GLOMERULONEPHRITIS Flashcards

1
Q

Which of the following is NOT a classic clinical feature of acute nephritic syndrome?
A. Hypertension
B. Hematuria
C. Nephrotic-range proteinuria
D. Red blood cell casts

A

C. Nephrotic-range proteinuria

Rationale: Acute nephritic syndrome is characterized by mild to moderate proteinuria, not nephrotic-range proteinuria (>3.5 g/day), which is seen in nephrotic syndrome.

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2
Q

What is the primary pathological process underlying acute nephritic syndrome?
A. Tubular atrophy
B. Glomerular inflammation
C. Vascular thrombosis
D. Obstruction of renal pelvis

A

B. Glomerular inflammation

Rationale: Acute nephritic syndrome results from extensive inflammatory damage to the glomeruli, which disrupts glomerular filtration and causes associated clinical features.

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3
Q

Which of the following findings in the urine sediment is pathognomonic for acute nephritic syndrome?
A. White blood cell casts
B. Red blood cell casts
C. Hyaline casts
D. Broad waxy casts

A

B. Red blood cell casts

Rationale: Red blood cell casts are a hallmark of glomerular inflammation and are diagnostic of acute nephritic syndrome.

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4
Q

A 7-year-old boy presents with facial swelling, hematuria, and hypertension. He had a sore throat two weeks ago that resolved without treatment. Physical examination reveals periorbital edema and blood pressure of 140/90 mmHg. Laboratory studies show the following:

Serum C3: Low
Serum C4: Normal
ASO titer: Elevated
Urinalysis: Hematuria, red blood cell casts, and mild proteinuria

What is the most likely diagnosis?
A. IgA nephropathy
B. Poststreptococcal glomerulonephritis
C. Membranous nephropathy
D. Minimal change disease

A

B. Poststreptococcal glomerulonephritis

Rationale: This patient presents with a classic nephritic syndrome following a recent streptococcal throat infection. The findings of low C3 with normal C4, elevated ASO titers, and RBC casts strongly support PSGN. IgA nephropathy is associated with synpharyngitic hematuria (hematuria occurring concurrently with the infection), whereas PSGN typically occurs 1–3 weeks after the infection.

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5
Q

Which of the following findings on renal biopsy is most characteristic of poststreptococcal glomerulonephritis?
A. Linear deposition of IgG along the glomerular basement membrane
B. Mesangial proliferation with IgA deposits
C. Subepithelial “humps” of immune complex deposits
D. Segmental sclerosis and podocyte effacement

A

C. Subepithelial “humps” of immune complex deposits

Rationale: PSGN is characterized by subepithelial immune complex deposits (“humps”) visible on electron microscopy. Linear IgG deposition (A) is seen in anti-GBM disease. Mesangial IgA deposits (B) are seen in IgA nephropathy, and segmental sclerosis with podocyte effacement (D) is associated with focal segmental glomerulosclerosis.

The renal biopsy in poststreptococcal glomerulonephritis demonstrates
hypercellularity of mesangial and endothelial cells; glomerular infiltrates of polymorphonuclear leukocytes; granular subendothelial immune deposits of IgG, IgM, C3, C4, and C5–9; and subepithelial deposits (which appear as “humps”)

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6
Q

A 12-year-old girl presents with hematuria and hypertension. She had impetigo 3 weeks ago. Her laboratory results show a low C3 level, a normal C4 level, and elevated anti-DNAse B titers. Which of the following is the primary mechanism of her kidney disease?
A. Autoantibodies against the glomerular basement membrane
B. Circulating immune complexes and complement activation
C. Direct bacterial invasion of the kidney
D. T-cell mediated podocyte injury

A

B. Circulating immune complexes and complement activation

Rationale: PSGN is an immune-mediated disease caused by nephritogenic streptococcal antigens, circulating immune complexes, and complement activation. The characteristic low C3 with normal C4 levels supports this mechanism. Autoantibodies against the GBM (A) cause Goodpasture syndrome. Direct bacterial invasion (C) is not typical of PSGN, and T-cell mediated podocyte injury (D) is associated with minimal change disease.

