Nephrology Practice Questions

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.

Q: Characteristic feature of Goodpasture's syndrome?

Serum antibodies against alpha 3 NC 1 domain of collagen-IV. ***Serum antibodies against alpha 3 NC 1 domain of collagen-IV*** - Goodpasture's syndrome is characterized by the presence of **autoantibodies** specifically targeting the **alpha 3 non-collagenous 1 (NC1) domain of type IV collagen**, found in the glomerular and alveolar basement membranes. - These antibodies lead to a **rapidly progressive glomerulonephritis** and often **pulmonary hemorrhage** [1]. *Anti DNAse antibodies positive* - **Anti-DNase B antibodies** are typically associated with **post-streptococcal glomerulonephritis**, not Goodpasture's syndrome. - While post-streptococcal glomerulonephritis can cause kidney damage, it has a different immunological mechanism and target antigens. *Serum antibodies against alpha 1 NC 1 domain of collagen III* - Antibodies against **collagen III** are not characteristic of Goodpasture's syndrome. - Goodpasture's disease specifically targets type IV collagen, which forms a crucial component of basement membranes. *Lumpy-bumpy deposits on immunofluorescence* - **Lumpy-bumpy deposits** on immunofluorescence are characteristic of **immune complex-mediated glomerulonephritis**, such as **post-streptococcal glomerulonephritis** [2]. - In contrast, Goodpasture's syndrome typically shows a **linear pattern of IgG deposition** along the glomerular basement membrane due to the direct binding of autoantibodies [2].

Q: Which of following is not seen in nephritic syndrome -

Hypocholestremia. ***Hypocholestremia*** - **Hypocholesterolemia** (low cholesterol) is not characteristic of nephritic syndrome; rather, **hypercholesterolemia** is a feature often associated with nephrotic syndrome [1] due to increased hepatic lipoprotein synthesis. - Nephritic syndrome is primarily associated with **inflammation** and **glomerular damage**, leading to hematuria, proteinuria, and renal impairment [1], without directly causing hypocholesterolemia. *HTN* - **Hypertension** is a common finding in nephritic syndrome due to fluid retention [2] and activation of the **renin-angiotensin-aldosterone system** (RAAS) resulting from impaired renal function. - The inflammatory damage to the glomeruli reduces the kidney's ability to excrete sodium and water, contributing to elevated blood pressure. *Hematuria* - **Hematuria** (blood in the urine), often macroscopic or microscopic, is a hallmark of nephritic syndrome due to the inflammatory damage to the **glomerular basement membrane**, allowing red blood cells to leak into the urine [1]. - The presence of **red blood cell casts** in the urine strongly indicates a nephritic process. *Edema* - **Edema** (swelling), particularly periorbital and peripheral, is frequently observed in nephritic syndrome as a result of **sodium and water retention** by the impaired kidneys [1][2]. - This fluid overload occurs even with relatively modest proteinuria, differentiating it from the more severe edema seen in nephrotic syndrome which is primarily due to hypoalbuminemia.

Q: Hypermagnesemia may be observed in:

Acute Kidney Injury. ***Acute Kidney Injury*** - When the kidneys are unable to adequately excrete excess magnesium, it accumulates in the body, leading to **hypermagnesemia**. - This is a common cause of hypermagnesemia, especially in patients who are also receiving **magnesium-containing medications** (e.g., antacids, laxatives). *Hypothyroidism* - Hypothyroidism is typically associated with **hypo**magnesemia due to altered renal handling and increased urinary excretion. - It is also commonly linked with **hypo**calcemia. *Primary hypoparathyroidism* - Primary hypoparathyroidism is characterized by **decreased parathyroid hormone (PTH)**, leading to **hypocalcemia** [1] and often **hyperphosphatemia**. - Magnesium levels are typically normal or slightly reduced, as PTH plays a role in magnesium reabsorption in the tubule [2]. *Adrenal insufficiency* - Adrenal insufficiency (Addison's disease) is characterized by a deficiency in mineralocorticoids, leading to **hyponatremia** and **hyperkalemia**. - Magnesium levels are usually normal or can be slightly elevated due to hemoconcentration, but it is not a direct cause of significant hypermagnesemia.

