Nephrology Practice Questions

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.

Q: The best response to steroids is observed with –

Lipoid nephrosis. ***Lipoid nephrosis*** - Also known as **Minimal Change Disease**, it is the most common cause of **nephrotic syndrome in children** and responds very well to steroid therapy [1]. - The disease involves effacement of podocyte foot processes without significant visible damage under light microscopy, leading to increased glomerular permeability to protein, but the condition is highly responsive to **immunosuppression with corticosteroids** [1]. *Focal glomerulonephritis* - This term usually refers to **Focal Segmental Glomerulosclerosis (FSGS)**, which typically has a much poorer response to steroids compared to minimal change disease [1]. - While some variants of FSGS can respond to steroids, the response rate is significantly lower than that seen in lipoid nephrosis, and it often progresses to **end-stage renal disease**. *Membranous GN* - **Membranous glomerulonephritis** has a variable response to steroids, with some patients achieving remission but many requiring more aggressive immunosuppression or demonstrating steroid resistance. - It is characterized by **subepithelial immune complex deposition** and glomerular basement membrane thickening, which is a different pathological process from lipoid nephrosis. *Membranoproliferative GN* - **Membranoproliferative glomerulonephritis (MPGN)** typically responds poorly to corticosteroids and often requires more potent immunosuppressive agents or specific therapies depending on its underlying cause (e.g., complement-mediated). - MPGN involves mesangial and endothelial proliferation, along with characteristic changes in the glomerular basement membrane, indicating a more severe and less steroid-responsive form of glomerular injury.

Question 1

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 2

Which of following is not seen in nephritic syndrome -

Accepted Answer

Hypocholestremia

Answer

HTN

Answer

Hematuria

Answer

Edema

Question 3

Hypermagnesemia may be observed in:

Accepted Answer

Acute Kidney Injury

Answer

Hypothyroidism

Answer

Primary hypoparathyroidism

Answer

Adrenal insufficiency

Question 4

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 5

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 6

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 7

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

Accepted Answer

Coagulopathy

Answer

Microangiopathic hemolytic anemia

Answer

Renal insufficiency

Answer

Thrombocytopenia

Question 8

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 9

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

Accepted Answer

Hypocalcemia

Answer

Hypophosphatemia

Answer

Hypokalemia

Answer

Hyponatremia

Question 10

The best response to steroids is observed with –

Accepted Answer

Lipoid nephrosis

Answer

Focal glomerulonephritis

Answer

Membranous GN

Answer

Membranoproliferative GN

Nephrology — MCQs

Nephrology — MCQs

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