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7
Q

Which of the following is a common laboratory finding in poststreptococcal glomerulonephritis?
A. Elevated CH50 and normal C3
B. Positive rheumatoid factor and decreased C3
C. Low C3 and low C4
D. Normal C3 and elevated cryoglobulins

A

B. Positive rheumatoid factor and decreased C3

Rationale: PSGN is associated with low C3 and normal C4 levels, reflecting activation of the alternative complement pathway. Rheumatoid factor may be elevated in some cases. CH50 is typically low, and C4 levels remain normal.

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8
Q

A 55-year-old man with poorly controlled diabetes presents with hematuria, hypertension, and edema. He recently recovered from a streptococcal throat infection. Which of the following features would suggest the diagnosis of poststreptococcal glomerulonephritis?
A. Subepithelial immune complex deposits on renal biopsy
B. Deposition of IgA in the mesangium
C. Rapid progression to end-stage kidney disease within weeks
D. Persistent proteinuria with normal complement levels

A

A. Subepithelial immune complex deposits on renal biopsy

Rationale: The hallmark of PSGN on biopsy is subepithelial immune complex deposits (“humps”). Mesangial IgA deposits (B) suggest IgA nephropathy. Rapid progression to ESRD (C) suggests RPGN, and normal complement levels (D) are not typical of PSGN.

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9
Q

Which of the following is the mainstay of treatment for poststreptococcal glomerulonephritis?
A. High-dose corticosteroids
B. Antibiotics to treat cohabitants with active streptococcal infection
C. Long-term immunosuppressive therapy
D. Supportive care including hypertension and edema control

A

D. Supportive care including hypertension and edema control

Rationale: The primary treatment for PSGN is supportive care aimed at controlling hypertension, managing edema, and providing dialysis if needed. Antibiotics are only indicated for active streptococcal infections, not for the glomerulonephritis itself. Immunosuppressive therapy, including corticosteroids, has no role in PSGN, even in the presence of crescents.

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10
Q

What is the typical prognosis of poststreptococcal glomerulonephritis in children?
A. ESRD occurs in 50% of cases
B. Most children recover fully within 3–6 weeks
C. Persistent hematuria and proteinuria are common and progressive
D. High mortality is observed due to hypertension-related complications

A

B. Most children recover fully within 3–6 weeks

Rationale: The majority of children with PSGN experience complete resolution of azotemia, hematuria, and proteinuria within 3–6 weeks. Persistent microscopic hematuria or nonnephrotic proteinuria occurs in a small percentage of cases but is usually not progressive. ESRD is rare in children.

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11
Q

What is the primary mechanism leading to renal damage in lupus nephritis?
A. Bacterial infection of the renal parenchyma
B. Deposition of circulating immune complexes and complement activation
C. Autoantibodies targeting renal tubules
D. Direct cytotoxic effects of T cells on renal glomeruli

A

B. Deposition of circulating immune complexes and complement activation

Rationale: Lupus nephritis results from the deposition of circulating immune complexes, primarily DNA and anti-DNA, which activate the complement cascade. This leads to complement-mediated damage, leukocyte infiltration, and cytokine release.

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12
Q

What laboratory findings are most strongly associated with lupus nephritis?
A. Low levels of C-reactive protein (CRP)
B. Elevated anti-dsDNA antibodies and hypocomplementemia
C. Increased serum albumin and normal complement levels
D. Positive rheumatoid factor

A

B. Elevated anti-dsDNA antibodies and hypocomplementemia

Rationale: Anti-dsDNA antibodies that fix complement correlate best with renal involvement in SLE. Hypocomplementemia (low C3 and C4 levels) is common during active lupus nephritis and may precede a flare.

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13
Q

A kidney biopsy is essential in lupus nephritis primarily to:
A. Confirm the diagnosis of systemic lupus erythematosus.
B. Establish the histologic class, which guides therapy.
C. Evaluate for bacterial or fungal infection.
D. Determine the need for immediate dialysis.

A

B. Establish the histologic class, which guides therapy.

Rationale: The histologic classification of lupus nephritis (e.g., Class I–VI) provides critical information for determining the severity and type of renal involvement, which directly influences treatment decisions.

