Nephrology (CKD, glomerular diseases) US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Nephrology (CKD, glomerular diseases). These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Nephrology (CKD, glomerular diseases) US Medical PG Question 1: A 45-year-old woman comes to the physician because of a 3-month history of worsening fatigue, loss of appetite, itching of the skin, and progressive leg swelling. Although she has been drinking 2–3 L of water daily, she has been passing only small amounts of urine. She has type 1 diabetes mellitus, chronic kidney disease, hypertension, and diabetic polyneuropathy. Her current medications include insulin, torasemide, lisinopril, and synthetic erythropoietin. Her temperature is 36.7°C (98°F), pulse is 87/min, and blood pressure is 138/89 mm Hg. She appears pale. There is 2+ pitting edema in the lower extremities. Sensation to pinprick and light touch is decreased over the feet and legs bilaterally. Laboratory studies show:
Hemoglobin 11.4 g/dL
Leukocyte count 6000/mm3
Platelet count 280,000/mm3
Serum
Na+ 137 mEq/L
K+ 5.3 mEq/L
Cl− 100 mEq/L
HCO3− 20 mEq/L
Urea nitrogen 85 mg/dL
Creatinine 8 mg/dL
pH 7.25
Which of the following long-term treatments would best improve quality of life and maximize survival in this patient?
- A. Peritoneal dialysis
- B. Living donor kidney transplant (Correct Answer)
- C. Cadaveric kidney transplant
- D. Hemofiltration
- E. Fluid restriction
Nephrology (CKD, glomerular diseases) Explanation: ***Living donor kidney transplant***
- A **living donor kidney transplant** offers the best outcomes for **quality of life and survival** in eligible patients with end-stage renal disease (ESRD), particularly when compared to dialysis, due to better graft survival rates and reduced complications.
- The patient's symptoms (fatigue, itching, leg swelling, oliguria, high urea nitrogen, creatinine, hyperkalemia, metabolic acidosis) are consistent with **ESRD**, and while she has several comorbidities, she is not explicitly stated to have contraindications for transplantation.
*Peritoneal dialysis*
- While an effective treatment for ESRD, **dialysis generally provides lower quality of life** and survival benefits compared to successful kidney transplantation.
- She already has significant fluid overload symptoms and **oliguria**, making adequate fluid removal through peritoneal dialysis potentially challenging without strict management and impacting her overall well-being.
*Cadaveric kidney transplant*
- A **cadaveric kidney transplant** is a viable option and offers better outcomes than dialysis, but it generally has **poorer graft survival** and a longer wait time compared to a living donor transplant due to delayed graft function and cold ischemia time.
- Given the option, a **living donor transplant is superior** in terms of long-term outcomes and reduces the time spent on dialysis.
*Hemofiltration*
- **Hemofiltration is a form of renal replacement therapy**, similar to hemodialysis, often used in acute settings or for critically ill patients with severe fluid overload or electrolyte imbalances.
- While it can manage her symptoms, it is not a long-term treatment that **improves quality of life or maximizes survival** better than transplantation for ESRD.
*Fluid restriction*
- **Fluid restriction** is a supportive measure to manage fluid overload in patients with ESRD; however, it addresses symptoms rather than the underlying progressive renal failure.
- While necessary as part of supportive care, it does not offer a definitive long-term solution or improve survival for ESRD, which requires **renal replacement therapy or transplantation**.
Nephrology (CKD, glomerular diseases) US Medical PG Question 2: 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
Nephrology (CKD, glomerular diseases) 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.
Nephrology (CKD, glomerular diseases) US Medical PG Question 3: A 45-year-old man presents with a 3-day history of right-sided flank pain due to a lodged ureteral stone. What changes would be expected to be seen at the level of glomerular filtration?
- A. Increase in glomerular capillary oncotic pressure
- B. Increase in Bowman's space oncotic pressure
- C. Increase in filtration fraction
- D. Increase in Bowman's space hydrostatic pressure (Correct Answer)
- E. No change in filtration fraction
Nephrology (CKD, glomerular diseases) Explanation: ***Increase in Bowman's space hydrostatic pressure***
- A lodged ureteral stone causes **obstruction** of urine flow, leading to a backup of fluid in the renal tubules and eventually into **Bowman's space**.
- This increased fluid volume in Bowman's space directly raises its **hydrostatic pressure**, which opposes glomerular filtration, thereby reducing the net filtration pressure.
*Increase in glomerular capillary oncotic pressure*
- **Glomerular capillary oncotic pressure** primarily reflects the protein concentration within the glomerular capillaries, which would not be directly increased by a ureteral stone.
- This parameter typically rises when fluid is filtered out, increasing protein concentration in the remaining blood, but not as the initial insult from obstruction.
*Increase in Bowman's space oncotic pressure*
- **Bowman's space oncotic pressure** is normally very low because the glomerular filtration barrier prevents significant protein filtration.
- An increase in this pressure would imply increased protein leakage into Bowman's space, which is not a direct consequence of a ureteral obstruction.
*Increase in filtration fraction*
- The **filtration fraction** is the ratio of glomerular filtration rate (GFR) to renal plasma flow.
- Ureteral obstruction typically **decreases GFR** due to increased Bowman's space hydrostatic pressure, which would lead to a reduction, not an increase, in the filtration fraction, assuming renal plasma flow remains stable or slightly reduced.
*No change in filtration fraction*
- Ureteral obstruction significantly impacts the forces driving glomerular filtration, primarily by increasing **Bowman's space hydrostatic pressure**.
- This change inevitably leads to a **decrease in GFR**, thus altering the filtration fraction, meaning it would not remain unchanged.
Nephrology (CKD, glomerular diseases) US Medical PG Question 4: 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)
Nephrology (CKD, glomerular diseases) 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.
Nephrology (CKD, glomerular diseases) US Medical PG Question 5: 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
Nephrology (CKD, glomerular diseases) 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.
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