Q: In which of the following condition normal anion gap metabolic acidosis is seen?

Diarrhoea. ***Diarrhoea*** - Diarrhoea causes a loss of **bicarbonate-rich fluid** from the gastrointestinal tract [2]. - This loss leads to an increase in **serum chloride** to maintain electroneutrality, resulting in a normal anion gap metabolic acidosis. *Lactic acidosis* - Lactic acidosis results from the overproduction or under-elimination of **lactic acid** [1]. - Lactic acid is an **unmeasured anion**, leading to an **increased anion gap** metabolic acidosis. *Diabetic ketoacidosis* - Diabetic ketoacidosis involves the accumulation of **ketone bodies** (beta-hydroxybutyrate, acetoacetate), which are unmeasured anions [2]. - This accumulation causes an **increased anion gap** metabolic acidosis. *Renal failure* - Chronic renal failure can cause metabolic acidosis through the retention of **phosphate** and **sulfate**, which are unmeasured anions [2]. - This typically results in an **increased anion gap** metabolic acidosis, although some forms of renal tubular acidosis can cause a normal anion gap [1].

Q: Cystinuria is characterised by –

Recurrent urinary caliculi. Cystinuria is characterised by – ***Recurrent urinary calculi*** - **Cystinuria** is a genetic disorder of amino acid transport characterized by impaired reabsorption of **cystine** and other dibasic amino acids in the renal tubules. - The elevated urinary concentration of poorly soluble **cystine** leads to the formation of **cystine stones** in the urinary tract, causing recurrent urinary calculi. *Generalised aminoaciduria* - While cystinuria involves an aminoaciduria, it is specifically for **dibasic amino acids** (cystine, ornithine, lysine, and arginine), not a generalized aminoaciduria. - Generalized aminoaciduria would imply increased excretion of many different amino acids, which is not the primary feature of cystinuria. *Systemic acidosis* - **Systemic acidosis** is not a primary characteristic of cystinuria; the disorder mainly affects amino acid transport and stone formation. - Conditions like **renal tubular acidosis** can cause systemic acidosis, but this is a distinct pathology from cystinuria. *Deposition of cystine crystals in Renal tubular cells* - Cystinuria involves the **impaired reabsorption** and **excretion** of cystine in the urine, leading to stone formation in the urinary tract. - The crystals typically form in the **urine** and urinary tract lumen, not as intracellular deposits within renal tubular cells.

Q: Low complement levels are seen in:

All of the above. ***All of the above*** - **Low complement levels** are a characteristic feature of several immune-mediated conditions, including **MPGN**, **Infective endocarditis**, and **PSGN**. - Complement activation and consumption, often due to **immune complex formation** [1], lead to depleted complement protein levels. *MPGN (Membranoproliferative glomerulonephritis)* - **MPGN types I and III** are strongly associated with **hypocomplementemia** due to chronic activation and consumption of the complement system [2]. - This is often driven by **circulating immune complexes** or, in type II, by **C3 nephritic factor** causing persistent C3 convertase activity. *Infective endocarditis* - **Immune complex formation** in infective endocarditis can lead to complement activation and subsequent **reduction in C3 and C4 levels** [1]. - This hypocomplementemia is particularly noted in cases with **glomerulonephritis** secondary to infective endocarditis. *PSGN (Post-streptococcal glomerulonephritis)* - **PSGN** is typically characterized by transient but significant **low C3 levels** due to classical and alternative pathway activation by immune complexes containing streptococcal antigens [1]. - **C4 levels** are usually normal or only mildly decreased, distinguishing it from conditions with widespread C1q, C4, and C2 activation.

Q: Which is not included in the triad of hemolytic uremic syndrome?

