Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 661: Characteristic feature of Goodpasture's syndrome?

A. Anti DNAse antibodies positive
B. Serum antibodies against alpha 1 NC 1 domain of collagen III
C. Serum antibodies against alpha 3 NC 1 domain of collagen-IV (Correct Answer)
D. Lumpy-bumpy deposits on immunofluorescence

Explanation: ***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].

Question 662: Which of following is not seen in nephritic syndrome -

A. HTN
B. Hypocholestremia (Correct Answer)
C. Hematuria
D. Edema

Explanation: ***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.

Question 663: Hypermagnesemia may be observed in:

A. Hypothyroidism
B. Primary hypoparathyroidism
C. Acute Kidney Injury (Correct Answer)
D. Adrenal insufficiency

Explanation: ***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.

Question 664: In which of the following condition normal anion gap metabolic acidosis is seen?

A. Lactic acidosis
B. Diabetic ketoacidosis
C. Diarrhoea (Correct Answer)
D. Renal failure

Explanation: ***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].

Question 665: In Henoch–Schönlein purpura, renal involvement is generally not seen if there is no involvement by:

A. 3 month after onset
B. 1 month after onset
C. 4 month after onset (Correct Answer)
D. 2 month after onset

Explanation: ***4 month after onset*** - Renal involvement in **Henoch-Schönlein Purpura (HSP)** typically manifests within the first 4 to 6 weeks of disease onset. - If **renal complications** have not appeared by 4 months, it is highly unlikely they will develop later. *3 month after onset* - While most renal involvement occurs earlier, waiting until 3 months may miss some cases, as the window extends slightly beyond this. - The critical period for **HSP nephritis** is usually considered to be within the first 6-8 weeks. *1 month after onset* - This period is too short to completely rule out renal involvement, as some cases may still emerge between 1 and 4 months. - Many patients, especially children, can develop **renal complications** even after the first month. *2 month after onset* - Similar to the 1-month mark, 2 months is still within the active window where **HSP nephritis** can develop. - The risk significantly decreases after this point, but it's not completely negligible until later.

Question 666: Cystinuria is characterised by –

A. Generalised aminoaciduria
B. Recurrent urinary caliculi (Correct Answer)
C. Systemic acidosis
D. Deposition of cystine crystals in Renal tubular cells

Explanation: 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.

Question 667: Which is not included in the triad of hemolytic uremic syndrome?

A. Coagulopathy (Correct Answer)
B. Microangiopathic hemolytic anemia
C. Renal insufficiency
D. Thrombocytopenia

Explanation: ***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.

Question 668: What is the most common immunosuppressant regimen used in renal transplant for maintenance?

A. Calcineurin inhibitors + Purine antagonists + Basliximab
B. Glucocorticoids + Cyclophosphamide
C. Cyclophosphamide + Purine antagonists + Glucocorticoids
D. Calcineurin inhibitors + Purine antagonists + Glucocorticoids (Correct Answer)

Explanation: ***Calcineurin inhibitors + Purine antagonists + Glucocorticoids*** - This triple therapy regimen is the **most common and effective** approach for long-term maintenance immunosuppression in renal transplant recipients [1]. - **Calcineurin inhibitors** (e.g., tacrolimus, cyclosporine) are the cornerstone for preventing T-cell activation, **purine antagonists** (e.g., mycophenolate mofetil, azathioprine) inhibit lymphocyte proliferation, and **glucocorticoids** provide broad anti-inflammatory effects [1]. *Calcineurin inhibitors + Purine antagonists + Basliximab* - **Basiliximab** is typically used for **induction therapy** (immediately post-transplant) to prevent acute rejection by blocking the IL-2 receptor, not as a long-term maintenance component. - The standard maintenance regimen *replaces* induction agents like basiliximab with a long-term steroid or calcineurin inhibitor alongside a purine antagonist. *Glucocorticoids + Cyclophosphamide* - **Cyclophosphamide** is a potent alkylating agent primarily used in specific autoimmune diseases or certain cancers, and its use in transplant is generally limited to cases of organ rejection resistant to standard therapy due to its significant toxicity. - This combination is **not a standard maintenance regimen** for renal transplant due to the high toxicity and side effects of cyclophosphamide. *Cyclophosphamide + Purine antagonists + Glucocorticoids* - As mentioned, **cyclophosphamide** is not a first-line agent for maintenance immunosuppression in renal transplant due to its severe side effect profile, including myelosuppression and hemorrhagic cystitis. - While purine antagonists and glucocorticoids are components of maintenance therapy, the inclusion of cyclophosphamide makes this an **uncommon and usually unfavorable regimen** for long-term use.

