Nephrology Practice Questions

Q: A 45-year-old Caucasian male with a history of chronic myeloid leukemia for which he is receiving chemotherapy presents to the emergency room with oliguria and colicky left flank pain. His serum creatinine is 3.0 mg/dL and his urine pH is 5.0. You diagnose nephrolithiasis. His kidney stones, however, are not visible on abdominal x-ray. His stone is most likely composed of which of the following?

Uric acid. ***Uric acid*** - The patient has **chronic myeloid leukemia (CML)** and is receiving **chemotherapy**, which can cause a rapid turnover of cells, leading to **hyperuricemia** and the formation of uric acid stones. - Uric acid stones are **radiolucent** (not visible on X-ray) and are associated with a **low urine pH** (5.0 in this case). *Cystine* - Cystine stones are caused by a **genetic defect** in amino acid transport, leading to high urinary cystine levels. - While they are also **radiolucent**, there is no clinical information to suggest a genetic predisposition for cystinuria in this patient. *Calcium phosphate* - Calcium phosphate stones are typically **radio-opaque** and usually form in alkaline urine, which contradicts the patient's low urine pH [1]. - They are often associated with conditions like **renal tubular acidosis** or hyperparathyroidism [1]. *Magnesium ammonium phosphate* - These are also known as **struvite stones** and are highly suggestive of **urinary tract infections** with urea-splitting organisms (e.g., *Proteus*) [1]. - They tend to grow large, form **staghorn calculi**, and are **radio-opaque** [1]. *Calcium oxalate* - Calcium oxalate stones are the **most common type** of kidney stone and are **radio-opaque**, making them visible on X-ray. - They are typically associated with conditions causing **hypercalciuria** or hyperoxaluria, which are not explicitly indicated here, and they would be visible on the X-ray.

Q: A 77-year-old man with a history of advanced dementia, hypertension, Parkinson’s disease, and diabetes mellitus type 2 is brought to the hospital from a nursing home after several days of non-bloody diarrhea and vomiting. The patient is evaluated and admitted to the hospital. Physical examination shows a grade 2/6 holosystolic murmur over the left upper sternal border, clear lung sounds, a distended abdomen with normal bowel sounds, a resting tremor, and 2+ edema of the lower extremities up to the ankle. Over the next few hours, the nurse records a total of 21 cc of urine output over the past 5 hours. Which of the following criteria suggest pre-renal failure?

Fractional excretion of sodium of 0.5%. ***Fractional excretion of sodium of 0.5%*** - A **fractional excretion of sodium (FENa)** less than 1% is a hallmark of **pre-renal acute kidney injury (AKI)**, indicating that the kidneys are attempting to conserve sodium and water due to decreased renal perfusion. - In pre-renal failure, the kidneys are structurally intact but functionally impaired due to **hypoperfusion**, leading to increased reabsorption of sodium and water in an effort to restore circulating volume. *Urine/plasma creatinine ratio of 10* - A **urine/plasma creatinine ratio** of less than 15 is observed in **intrinsic renal failure**, not pre-renal failure. - In **pre-renal failure**, the ratio is typically **greater than 20**, reflecting the kidney's ability to concentrate urine. *Urine osmolarity of 280 mOsm/kg* - A **urine osmolarity** of 280 mOsm/kg is close to **plasma osmolarity** and suggests an inability to concentrate urine, which is characteristic of **intrinsic renal failure**, particularly acute tubular necrosis. - In **pre-renal failure**, the kidneys actively reabsorb water, leading to a **high urine osmolarity** (typically >500 mOsm/kg) [1]. *Urine Na of 80 mEq/L* - A **urine sodium** concentration of 80 mEq/L is high and indicates significant sodium excretion, which is typical of **intrinsic renal failure** due to tubular damage. - In **pre-renal failure**, the kidneys conserve sodium, resulting in a **low urine sodium concentration** (typically <20 mEq/L). *Urine/plasma osmolarity ratio of 0.8* - A **urine/plasma osmolarity ratio** of 0.8 indicates that the urine is less concentrated than plasma, suggesting impaired concentrating ability, which is seen in **intrinsic renal failure**. - In **pre-renal failure**, the kidneys actively conserve water, leading to a ratio **greater than 1.5**, indicating highly concentrated urine.