Coagulopathy. ***Coagulopathy*** - While bleeding and clotting abnormalities can occur in severe cases due to multiple organ dysfunction, **coagulopathy is not a primary component** of the classic HUS triad. [1] - The classic triad focuses on specific hematologic and renal manifestations rather than broader coagulation defects. *Microangiopathic hemolytic anemia* - This is a core component of the HUS triad, characterized by **mechanical destruction of red blood cells** in small blood vessels. [1][2] - It leads to schistocytes on peripheral blood smear and signs of hemolysis, such as elevated **LDH** and **indirect bilirubin**. *Renal insufficiency* - This is a hallmark feature of HUS, caused by widespread **thrombi in the renal microvasculature** leading to kidney injury. [1][2] - It manifests as elevated creatinine, reduced urine output, and potentially acute kidney failure requiring dialysis. *Thrombocytopenia* - This is an essential component of the HUS triad, resulting from the **consumption of platelets** in the formation of microthrombi within small blood vessels. [1][2] - It leads to a low platelet count, increasing the risk of bleeding.

Q: Episodic generalized weakness can occur due to all of the following acute electrolyte disturbances, EXCEPT:

Hypocalcemia. ***Hypocalcemia*** - While hypocalcemia can cause symptoms like **tetany**, muscle cramps, and paresthesias, it typically does not manifest as **episodic generalized weakness** in the same way that other electrolyte disturbances do. - Its neuromuscular effects are primarily due to increased neuromuscular excitability rather than generalized muscle weakness. *Hypophosphatemia* - Severe hypophosphatemia can lead to **generalized muscle weakness** due to impaired ATP production and cellular energy. - This weakness can be profound and include **rhabdomyolysis** in severe cases, making it a cause of acute generalized weakness. *Hypokalemia* - Low potassium levels can cause **muscle weakness** ranging from mild to severe, including paralysis, due to its critical role in muscle cell membrane potential and neuromuscular function. - This can be episodic, especially in conditions like **hypokalemic periodic paralysis**. *Hyponatremia* - Acute hyponatremia can cause rapid fluid shifts into cells, including muscle cells, leading to **generalized weakness**, lethargy, and altered mental status. - This can be episodic depending on the cause of the acute drop in sodium levels.

Question 1

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

Question 2

Characteristic feature of Goodpasture's syndrome?

Accepted Answer

Serum antibodies against alpha 3 NC 1 domain of collagen-IV

Answer

Anti DNAse antibodies positive

Answer

Serum antibodies against alpha 1 NC 1 domain of collagen III

Answer

Lumpy-bumpy deposits on immunofluorescence

Question 3

Which of following is not seen in nephritic syndrome -

Accepted Answer

Hypocholestremia

Answer

HTN

Answer

Hematuria

Answer

Edema

Question 4

Hypermagnesemia may be observed in:

Accepted Answer

Acute Kidney Injury

Answer

Hypothyroidism

Answer

Primary hypoparathyroidism

Answer

Adrenal insufficiency

Question 5

In which of the following condition normal anion gap metabolic acidosis is seen?

Accepted Answer

Diarrhoea

Answer

Lactic acidosis

Answer

Diabetic ketoacidosis

Answer

Renal failure

Question 6

Cystinuria is characterised by –

Accepted Answer

Recurrent urinary caliculi

Answer

Generalised aminoaciduria

Answer

Systemic acidosis

Answer

Deposition of cystine crystals in Renal tubular cells

Question 7

Low complement levels are seen in:

Accepted Answer

All of the above

Answer

MPGN (Membranoproliferative glomerulonephritis)

Answer

Infective endocarditis

Answer

PSGN (Post-streptococcal glomerulonephritis)

Question 8

Which is not included in the triad of hemolytic uremic syndrome?

Accepted Answer

Coagulopathy

Answer

Microangiopathic hemolytic anemia

Answer

Renal insufficiency

Answer

Thrombocytopenia

Question 9

What is the most common immunosuppressant regimen used in renal transplant for maintenance?

Accepted Answer

Calcineurin inhibitors + Purine antagonists + Glucocorticoids

Answer

Calcineurin inhibitors + Purine antagonists + Basliximab

Answer

Glucocorticoids + Cyclophosphamide

Answer

Cyclophosphamide + Purine antagonists + Glucocorticoids

Question 10

Episodic generalized weakness can occur due to all of the following acute electrolyte disturbances, EXCEPT:

Accepted Answer

Hypocalcemia

Answer

Hypophosphatemia

Answer

Hypokalemia

Answer

Hyponatremia

Nephrology — MCQs

Nephrology — MCQs

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