Question 669: The best response to steroids is observed with –

A. Focal glomerulonephritis
B. Lipoid nephrosis (Correct Answer)
C. Membranous GN
D. Membranoproliferative GN

Explanation: ***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 670: What is the most common cause of normal anion gap metabolic acidosis?

A. Ingestion of ammonium chloride
B. Lactic acidosis
C. Ethylene glycol intoxication
D. Renal tubular acidosis
E. Salicylate intoxication
F. External pancreatic drainage
. Diarrhoea (Correct Answer)
. Chronic renal failure
. Methanol/Formaldehyde intoxication
. Uterosigmoidostomy
. Ketoacidosis

Explanation: ***Diarrhoea*** - Diarrhoea causes a **loss of bicarbonate** from the gastrointestinal tract, leading to a **normal anion gap metabolic acidosis** [2]. - The loss of bicarbonate is compensated by an **increase in chloride reabsorption** in the kidneys, maintaining a normal anion gap. *Ingestion of ammonium chloride* - Ingestion of ammonium chloride leads to **hyperchloremic metabolic acidosis** by contributing to a net gain of hydrogen ions. - While it causes a normal anion gap metabolic acidosis, it is **not the most common cause** in clinical practice. *Lactic acidosis* - Lactic acidosis results from the accumulation of **lactic acid**, an unmeasured anion, leading to a **high anion gap metabolic acidosis** [1]. - This typically occurs in conditions of **tissue hypoxia** or impaired lactate metabolism [1]. *Ethylene glycol intoxication* - Ethylene glycol metabolism produces various organic acids (e.g., **glycolic acid, oxalic acid**), which are unmeasured anions, causing a **high anion gap metabolic acidosis**. - It is often associated with acute **kidney injury** and neurological symptoms. *Renal tubular acidosis* - Renal tubular acidosis (RTA) involves impaired acid excretion or bicarbonate reabsorption by the kidneys, resulting in a **normal anion gap metabolic acidosis** [1]. - While a significant cause, it is **less common globally** than diarrhoea as a cause of normal anion gap metabolic acidosis. *Salicylate intoxication* - Salicylate intoxication initially causes **respiratory alkalosis** due to central respiratory stimulation [1]. - At toxic levels, it can lead to **high anion gap metabolic acidosis** due to the accumulation of organic acids and uncoupling of oxidative phosphorylation. *External pancreatic drainage* - External pancreatic drainage can lead to significant **bicarbonate loss**, as pancreatic fluid is rich in bicarbonate. - This loss causes a **normal anion gap metabolic acidosis**, similar to severe diarrhoea. *Chronic renal failure* - Chronic renal failure can cause metabolic acidosis, but it's typically a **high anion gap metabolic acidosis** due to the accumulation of unexcreted organic acids (e.g., phosphates, sulfates). - In earlier stages, or when accompanied by specific renal tubular defects, it can sometimes present as normal anion gap acidosis. *Methanol/Formaldehyde intoxication* - Methanol and formaldehyde intoxication lead to **high anion gap metabolic acidosis** due to their metabolism into highly toxic substances like **formic acid**. - These are characterized by severe systemic toxicity and visual disturbances. *Uterosigmoidostomy* - Uterosigmoidostomy involves diverting urine into the sigmoid colon, allowing for the reabsorption of **chloride** and the loss of **bicarbonate** from the body. - This results in a **normal anion gap metabolic acidosis**, also known as **hyperchloremic metabolic acidosis**. *Ketoacidosis* - Ketoacidosis (e.g., diabetic ketoacidosis, alcoholic ketoacidosis) is characterized by the overproduction of **ketoacids** (beta-hydroxybutyrate, acetoacetate). - These are unmeasured anions, leading to a prominent **high anion gap metabolic acidosis**.

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Acute Kidney Injury

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Chronic Kidney Disease

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Glomerular Diseases

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Tubulointerstitial Diseases

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Nephrotic and Nephritic Syndromes

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Urinary Tract Infections

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Renal Replacement Therapy

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Fluid and Electrolyte Disorders

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Acid-Base Disorders

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Kidney in Systemic Diseases

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Kidney Stones and Obstructive Uropathy

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Hypertension in Kidney Disease

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Nephrology — MCQs

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