Q: MC cause of nephrotic syndrome in adults:-

Focal segmental glomerulosclerosis. **Focal segmental glomerulosclerosis** - **Focal segmental glomerulosclerosis (FSGS)** is the most common cause of **primary nephrotic syndrome in adults**, particularly in African Americans and individuals with HIV or obesity [1]. - It involves **scarring** of some glomeruli (focal) and only parts of affected glomeruli (segmental), leading to **proteinuria** and progression to end-stage renal disease [2]. *Minimal change disease* - While it is the most common cause of **nephrotic syndrome in children**, it accounts for a smaller proportion of adult cases [1]. - Characterized by normal-appearing glomeruli on light microscopy but **effacement of foot processes** on electron microscopy. *Good-pasture syndrome* - This is an **autoimmune disease** causing rapidly progressive glomerulonephritis, often associated with **pulmonary hemorrhage** [3]. - It is a much rarer cause of nephrotic syndrome and is characterized by **anti-GBM antibodies** [3]. *Membranous GN* - It is a common cause of **nephrotic syndrome in adults**, particularly in Caucasians, but **Focal Segmental Glomerulosclerosis (FSGS)** has surpassed it as the overall most common primary cause. - Characterized by thickening of the **glomerular basement membrane** due to immune complex deposition, often detected by **anti-PLA2R antibodies** [2].

Q: Which is the primary organ involved in Goodpasture syndrome?

Kidney. Kidney - Goodpasture syndrome is an autoimmune disease primarily characterized by the production of antibodies against the alpha-3 chain of type IV collagen in the glomerular basement membrane (GBM) and alveolar basement membrane [1]. - This leads to rapidly progressive glomerulonephritis and pulmonary hemorrhage, making the kidneys and lungs the main affected organs, with the kidneys being the primary and universally involved organ [1]. Adrenals - The adrenal glands are not directly involved in the pathogenesis or primary pathology of Goodpasture syndrome. - Conditions like Addison's disease or Cushing's syndrome affect the adrenals, which are distinct from Goodpasture syndrome. Liver - The liver is not a target organ for the antibodies involved in Goodpasture syndrome. - Diseases like autoimmune hepatitis or primary biliary cholangitis primarily affect the liver. Brain - The brain is not affected by the specific autoantibodies targeting type IV collagen in Goodpasture syndrome. - Neurological conditions such as vasculitis of the central nervous system or multiple sclerosis involve the brain.

Q: All the following are feature of polycystic disease of kidneys except:-

Erythrocytosis. Polycystic kidney disease (PKD) is an autosomal dominant condition where multiple cysts enlarge slowly, compressing and damaging surrounding kidney tissue [1]. ***Erythrocytosis*** - **Polycystic kidney disease (PKD)** typically leads to **anemia** due to reduced erythropoietin production by the damaged kidneys [2]. - **Erythrocytosis** (an abnormally high red blood cell count) is not a common feature of PKD; it is more often associated with conditions like **renal cell carcinoma** or certain chronic hypoxic states. *Renal failure* - **Progressive cyst growth** in PKD eventually destroys functional kidney tissue, leading to a decline in renal function and often culminating in **end-stage renal disease**, which occurs in about 50% of PKD1 patients [1]. - **Renal failure** is a common and serious complication of PKD, necessitating dialysis or kidney transplantation. *Hematuria* - **Cysts in PKD** can rupture into the collecting system, leading to **gross hematuria** (visible blood in urine) or microscopic hematuria [1]. - Trauma to the flank or infection within a cyst can trigger an episode of **hematuria** [1]. *Hypertension* - **Hypertension** is a very common early manifestation of PKD, often preceding any significant decline in glomerular filtration rate. - It results from activation of the **renin-angiotensin-aldosterone system (RAAS)** due to renal ischemia caused by cyst enlargement [1].

Q: Oliguria is defined as:-

Less than 400 ml of urine excreted in a day. ***Less than 400 ml of urine excreted in a day*** - Oliguria is clinically defined as **urine production** of less than **400-500 mL per 24 hours** in adults. - This reduction in urine output is often a critical sign of acute kidney injury or other underlying medical conditions impacting **renal function**. *More than 900 ml of urine excreted in a day* - This volume is within the normal range of **daily urine output** for an adult, which is typically between **800 mL and 2000 mL**. - It does not represent oliguria, which indicates a significantly **decreased urine production**. *Absence of urine production* - The complete absence of urine production is known as **anuria**, which is a more severe condition than oliguria. - Anuria is typically defined as less than **50 mL of urine per 24 hours**. *600 ml to 700 ml of urine excreted in a day* - While this volume is below the typical average, it does not meet the strict clinical definition of oliguria, which is typically set at **less than 400-500 mL/day**. - This range might be considered **borderline decreased** but is not severe enough to be classified as oliguric by most standards.

