Glomerulonephritis Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Glomerulonephritis. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Glomerulonephritis Indian Medical PG Question 1: Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
- A. HTN
- B. Increased urea
- C. Increased creatinine
- D. Normal C3 level (Correct Answer)
Glomerulonephritis Explanation: ***Normal C3 level***
- In Post-streptococcal glomerulonephritis (PSGN), **C3 levels are typically decreased** due to complement consumption during the inflammatory process. [1]
- A **normal C3 level** would not be consistent with PSGN, as it suggests no significant complement activation.
*Increased urea*
- Increased urea can occur due to **impaired renal function**, which is common in PSGN due to glomerular inflammation. [1]
- It's a typical finding reflecting the kidneys' inability to excrete waste products properly.
*HTN*
- Hypertension is frequently associated with PSGN due to **volume overload** and activation of the renin-angiotensin system. [1] [2]
- It is a common clinical feature that results from increased fluid retention.
*Increased creatinine*
- Increased creatinine levels indicate **renal impairment**, which is characteristic of PSGN as kidney function is affected during this condition. [1]
- This finding highlights the reduction in glomerular filtration rate (GFR), typical in glomerulonephritis. [2]
Glomerulonephritis Indian Medical PG Question 2: Which of the following is associated with pauci-immune glomerulonephritis?
- A. Anti-GBM glomerulonephritis
- B. SLE nephritis
- C. IgA nephropathy
- D. Granulomatosis with polyangiitis (GPA) (Correct Answer)
Glomerulonephritis Explanation: ***Granulomatosis with polyangiitis (GPA)***
- **Pauci-immune glomerulonephritis** is characterized by the absence or scarcity of immune complex deposits in the glomeruli.
- This is typical of **ANCA-associated vasculitides**, such as GPA (formerly Wegener's granulomatosis), which cause severe necrotising glomerulonephritis with few immune deposits [1].
*Anti-GBM glomerulonephritis*
- This condition is characterized by **linear deposition of anti-GBM antibodies** along the glomerular basement membrane, making it an **immune complex-mediated disease**, not pauci-immune [1].
- It involves autoantibodies attacking the **collagen type IV** in the GBM.
*SLE nephritis*
- Systemic lupus erythematosus (SLE) nephritis is a classic example of **immune complex-mediated glomerulonephritis**, with abundant immune deposits containing immunoglobulins and complement [1].
- The pathology often shows **full-house immunofluorescence** with IgG, IgA, IgM, C3, and C1q.
*IgA nephropathy*
- This is characterized by prominent **mesangial deposition of IgA immune complexes**, which is clearly an immune complex-mediated process [1].
- While it can present with different histological patterns, the presence of **IgA deposition** means it is not pauci-immune [1].
Glomerulonephritis Indian Medical PG Question 3: A child presents with brown colored urine and oliguria for last 3 days. He has mild facial and pedal edema. His blood pressure is 126/90. He has +3 proteinuria with 100 red cell and a few granular casts. His creatinine is 0.9, urea is 56. What is his diagnosis?
- A. PSGN (Correct Answer)
- B. FSGS
- C. IgA Nephropathy
- D. Nephrolithiasis
Glomerulonephritis Explanation: ***PSGN***
- The presentation with **brown urine**, **oliguria**, **edema**, **hypertension**, and **hematuria with red cell casts** is classic for an acute nephritic syndrome.
- Given the patient is a child, and the constellation of symptoms including **sudden onset**, **significant hypertension**, and **granular casts**, **Post-Streptococcal Glomerulonephritis (PSGN)** is the most likely diagnosis.
- PSGN typically follows streptococcal pharyngitis or skin infection by 1-3 weeks and presents with acute nephritic syndrome.
*FSGS*
- **Focal Segmental Glomerulosclerosis (FSGS)** typically presents with **nephrotic syndrome** (heavy proteinuria, hypoalbuminemia, severe edema), not primarily with nephritic features.
- While it can cause proteinuria, the presence of **red cell casts** and significant hematuria with acute hypertension points to an inflammatory glomerulonephritis, not FSGS.
