorders, not uncompensated hypovolemia.
- In prerenal AKI, the body actively reabsorbs sodium to expand volume, leading to low rather than high FeNa+ and urine Na+.
*Low urine osmolality, high FeNa+, low urine Na+*
- This combination is inconsistent. High FeNa+ and low urine Na+ do not usually occur together in a state of hypovolemia. If FeNa+ is high, it implies significant sodium excretion, which would typically be accompanied by higher urine Na+.
- Low urine osmolality also suggests impaired concentrating ability, which is not characteristic of the compensatory mechanisms in prerenal AKI.
*Low urine osmolality, low FeNa+, high urine Na+*
- This combination is also contradictory. Low urine osmolality with low FeNa+ and high urine Na+ does not align with typical kidney responses to dehydration or specific AKI etiologies.
- Low FeNa+ and high urine Na+ are conflicting, as low FeNa+ implies sodium conservation, while high urine Na+ indicates sodium excretion.
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