Glomerular Diseases Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Glomerular Diseases. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Glomerular Diseases Indian Medical PG Question 1: All are seen in Nephrotic syndrome except
- A. Atherosclerosis
- B. Thrombo-embolism
- C. Lipiduria
- D. Increased protein C levels (Correct Answer)
Glomerular Diseases Explanation: ***Increased protein C levels***
- In **nephrotic syndrome**, there is an **increased urinary loss of anticoagulant proteins**, including **Protein C** and **Protein S**, leading to a state of **hypercoagulability**. [1]
- Therefore, **Protein C levels are decreased**, not increased, making this the exception.
*Atherosclerosis*
- **Hyperlipidemia**, a hallmark of nephrotic syndrome, contributes significantly to **accelerated atherosclerosis** due to dysregulation of lipid metabolism.
- The increased levels of **LDL cholesterol** and other lipoproteins promote plaque formation and arterial stiffening.
*Thrombo-embolism*
- Patients with nephrotic syndrome are at a significantly **increased risk of thromboembolic events**, such as deep vein thrombosis and pulmonary embolism, due to a **hypercoagulable state**.
- This state results from the **urinary loss of anticoagulant proteins** (e.g., antithrombin III, Protein C, Protein S) and increased levels of procoagulant factors (e.g., fibrinogen, factor V, factor VIII).
*Lipiduria*
- **Lipiduria**, the presence of lipids in the urine, is a characteristic feature of nephrotic syndrome, often manifested as **oval fat bodies** and **fatty casts**. [1]
- This occurs due to the increased glomerular permeability that allows lipoproteins to filter into the urine. [1]
Glomerular Diseases Indian Medical PG Question 2: Which of the following is the LEAST common characteristic of nephrotic syndrome?
- A. Lipiduria (Correct Answer)
- B. Hyperlipidemia
- C. Hypoalbuminemia
- D. Proteinuria > 3.5 gm per 1.73 m2 per 24 hours
Glomerular Diseases Explanation: ***Lipiduria***
- While lipiduria can occur in nephrotic syndrome, particularly with **severe proteinuria**, it is not a universally present clinical diagnostic criterion.
- Its presence is a consequence of lipoprotein filtration rather than a direct defining feature of the syndrome itself.
*Hypoalbuminemia*
- This is a cardinal feature, defined as **serum albumin < 3.0 g/dL**, resulting from significant urinary protein loss.
- It drives the generalized edema characteristic of nephrotic syndrome by reducing plasma oncotic pressure [1].
*Hyperlipidemia*
- This is a very common characteristic due to increased hepatic synthesis of lipoproteins and decreased catabolism, often presenting as elevated **cholesterol and triglycerides**.
- It is a risk factor for cardiovascular complications in nephrotic patients [1].
*Proteinuria > 3.5 gm per 1.73 m2 per 24 hours*
- This is the **defining feature** of nephrotic syndrome, indicating significant damage to the glomerular filtration barrier [1].
- Massive proteinuria leads to the other key clinical manifestations of the syndrome.
Glomerular Diseases Indian Medical PG Question 3: An asymptomatic patient has proteinuria and hematuria that is glomerular in origin on a routine urinalysis. Which of the following is the most likely diagnosis?
- A. immunoglobulin A (IgA) nephropathy (Berger's disease) (Correct Answer)
- B. diabetes mellitus (DM) - nephropathy
- C. amyloidosis - nephropathy
- D. focal glomerulosclerosis - nephropathy
Glomerular Diseases Explanation: ***immunoglobulin A (IgA) nephropathy (Berger's disease)***
- **IgA nephropathy** often presents with **asymptomatic gross or microscopic hematuria** and proteinuria, which can be glomerular in origin [1].
- It is one of the most common causes of **glomerular hematuria** and can be discovered incidentally on routine urinalysis [1].
*diabetes mellitus (DM) - nephropathy*
- While **diabetic nephropathy** causes proteinuria, **hematuria is not a primary or prominent feature** in the early stages; it typically presents with progressive proteinuria and kidney function decline [2].