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14
Q

Which of the following best describes the histologic findings in Class I lupus nephritis?
A. Mesangial immune complexes with mesangial proliferation
B. Normal glomerular histology on light microscopy with minimal mesangial deposits
C. Subendothelial immune deposits with diffuse glomerular proliferation
D. Thickened glomerular basement membrane with subepithelial deposits

A

B. Normal glomerular histology on light microscopy with minimal mesangial deposits

Rationale: Class I lupus nephritis is characterized by normal glomerular appearance on light microscopy but with minimal mesangial immune deposits detected by immunofluorescence or electron microscopy.

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15
Q

Which statement is true regarding Class II lupus nephritis?
A. It is associated with severe renal manifestations and poor prognosis.
B. It features mesangial immune complex deposition with mesangial proliferation.
C. It often progresses to Class V lupus nephritis.
D. It requires aggressive immunosuppressive therapy.

A

B. It features mesangial immune complex deposition with mesangial proliferation.

Rationale: Class II lupus nephritis involves mesangial immune deposits accompanied by mesangial proliferation, typically with minimal clinical renal manifestations and a favorable prognosis.

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16
Q

Patients with lupus nephritis limited to the renal mesangium (Class I and II) typically present with:
A. Nephrotic syndrome and acute kidney injury
B. Hypertension and hematuria
C. Minimal renal manifestations and normal renal function
D. Rapidly progressive glomerulonephritis

A

C. Minimal renal manifestations and normal renal function

Rationale: Lesions limited to the mesangium (Class I and II) are usually associated with minimal renal symptoms and normal renal function. Nephrotic syndrome is rare in these classes.

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17
Q

What is the most appropriate management for a patient with Class I or II lupus nephritis and no significant renal manifestations?
A. High-dose corticosteroids and cyclophosphamide
B. Supportive care without specific therapy for lupus nephritis
C. Plasmapheresis and intravenous immunoglobulin (IVIG)
D. Renal transplantation

A

B. Supportive care without specific therapy for lupus nephritis

Rationale: Class I and II lupus nephritis have an excellent prognosis and usually do not require specific treatment beyond general supportive care for systemic lupus erythematosus (SLE).

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18
Q

Which of the following findings is most characteristic of Class III lupus nephritis?
A. Proliferative lesions involving >50% of glomeruli
B. Focal lesions involving <50% of glomeruli with segmental proliferation or scarring
C. Nephrotic syndrome without hematuria
D. Normal glomerular histology with minimal mesangial deposits

A

B. Focal lesions involving <50% of glomeruli with segmental proliferation or scarring

Rationale: Class III lupus nephritis is characterized by focal involvement of <50% of glomeruli, often with segmental proliferation or scarring. The clinical course can vary widely depending on the severity of the lesions.

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19
Q

What is the primary difference between Class IV-S and Class IV-G lupus nephritis?
A. Presence of mesangial proliferation in IV-S but not in IV-G
B. Degree of proteinuria, which is higher in IV-S than in IV-G
C. Extent of glomerular tuft involvement in diffuse lesions
D. Response to treatment, with IV-G having a better prognosis

A

C. Extent of glomerular tuft involvement in diffuse lesions

Rationale: In Class IV lupus nephritis, segmental lesions (IV-S) involve <50% of the glomerular tuft, while global lesions (IV-G) involve >50%. Both are diffuse, affecting >50% of the glomeruli.

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20
Q

Which of the following is most associated with a poor prognosis in Class IV lupus nephritis?
A. Low serum complement levels and high anti-dsDNA antibody titers
B. Hematuria and mild proteinuria
C. Mesangial immune deposits without crescents
D. Normal renal function at presentation

A

A. Low serum complement levels and high anti-dsDNA antibody titers

Rationale: Class IV lupus nephritis commonly involves aggressive disease with immune complex deposition, low complement levels, high anti-dsDNA antibody titers, and crescents on biopsy, all associated with a poor prognosis if untreated.

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21
Q

What is the recommended initial treatment for severe Class IV lupus nephritis?
A. Supportive care only, as the prognosis is poor regardless of treatment
B. High-dose corticosteroids with cyclophosphamide or mycophenolate mofetil for induction
C. Low-dose corticosteroids and azathioprine for maintenance
D. Antihypertensive therapy to control blood pressure and prevent further progression

A

B. High-dose corticosteroids with cyclophosphamide or mycophenolate mofetil for induction

Rationale: The standard treatment for severe Class IV lupus nephritis involves an induction phase with high-dose corticosteroids and either cyclophosphamide or mycophenolate mofetil to achieve remission, followed by maintenance therapy.