*IgA Nephropathy*
- **IgA Nephropathy (Berger's disease)** can also cause nephritic syndrome in children with hematuria and RBC casts.
- However, it typically presents with **recurrent episodes of gross hematuria** occurring **during or immediately after** upper respiratory infections (synpharyngitic hematuria), rather than the delayed presentation seen here.
- It usually has a more chronic course with less prominent edema and hypertension compared to PSGN.
*Nephrolithiasis*
- **Nephrolithiasis (kidney stones)** would typically present with **colicky flank pain** and hematuria.
- It would not explain the prominent **edema**, **hypertension**, **significant proteinuria**, or presence of **red cell casts** seen in this patient.
Glomerulonephritis Indian Medical PG Question 4: Proteoglycan present in the glomerular basement membrane is?
- A. Keratan sulfate 1
- B. Keratan sulfate 2
- C. Heparan sulfate (Correct Answer)
- D. Chondroitin sulfate
Glomerulonephritis Explanation: ***Heparan sulphate***
- Heparan sulphate is a key component of the **glomerular basement membrane** (GBM), crucial for its **negative charge and filtration function** [1][2].
- It plays a significant role in **filtration barrier** properties and affects the permeability of the GBM to proteins [1].
*Keratan sulphate 1*
- Predominantly found in **cartilage** and **corneal tissue**, not associated with the glomerular basement membrane.
- It contributes to **mechanical support** but lacks the essential role in renal filtration.
*Keratan sulphate 2*
- Similar to Keratan sulphate 1, this variant is involved in **cartilage** but not in the structure of the glomerular basement membrane.
- Has distinct functions related to **tissue hydration** rather than the filtration dynamics of the GBM.
*Chondroitin sulphate*
- Commonly located in **cartilage** and connective tissues, it does not play a significant role in the structure of the glomerular basement membrane.
- While it assists in **cell signaling** and regeneration, it does not influence the GBM permeability like heparan sulphate.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 905-907.
[2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 34-35.
Glomerulonephritis Indian Medical PG Question 5: Which of the following is NOT a feature of nephrotic syndrome?
- A. Hematuria (Correct Answer)
- B. Edema
- C. Hypoalbuminemia
- D. Proteinuria
Glomerulonephritis Explanation: ### Original Explanation
***Hematuria***
- **Hematuria** is a characteristic feature of **nephritic syndrome**, which involves glomerular inflammation and damage leading to blood in the urine [1].
- In contrast, **nephrotic syndrome** is primarily characterized by increased glomerular permeability to protein, not red blood cells, resulting in significant **proteinuria** [1].
*Edema*
- **Edema** is a hallmark of nephrotic syndrome, resulting from severe **hypoalbuminemia** that reduces plasma oncotic pressure [2].
- This leads to fluid extravasation into the interstitial spaces, causing generalized swelling.
*Hypoalbuminemia*
- **Hypoalbuminemia** is a defining feature of nephrotic syndrome, caused by excessive urinary loss of albumin due to widespread glomerular damage [2].
- Reduced serum albumin levels contribute to the characteristic edema and increased lipid synthesis by the liver.
*Proteinuria*
- **Proteinuria**, specifically *massive proteinuria* (>3.5 g/day in adults), is the cardinal feature of nephrotic syndrome [1], [2].
- It signifies significant damage to the glomerular filtration barrier, allowing large amounts of protein to leak into the urine.
Glomerulonephritis Indian Medical PG Question 6: 2 year old child presented with sudden onset of altered sensorium. On examination, BP was 200/100. What is the most likely diagnosis?
- A. Essential hypertension
- B. Glomerulonephritis (Correct Answer)
- C. Renal artery stenosis
- D. Coarctation of the aorta
Glomerulonephritis Explanation: ***Glomerulonephritis***
- **Sudden onset of altered sensorium** in a child with severe **hypertension (BP 200/100)** is highly suggestive of hypertensive encephalopathy, a common complication of acute glomerulonephritis.
- **Acute glomerulonephritis** often presents with hypertension, edema, and hematuria, which can lead to neurological symptoms due to rapid and severe blood pressure elevation.