- Patients with **diabetic nephropathy** are usually symptomatic with **long-standing diabetes** and often associated complications.
*amyloidosis - nephropathy*
- **Nephropathy due to amyloidosis** primarily presents with **heavy proteinuria**, leading to **nephrotic syndrome**, but hematuria is uncommon.
- Systemic amyloidosis often involves other organs, and patients typically present with other associated symptoms like **fatigue, weight loss, or organ dysfunction**.
*focal glomerulosclerosis - nephropathy*
- **Focal segmental glomerulosclerosis (FSGS)** typically presents with **nephrotic syndrome** (heavy proteinuria, edema, hypoalbuminemia), with microscopic hematuria being inconsistent and often mild.
- While it can be primary (idiopathic), it more commonly presents with symptoms of **nephrotic range proteinuria** rather than isolated asymptomatic hematuria and proteinuria.
Glomerular Diseases Indian Medical PG Question 4: In glomerulus subendothelial deposits are seen in?
- A. Goodpasture syndrome (linear IgG deposits in the basement membrane)
- B. MPGN type I (subendothelial deposits) (Correct Answer)
- C. MPGN type II (intramembranous deposits)
- D. IgA nephropathy (mesangial IgA deposits)
Glomerular Diseases Explanation: ***MPGN type I***
- **Subendothelial deposits** are a hallmark of MPGN type I, often associated with **immune complex deposition** [1].
- This condition can present with **hematuria**, **proteinuria**, and can be triggered by infections or autoimmune diseases [1].
*Good pasture syndrome*
- Primarily involves **anti-GBM antibodies** leading to **glomerulonephritis** and pulmonary hemorrhage, not subendothelial deposits.
- Typically, it presents with **crescent formation** in the glomeruli rather than deposits.
*MPGN type II*
- Characterized by **dense deposit disease**, it features **intramembranous** rather than subendothelial deposits [1].
- It is often associated with **C3 nephritic factor** and does not show classic subendothelial pathology.
*IgA nephropathy*
- Characterized by **IgA deposits** primarily in the **mesangium**, not subendothelially.
- It presents with **hematuria** and recurrent episodes of **macrohematuria**, especially after infections.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.
Glomerular Diseases Indian Medical PG Question 5: Post streptococcal glomerulonephritis causes -
- A. Nephritic syndrome (Correct Answer)
- B. Primary Nephrotic syndrome
- C. Chronic renal failure
- D. Secondary Nephrotic syndrome
Glomerular Diseases Explanation: ***Nephritic syndrome***
- **Post-streptococcal glomerulonephritis (PSGN)** is a classic cause of **nephritic syndrome** [2], characterized by **glomerular inflammation** [1].
- Key features of nephritic syndrome include **hematuria**, **oliguria**, **hypertension**, and mild proteinuria with edema [2].
*Primary Nephrotic syndrome*
- **Nephrotic syndrome** is defined by massive **proteinuria** (>3.5g/day), **hypoalbuminemia**, **edema**, and **hyperlipidemia** [2].
- PSGN typically presents with **microscopic or gross hematuria** and only moderate proteinuria, not the heavy proteinuria characteristic of nephrotic syndrome [2].
*Chronic renal failure*
- While severe or recurrent cases of PSGN can eventually lead to **chronic kidney disease (CKD)** [3], it is not the immediate or primary presentation.
- PSGN typically presents as an **acute** glomerulonephritis [1].
*Secondary Nephrotic syndrome*
- **Secondary nephrotic syndrome** refers to nephrotic syndrome caused by systemic diseases (e.g., diabetes, lupus).
- PSGN is an inflammatory condition primarily affecting the glomeruli, leading to nephritic features rather than dominant nephrotic range proteinuria [2].
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-915.
[2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915.
[3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 916-917.
Glomerular Diseases Indian Medical PG Question 6: At what glomerular filtration rate (GFR) is the term "end-stage renal disease (ESRD)" typically classified?