Q: Hyperkalemia means more than

5.5 mEq/l. ***5.5 mEq/l*** - **Hyperkalemia** is defined as a serum potassium level greater than **5.5 mEq/L** [1]. - This elevated level can lead to significant cardiac and neurological complications if not promptly addressed. *4.5 mEq/l* - A potassium level of 4.5 mEq/L falls within the normal physiological range for serum potassium, which is typically **3.5 to 5.0 mEq/L** [1]. - Therefore, this value does not indicate hyperkalemia. *10.5 mEq/l* - While 10.5 mEq/L is indeed an elevated potassium level, it represents **severe hyperkalemia**, far exceeding the general threshold for diagnosis. - The definition of hyperkalemia begins at a lower threshold of **5.5 mEq/L** [1]. *7.5 mEq/l* - A potassium level of 7.5 mEq/L indicates **moderate to severe hyperkalemia** and is a critical finding requiring immediate medical intervention [2]. - However, the initial threshold for defining hyperkalemia is **5.5 mEq/L**, making this option too high for the general definition [1].

Q: Which of these is least effective as first-line treatment for dangerous hyperkalemia?

Intravenous sodium bicarbonate. ***Intravenous sodium bicarbonate*** - While it can drive potassium into cells, its effect is often **delayed and unreliable** in acute, dangerous hyperkalemia, especially without concurrent acidosis. - Its efficacy is most pronounced when hyperkalemia is associated with **metabolic acidosis**, which is not always the primary driving factor of dangerous hyperkalemia. *Calcium chloride injection* - This is a **first-line treatment** for dangerous hyperkalemia, as it **stabilizes the cardiac membrane** by antagonizing the direct effects of potassium on myocardial excitability [1]. - It does not lower serum potassium levels but **protects the heart** from life-threatening arrhythmias, buying time for other therapies to reduce potassium [1]. *Beta-2 agonist (Salbutamol)* - **Beta-2 agonists** like salbutamol are effective in shifting potassium **intracellularly**, thereby lowering serum potassium levels. - This effect is mediated by stimulating the **Na+/K+-ATPase pump** on cell membranes. *Dialysis (Hemodialysis)* - **Hemodialysis** is the **most effective and rapid** method for removing excess potassium from the body, especially in cases of severe or refractory hyperkalemia. - It provides definitive treatment by directly **filtering potassium** from the blood, and is often considered when other measures fail or in patients with kidney failure.

Q: Which of the following is the earliest finding seen in Diabetic nephropathy?

Microalbuminuria. ***Microalbuminuria*** - **Microalbuminuria** is defined as the excretion of 30-300 mg of albumin in urine per 24 hours and is the **earliest detectable sign** of diabetic nephropathy, preceding overt proteinuria [1], [3]. - Early detection allows for interventions to slow the progression of kidney damage, such as **strict glycemic control** and **blood pressure management** with ACE inhibitors or ARBs [3]. *Hematuria* - **Hematuria** (blood in the urine) is not typically an early or primary finding in diabetic nephropathy [2]. - While it can occur in some kidney diseases, it is more characteristic of conditions like **glomerulonephritis** or **urinary tract infections** [4]. *Exudates* - **Exudates** refer to leakage of fluid, protein, or cells into tissues, often associated with inflammation or injury, and are not a measure of kidney function. - It's possible this term is being confused with **retinal exudates** (hard exudates) which are a finding in diabetic retinopathy, but not diabetic nephropathy. *Macroalbuminuria* - **Macroalbuminuria** (or overt proteinuria) is the excretion of more than 300 mg of albumin per 24 hours, indicating more advanced kidney damage. - It is a **later finding** than microalbuminuria in the progression of diabetic nephropathy, signifying established kidney disease [3].

Q: A 69-year-old man with a history of recurrent pancreatitis treated with corticosteroids now has increasing fatigue for 2 years. He does not drink alcohol and has no evidence of gallbladder disease. On examination, there are no abnormalities. Laboratory studies show his serum creatinine is 5 mg/dL and urea nitrogen is 48 mg/ dL. His serum IgG4 is elevated. Ultrasound imaging shows bilateral hydronephrosis. What is abdominal CT imaging most likely to show in this man?