*Essential hypertension*
- **Essential hypertension** is extremely rare in a 2-year-old child; hypertension in this age group is typically secondary to an underlying condition.
- The sudden onset of severe hypertension with neurological symptoms points away from primary hypertension, which usually develops gradually.
*Renal artery stenosis*
- While **renal artery stenosis** can cause hypertension, it usually presents as sustained hypertension and is less likely to cause a sudden, acute presentation with altered sensorium in a 2-year-old compared to acute glomerulonephritis.
- Renal artery stenosis often causes **renovascular hypertension**, which may be indicated by abdominal bruits, but the acute neurological crisis is more characteristic of the rapid blood pressure rise seen in glomerulonephritis.
*Coarctation of the aorta*
- **Coarctation of the aorta** causes hypertension, but it typically presents with a **difference in blood pressure between the upper and lower extremities** or absent/diminished femoral pulses.
- While it can lead to severe hypertension, the sudden onset of altered sensorium as the primary presenting feature is less typical; other signs related to the anatomical defect would usually be present.
Glomerulonephritis Indian Medical PG Question 7: A 2-year-old child presents with sudden onset of altered sensorium. On examination, blood pressure is 200/100 mmHg. What is the most likely diagnosis?
- A. Renal artery stenosis
- B. Essential hypertension
- C. Glomerulonephritis (Correct Answer)
- D. Coarctation of Aorta
Glomerulonephritis Explanation: ***Glomerulonephritis***
- The sudden onset of **altered sensorium** in a 2-year-old with severe **hypertension** (200/100 mmHg) is highly suggestive of **hypertensive encephalopathy**, a serious complication often seen in acute glomerulonephritis.
- **Acute glomerulonephritis**, particularly post-streptococcal glomerulonephritis, frequently presents with sudden onset of hypertension, fluid retention, and neurological symptoms such as altered sensorium in young children.
*Renal artery stenosis*
- While renal artery stenosis can cause severe hypertension, it typically does not present with such an acute and dramatic onset of altered sensorium in a 2-year-old, unless there's a thrombotic event.
- Hypertensive encephalopathy secondary to renal artery stenosis is possible but less common as the initial presentation in this age group compared to acute glomerulonephritis.
*Essential hypertension*
- **Essential hypertension** is extremely rare in a 2-year-old and would not typically present with such a severe, sudden onset of hypertension leading to altered sensorium.
- When hypertension is diagnosed in young children, an underlying **secondary cause** is almost always present and must be aggressively investigated.
*Coarctation of Aorta*
- **Coarctation of the aorta** causes hypertension, but the hypertension is usually present from birth or early infancy and would typically manifest with a **difference in blood pressure** between the upper and lower extremities and specific murmur.
- While it can lead to high blood pressure, an acute presentation with sudden altered sensorium due to extremely high pressure is less characteristic compared to the acute inflammatory process of glomerulonephritis.
Glomerulonephritis Indian Medical PG Question 8: Which of the following is not a hallmark of nephrotic syndrome in children?
- A. Hypoalbuminemia < 2.5 g/dL
- B. Edema
- C. Severe proteinuria >2 gm/m2/day
- D. Gross hematuria (Correct Answer)
Glomerulonephritis Explanation: ***Gross hematuria***
- While some glomerular disorders that cause nephrotic syndrome can also present with microscopic hematuria, **gross hematuria** is a hallmark feature of **nephritic syndrome**, not nephrotic syndrome.
- Nephritic syndrome typically involves significant inflammation and damage to the glomeruli, leading to blood in the urine, often accompanied by hypertension and acute kidney injury.
*Severe proteinuria >2 gm/m2/day*
- **Severe proteinuria** (typically defined as >40 mg/m2/hr or >50 mg/kg/day, or >3.5 g/day in adults, which translates to high values in children) is a **defining characteristic** of nephrotic syndrome, resulting from increased glomerular permeability.
- The excessive loss of protein in the urine is responsible for many of the other clinical manifestations of the syndrome.
*Hypoalbuminemia < 2.5 g/dL*
- **Hypoalbuminemia** is a direct consequence of the massive proteinuria, as the liver cannot synthesize albumin quickly enough to compensate for its loss.