- A. less than 15% of normal (Correct Answer)
- B. 10%—25% of normal
- C. 15%—25% of normal
- D. 5%—10% of normal
Glomerular Diseases Explanation: ***Less than 15% of normal***
- **End-stage renal disease (ESRD)** is defined by a **glomerular filtration rate (GFR)** that falls below **15 mL/min/1.73 m²**, which is approximately **less than 15% of normal function**.
- At this stage, **renal replacement therapy** (dialysis or transplantation) is typically required to sustain life.
*15%—25% of normal*
- This GFR range (15-25 mL/min/1.73 m²) corresponds to **Stage 4 chronic kidney disease (CKD)**, which is severe but not yet formally "end-stage."
- Patients in this stage require careful monitoring and management, but may not immediately need renal replacement therapy.
*10%—25% of normal*
- This range overlaps with both **severe CKD (Stage 4)** and the beginning of **ESRD (Stage 5)**, but it is not the precise definition for ESRD.
- The critical threshold for ESRD is uniformly established as GFR below 15 mL/min/1.73 m².
*5%—10% of normal*
- While a GFR in this range certainly indicates **ESRD**, the official classification includes any GFR **below 15% of normal** (or below 15 mL/min/1.73 m²), making "less than 15%" the most accurate and inclusive answer.
- This smaller range describes a more advanced state within ESRD, but not the general definition.
Glomerular Diseases Indian Medical PG Question 7: 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
Glomerular Diseases 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].
Glomerular Diseases Indian Medical PG Question 8: In case of PSGN complication commonly seen are all except :
- A. Hypertensive encephalopathy
- B. Bleeding diathesis (Correct Answer)
- C. Hyperkalemia
- D. LVF
Glomerular Diseases Explanation: ***Bleeding diathesis***
- **Post-streptococcal glomerulonephritis (PSGN)** typically does not cause **bleeding diathesis**. Bleeding diathesis is primarily associated with **liver disease**, **bone marrow suppression**, or certain genetic disorders, not directly with PSGN.
- While severe kidney failure can indirectly affect coagulation, it's not a common or direct complication leading to **bleeding diathesis** in PSGN.
*Hypertensive encephalopathy*
- PSGN often leads to **fluid overload** and **renin-angiotensin system activation**, causing severe **hypertension** [1].
- Uncontrolled hypertension can result in **hypertensive encephalopathy**, characterized by headaches, seizures, and altered mental status.
*Hyperkalemia*
- Renal insufficiency, common in PSGN, impairs the kidneys' ability to excrete **potassium**.
- This can lead to **hyperkalemia**, a life-threatening electrolyte imbalance that can cause cardiac arrhythmias.
*LVF*
- **Fluid overload** and severe **hypertension** in PSGN can overwhelm the heart's pumping capacity [1].
- This can precipitate **left ventricular failure (LVF)**, leading to symptoms like dyspnea and pulmonary edema.
Glomerular Diseases Indian Medical PG Question 9: A 63-year-old woman with long-standing type 2 diabetes, hypertension, osteoarthritis, and controlled systolic congestive heart failure following a previous anterior myocardial infarction presents for a routine office visit. She denies any significant complaints. The patient faithfully takes her glargine insulin, lisinopril, carvedilol, furosemide, and aspirin. On examination, her blood pressure is 122/82 mmHg, pulse is 85 beats per minute, respiratory rate is 14 breaths per minute, with clear lungs, regular heartbeat, and 1+ bilateral pedal edema. Review of her chart reveals a baseline creatinine of 1.5 mg/dL with an estimated glomerular filtration rate of 42 mL/min. Laboratory studies drawn early in the morning of the visit show: sodium 138 mEq/L, potassium 6.0 mEq/L, bicarbonate 15 mEq/L, chloride 120 mEq/L, blood urea nitrogen 20 mg/dL, creatinine 1.8 mg/dL, and glucose 183 mg/dL. Given these findings, what is the most common pathophysiologic scenario leading to a diagnosis of type 4 renal tubular acidosis?