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22
Q

Which of the following best describes the histopathological findings in Class V lupus nephritis?
A. Mesangial immune deposits with proliferation
B. Subepithelial immune deposits producing a membranous pattern
C. Focal proliferative lesions involving <50% of glomeruli
D. Diffuse proliferative lesions involving >50% of glomeruli

A

B. Subepithelial immune deposits producing a membranous pattern

Rationale: Class V lupus nephritis is characterized by subepithelial immune deposits that create a membranous pattern, similar to idiopathic membranous nephropathy.

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23
Q

Which condition predisposes patients with Class V lupus nephritis to renal vein thrombosis?
A. Nephrotic syndrome
B. Elevated complement levels
C. Lack of proteinuria
D. Hypertension

A

A. Nephrotic syndrome

Rationale: Nephrotic syndrome in Class V lupus nephritis is associated with hypercoagulability, predisposing patients to renal vein thrombosis and other thrombotic complications.

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24
Q

Class VI lupus nephritis is defined by which of the following?
A. Subepithelial immune deposits
B. >90% sclerotic glomeruli and interstitial fibrosis
C. Diffuse proliferative endocapillary lesions
D. Focal proliferative lesions with crescents

A

B. >90% sclerotic glomeruli and interstitial fibrosis

Rationale: Class VI lupus nephritis represents advanced chronic kidney disease with >90% sclerotic glomeruli, extensive interstitial fibrosis, and is typically associated with end-stage renal disease (ESRD).

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25
Q

Which of the following is recommended for lupus patients with ESRD due to Class VI lupus nephritis?
A. Immediate renal transplantation without waiting for disease inactivity
B. Renal transplantation after ~6 months of inactive disease
C. High-dose corticosteroids to reverse ESRD
D. Conservative management without transplantation

A

B. Renal transplantation after ~6 months of inactive disease

Rationale: Patients with ESRD due to lupus nephritis often undergo renal transplantation after ~6 months of inactive disease, which provides comparable allograft survival rates to other causes of ESRD.

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26
Q

Goodpasture’s syndrome is characterized by which of the following clinical features?
A. Isolated lung hemorrhage without renal involvement
B. Pulmonary hemorrhage and glomerulonephritis
C. Nephrotic syndrome with no pulmonary symptoms
D. Acute interstitial nephritis without antibody involvement

A

B. Pulmonary hemorrhage and glomerulonephritis

Rationale: Goodpasture’s syndrome is a pulmonary-renal syndrome characterized by the combination of lung hemorrhage and glomerulonephritis caused by autoantibodies targeting the α3 NC1 domain of collagen IV

27
Q

Which of the following is the primary autoimmune target in Goodpasture’s syndrome?
A. α1 NC1 domain of collagen IV
B. α3 NC1 domain of collagen IV
C. Mesangial immune deposits
D. Myeloperoxidase

A

B. α3 NC1 domain of collagen IV

Rationale: The autoimmune target in Goodpasture’s syndrome is the α3 NC1 domain of collagen IV, which becomes exposed due to environmental or inflammatory triggers.

28
Q

What biopsy finding is characteristic of Goodpasture’s syndrome?
A. Granular immune deposits in the glomerulus
B. Linear immunofluorescent staining for IgG
C. Subepithelial humps on electron microscopy
D. Mesangial proliferation

A

B. Linear immunofluorescent staining for IgG

Rationale: Renal biopsies in Goodpasture’s syndrome show linear immunofluorescent staining for IgG along the glomerular basement membrane, reflecting anti-GBM antibody deposition.

29
Q

Which clinical or pathological feature is associated with a worse prognosis in Goodpasture’s syndrome?
A. Presence of hemoptysis
B. Normal serum creatinine at presentation
C. >50% crescents on renal biopsy with advanced fibrosis
D. Mild proteinuria

A

C. >50% crescents on renal biopsy with advanced fibrosis

Rationale: A worse prognosis is associated with >50% crescents on biopsy, advanced fibrosis, high serum creatinine (>5–6 mg/dL), oliguria, or the need for acute dialysis at presentation.