Retroperitoneal fibrosis. ***Retroperitoneal fibrosis*** - The patient's history of **recurrent pancreatitis** treated with corticosteroids, elevated **IgG4**, and bilateral **hydronephrosis** strongly suggest IgG4-related sclerosing disease manifesting as retroperitoneal fibrosis [1]. - Abdominal CT would likely show a **soft tissue mass** encapsulating the great vessels and ureters, leading to ureteral obstruction and hydronephrosis. *Renal cell carcinoma* - While it can cause hydronephrosis if locally advanced, it typically presents as a **renal mass**, and is not associated with elevated IgG4 or recurrent pancreatitis in this manner. - Would not explain the classic features of a systemic **IgG4-related disease** or the symmetrical obstruction implied by bilateral hydronephrosis without a directly obstructing renal tumor. *Nephrolithiasis* - This would present with **renal colic** and typically show **calculi** on imaging, which is not indicated by the patient's symptoms or lab findings. - Bilateral hydronephrosis caused by stones would usually imply multiple or strategically placed stones, and would not be associated with a history of IgG4-related pancreatitis or the systemic features observed. *Polypoid cystitis* - This condition involves inflammation and **polypoid changes** in the bladder, typically causing irritative voiding symptoms or hematuria. - It would not explain the **bilateral hydronephrosis** or the systemic features like elevated IgG4 and recurrent pancreatitis that point to a broader systemic inflammatory process.

Question 1

A 45-year-old Caucasian male with a history of chronic myeloid leukemia for which he is receiving chemotherapy presents to the emergency room with oliguria and colicky left flank pain. His serum creatinine is 3.0 mg/dL and his urine pH is 5.0. You diagnose nephrolithiasis. His kidney stones, however, are not visible on abdominal x-ray. His stone is most likely composed of which of the following?

Accepted Answer

Uric acid

Answer

Cystine

Answer

Calcium phosphate

Answer

Magnesium ammonium phosphate

Answer

Calcium oxalate

Question 2

A 77-year-old man with a history of advanced dementia, hypertension, Parkinson’s disease, and diabetes mellitus type 2 is brought to the hospital from a nursing home after several days of non-bloody diarrhea and vomiting. The patient is evaluated and admitted to the hospital. Physical examination shows a grade 2/6 holosystolic murmur over the left upper sternal border, clear lung sounds, a distended abdomen with normal bowel sounds, a resting tremor, and 2+ edema of the lower extremities up to the ankle. Over the next few hours, the nurse records a total of 21 cc of urine output over the past 5 hours. Which of the following criteria suggest pre-renal failure?

Accepted Answer

Fractional excretion of sodium of 0.5%

Answer

Urine/plasma creatinine ratio of 10

Answer

Urine osmolarity of 280 mOsm/kg

Answer

Urine Na of 80 mEq/L

Answer

Urine/plasma osmolarity ratio of 0.8

Question 3

MC cause of nephrotic syndrome in adults:-

Accepted Answer

Focal segmental glomerulosclerosis

Answer

Minimal change disease

Answer

Good-pasture syndrome

Answer

Membranous GN

Question 4

Which is the primary organ involved in Goodpasture syndrome?

Accepted Answer

Kidney

Answer

Adrenals

Answer

Liver

Answer

Brain

Question 5

All the following are feature of polycystic disease of kidneys except:-

Accepted Answer

Erythrocytosis

Answer

Renal failure

Answer

Hematuria

Answer

Hypertension

Question 6

Oliguria is defined as:-

Accepted Answer

Less than 400 ml of urine excreted in a day

Answer

More than 900 ml of urine excreted in a day

Answer

Absence of urine production

Answer

600 ml to 700 ml of urine excreted in a day

Question 7

Hyperkalemia means more than

Accepted Answer

5.5 mEq/l

Answer

4.5 mEq/l

Answer

10.5 mEq/l

Answer

7.5 mEq/l

Question 8

Which of these is least effective as first-line treatment for dangerous hyperkalemia?

Accepted Answer

Intravenous sodium bicarbonate

Answer

Calcium chloride injection

Answer

Beta-2 agonist (Salbutamol)

Answer

Dialysis (Hemodialysis)

Question 9

Which of the following is the earliest finding seen in Diabetic nephropathy?

Accepted Answer

Microalbuminuria

Answer

Hematuria

Answer

Exudates

Answer

Macroalbuminuria

Question 10

A 69-year-old man with a history of recurrent pancreatitis treated with corticosteroids now has increasing fatigue for 2 years. He does not drink alcohol and has no evidence of gallbladder disease. On examination, there are no abnormalities. Laboratory studies show his serum creatinine is 5 mg/dL and urea nitrogen is 48 mg/ dL. His serum IgG4 is elevated. Ultrasound imaging shows bilateral hydronephrosis. What is abdominal CT imaging most likely to show in this man?

Accepted Answer

Retroperitoneal fibrosis

Answer

Renal cell carcinoma

Answer

Nephrolithiasis

Answer

Polypoid cystitis

Nephrology — MCQs

Nephrology — MCQs

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