- A. The combination of long-standing diabetes and hypertension has led to distal nephron dysfunction inhibiting both acid and potassium secretion. (Correct Answer)
- B. The patient has been overtreated with diuretics leading to intravascular volume depletion and acidosis.
- C. The patient's aspirin use has led to toxicity in the setting of acute kidney injury and hence the metabolic acidosis.
- D. The patient's heart failure may contribute to renal dysfunction due to decreased renal perfusion, leading to the metabolic abnormalities.
Glomerular Diseases Explanation: ### **The combination of long-standing diabetes and hypertension has led to distal nephron dysfunction inhibiting both acid and potassium secretion.**
- This patient's laboratory values show **hyperkalemia (6.0 mEq/L)**, **non-anion gap metabolic acidosis (bicarbonate 15 mEq/L)**, and **impaired renal function (creatinine 1.8 mg/dL, baseline 1.5 mg/dL)**, which are characteristic of **Type 4 renal tubular acidosis (RTA)** [1].
- **Type 4 RTA** is typically caused by **hypoaldosteronism** or **renal tubular unresponsiveness to aldosterone**, often seen in patients with long-standing diabetes and hypertension due to damage to the juxtaglomerular apparatus and distal tubules, leading to impaired potassium and acid secretion.
### *The patient has been overtreated with diuretics leading to intravascular volume depletion and acidosis.*
- While **diuretic use** can cause electrolyte imbalances, **furosemide** typically causes **hypokalemia** and **metabolic alkalosis**, not hyperkalemia and non-anion gap metabolic acidosis [2].
- The patient's blood pressure is stable (122/82 mmHg) and she has 1+ pedal edema, making severe **volume depletion** unlikely.
### *The patient's aspirin use has led to toxicity in the setting of acute kidney injury and hence the metabolic acidosis.*
- **Aspirin toxicity** can cause metabolic acidosis, but it usually presents with a **high anion gap metabolic acidosis** and possibly respiratory alkalosis (due to stimulation of respiratory drive), which is not evident here given the **normal chloride** and **low bicarbonate** indicating a **non-anion gap acidosis** [1].
- While the creatinine has slightly increased, there are no other clear indicators of acute aspirin toxicity, such as tinnitus or altered mental status.
### *The patient's heart failure may contribute to renal dysfunction due to decreased renal perfusion, leading to the metabolic abnormalities.*
- While **heart failure** can lead to **renal dysfunction** (cardiorenal syndrome) due to reduced renal perfusion, this typically causes a general decline in GFR and potentially **high anion gap metabolic acidosis** due to accumulation of metabolic waste products.
- It does not specifically account for the combination of **hyperkalemia** and **non-anion gap metabolic acidosis** characteristic of Type 4 RTA.
Glomerular Diseases Indian Medical PG Question 10: Which of these conditions is classified as a nephritic syndrome?
- A. Minimal Change Disease
- B. Membranous Glomerulopathy
- C. Post Infectious Glomerulonephritis (Correct Answer)
- D. Focal Segmental Glomerulosclerosis
Glomerular Diseases Explanation: ***Post infectious Glomerulonephritis***
- Characterized by **hematuria, hypertension, and edema**, typically following an infection, such as streptococcal pharyngitis [2].
- Immune-mediated response leads to **decreased GFR** and signs of nephritic syndrome [1][2].
*Focal segmental glomerulosclerosis*
- Primarily causes **nephrotic syndrome**, characterized by proteinuria and edema rather than hematuria [2].
- Often associated with **secondary causes** like obesity or HIV, not typically post-infectious.
*Membranous Glomerulopathy*
- Results in significant **proteinuria** and is classified as a **nephrotic syndrome** rather than a nephritic one [2][3].
- It presents with **edema and hypoalbuminemia**, lacking the hallmark features of hematuria.
*Minimal change disease*
- Predominantly causes **nephrotic syndrome** with heavy proteinuria and little to no hematuria [2].
- Young children are commonly affected, and it responds well to **corticosteroid therapy** [1].
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