30
Q

What is the first-line treatment for Goodpasture’s syndrome?
A. High-dose steroids alone
B. Antibiotics and supportive care
C. Plasmapheresis combined with prednisone and cyclophosphamide
D. Rituximab as monotherapy

A

C. Plasmapheresis combined with prednisone and cyclophosphamide

Rationale: Plasmapheresis removes circulating anti-GBM antibodies, and immunosuppressive therapy with prednisone and cyclophosphamide reduces further antibody production and inflammation.

31
Q

Why should kidney transplantation be delayed in patients with Goodpasture’s syndrome?
A. Risk of immediate antibody-mediated rejection
B. Difficulty in matching HLA types
C. Need to confirm histologic subtype on biopsy
D. Requirement for undetectable serum anti-GBM antibodies

A

D. Requirement for undetectable serum anti-GBM antibodies

Rationale: Kidney transplantation should be delayed for at least 6 months until serum anti-GBM antibodies are undetectable to reduce the risk of recurrent disease in the allograft.

32
Q

Which of the following best describes the pathological hallmark of IgA nephropathy?
A) Thickening of the glomerular basement membrane with linear IgG deposits
B) Mesangial deposition of IgA immune complexes
C) Subepithelial humps with C3 deposition
D) Endothelial proliferation with anti-GBM antibodies

A

B) Mesangial deposition of IgA immune complexes

33
Q

A 25-year-old male presents with recurrent episodes of painless gross hematuria following upper respiratory infections. Which of the following is the most likely diagnosis?
A) Post-streptococcal glomerulonephritis
B) Membranous nephropathy
C) IgA nephropathy
D) Alport syndrome

A

C) IgA nephropathy

Rationale:
The classic presentation of IgA nephropathy includes recurrent episodes of gross hematuria, often triggered by mucosal infections such as upper respiratory tract infections. Post-streptococcal glomerulonephritis (A) typically occurs weeks after infection and presents with nephritic syndrome. Membranous nephropathy (B) is primarily nephrotic. Alport syndrome (D) is associated with hereditary hematuria and hearing loss.

34
Q

Which of the following clinical features is most commonly associated with IgA nephropathy?
A) Nephrotic syndrome with significant proteinuria
B) Episodic hematuria, often following mucosal infections
C) Rapidly progressive renal failure with crescents
D) Persistent hypocomplementemia

A

B) Episodic hematuria, often following mucosal infections

Rationale:
IgA nephropathy is characterized by episodic hematuria, typically occurring shortly after respiratory or gastrointestinal infections.

35
Q

Which of the following clinical features is most commonly associated with IgA nephropathy?
A) Nephrotic syndrome with significant proteinuria
B) Episodic hematuria, often following mucosal infections
C) Rapidly progressive renal failure with crescents
D) Persistent hypocomplementemia

A

B) Episodic hematuria, often following mucosal infections

Rationale:
IgA nephropathy is characterized by episodic hematuria, typically occurring shortly after respiratory or gastrointestinal infections.

36
Q

Which of the following systemic symptoms distinguishes Henoch-Schönlein purpura (HSP) from IgA nephropathy?
A) Hypertension
B) Arthralgia and palpable purpura
C) Rapidly progressive renal failure
D) Nephrotic-range proteinuria

A

B) Arthralgia and palpable purpura

Rationale:
HSP, also known as IgA vasculitis, is characterized by systemic symptoms such as palpable purpura (especially on the lower extremities), arthralgia, and abdominal pain, which are not typically seen in isolated IgA nephropathy. The other options are less specific or may occur in both conditions.

37
Q

A 10-year-old boy presents with abdominal pain, arthralgia, a purpuric rash on his legs, and hematuria. He was diagnosed with Henoch-Schönlein purpura. Which of the following best explains the renal involvement in this condition?
A) Subepithelial immune complex deposition
B) Linear IgG deposition along the glomerular basement membrane
C) Mesangial IgA deposition
D) Crescent formation with anti-GBM antibodies

A

C) Mesangial IgA deposition

Rationale: Renal involvement in Henoch-Schönlein purpura is due to mesangial IgA deposition, which is identical to the findings in IgA nephropathy. Subepithelial deposits (A) occur in post-streptococcal glomerulonephritis, linear IgG deposition (B) is seen in Goodpasture syndrome, and crescent formation with anti-GBM antibodies (D) is seen in anti-GBM disease.