- A serum albumin level of less than 2.5 g/dL is a key diagnostic criterion for nephrotic syndrome.
*Edema*
- **Edema**, particularly periorbital, scrotal, and lower extremity swelling, is a prominent clinical feature of nephrotic syndrome.
- It results from the reduced plasma oncotic pressure due to hypoalbuminemia, leading to fluid shifts from the intravascular space to the interstitial space.
Glomerulonephritis Indian Medical PG Question 9: A child was diagnosed as a case of pauci-immune crescentic glomerulonephritis. The treatment to be given in this child is –
- A. Immunoglobulins
- B. Cyclophosphamide
- C. Methylprednisolone
- D. Prednisolone + Cyclophosphamide (Correct Answer)
Glomerulonephritis Explanation: ***Prednisolone + Cyclophosphamide***
- **Pauci-immune crescentic glomerulonephritis** (also known as ANCA-associated vasculitis) is a rapidly progressive and severe autoimmune condition affecting the kidneys.
- **Combination therapy** with a corticosteroid (like prednisolone) and an immunosuppressant (like cyclophosphamide) is the standard and most effective initial treatment to control inflammation and suppress the immune response.
*Immunoglobulins*
- **Intravenous immunoglobulins (IVIG)** are sometimes used in autoimmune diseases, but they are not the first-line treatment for pauci-immune crescentic glomerulonephritis due to its aggressive nature.
- IVIG might be considered as an **adjunctive therapy** or in specific cases of refractory disease, but not as monotherapy.
*Cyclophosphamide*
- While **cyclophosphamide** is a critical component of treatment for **pauci-immune crescentic glomerulonephritis** due to its potent immunosuppressive effects, it is not used alone.
- It is typically combined with a **corticosteroid** (such as prednisolone) to achieve a more rapid and comprehensive anti-inflammatory and immunosuppressive effect.
*Methylprednisolone*
- **Methylprednisolone** (a corticosteroid) is routinely used in the initial management of **pauci-immune crescentic glomerulonephritis** to rapidly reduce inflammation.
- However, it is generally part of a **combination regimen** and is not sufficient as monotherapy for inducing remission in this severe form of glomerulonephritis.
Glomerulonephritis Indian Medical PG Question 10: A child presented with cola-colored urine, proteinuria 2+, and history of rash 2 weeks ago. What is the most probable diagnosis?
- A. Wegener Granulomatosis
- B. HUS
- C. IgA nephropathy
- D. HSP (Correct Answer)
Glomerulonephritis Explanation: ***HSP (Henoch-Schönlein Purpura)***
- This presentation, specifically **cola-colored urine (indicating hematuria), proteinuria**, and a **history of a rash**, is highly characteristic of **Henoch-Schönlein Purpura nephritis**, which is a common complication of HSP.
- HSP is a **small-vessel vasculitis** often preceded by an upper respiratory tract infection and typically presents with a **palpable purpuric rash**, arthralgia, abdominal pain, and renal involvement.
*Wegener Granulomatosis (Granulomatosis with Polyangiitis)*
- While it can cause hematuria and proteinuria, it typically presents with **upper and lower respiratory tract involvement** (e.g., sinusitis, lung nodules) and is often associated with positive **c-ANCA**.
- A preceding rash as described is not a typical initial feature, and its presentation often involves more systemic and severe organ damage.
*HUS (Hemolytic Uremic Syndrome)*
- HUS is characterized by a **triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury**, often preceded by diarrheal illness (especially shiga toxin-producing E. coli).
- While it causes renal involvement (hematuria and proteinuria), the primary distinguishing features are the hematological abnormalities (anemia and low platelets) and the typical absence of a preceding rash.
*IgA nephropathy*
- IgA nephropathy can cause **recurrent episodes of gross hematuria**, often occurring concurrent with or shortly after an **upper respiratory tract infection**.
- However, the characteristic **palpable purpuric rash** described (implied by "h/o rash") and the typical timing of presentation (often affecting young adults) make HSP a more probable diagnosis in this pediatric case.
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