38
Q

Which antibody is more commonly associated with granulomatosis with polyangiitis (GPA)?
A. Anti-MPO
B. Anti-PR3
C. Anti-dsDNA
D. Anti-Ro

A

B. Anti-PR3

Rationale: Anti-proteinase 3 (PR3) antibodies are more commonly associated with granulomatosis with polyangiitis (GPA), while anti-myeloperoxidase (MPO) antibodies are seen in microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (EGPA).

39
Q

Anti-MPO antibodies are more commonly seen in which conditions?
A. Granulomatosis with polyangiitis
B. Microscopic polyangiitis or Churg-Strauss syndrome
C. Systemic lupus erythematosus
D. Rheumatoid arthritis

A

B. Microscopic polyangiitis or Churg-Strauss syndrome

Rationale: Anti-MPO antibodies are most often associated with microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (formerly known as Churg-Strauss syndrome), distinguishing them from anti-PR3 antibodies, which are linked to GPA.

40
Q

What is the first-line induction therapy for ANCA-associated vasculitides?
A. Methotrexate and plasmapheresis
B. Glucocorticoids and cyclophosphamide or rituximab
C. Azathioprine and low-dose steroids
D. NSAIDs and anti-TNF agents

A

B. Glucocorticoids and cyclophosphamide or rituximab

Rationale: Induction therapy typically includes high-dose glucocorticoids combined with cyclophosphamide or rituximab to control inflammation and halt disease progression.

41
Q

Plasmapheresis is specifically recommended in ANCA-associated vasculitides for which situations?
A. Persistent nasal crusting
B. Rapidly progressive renal failure or pulmonary hemorrhage
C. Chronic fatigue and arthralgia
D. Maintenance therapy

A

B. Rapidly progressive renal failure or pulmonary hemorrhage

Rationale: Plasmapheresis is used in severe cases, such as rapidly progressive renal failure or life-threatening pulmonary hemorrhage, to remove pathogenic antibodies and inflammatory mediators.

42
Q

Which of the following is a classical feature of nephrotic syndrome?
A. Heavy proteinuria and hypercholesterolemia
B. Significant hematuria and hyperkalemia
C. Oliguria and metabolic acidosis
D. Hypoglycemia and hypokalemia

A

A. Heavy proteinuria and hypercholesterolemia

Rationale: Nephrotic syndrome is characterized by heavy proteinuria (>3.5 g/day), hypoalbuminemia, hypercholesterolemia, edema, and often minimal hematuria.

43
Q

Why are lipid-lowering agents recommended for patients with nephrotic syndrome?
A. To reduce hypercoagulability
B. To decrease the risk of cardiovascular disease
C. To treat hypoalbuminemia
D. To prevent hematuria

A

B. To decrease the risk of cardiovascular disease

Rationale: Hypercholesterolemia, a common complication of nephrotic syndrome, increases the risk of cardiovascular disease. Lipid-lowering agents help mitigate this risk.

44
Q

Which complication of nephrotic syndrome is treated with anticoagulants?
A. Hypercholesterolemia
B. Venous thromboembolism
C. Hypoalbuminemia
D. Hypertension

A

B. Venous thromboembolism

Rationale: Nephrotic syndrome creates a hypercoagulable state due to loss of anticoagulant proteins in the urine, which predisposes patients to venous thromboembolism. Anticoagulants are used for treatment.

45
Q

What is the hallmark finding on electron microscopy in minimal change disease?
A. Glomerular sclerosis
B. Immune complex deposits
C. Effacement of podocyte foot processes
D. Thickening of the glomerular basement membrane

A

C. Effacement of podocyte foot processes

Rationale: Electron microscopy consistently reveals podocyte foot process effacement and weakening of the slit-pore membranes, which are the defining features of MCD.

46
Q

What would be the findings on light microscopy and immunofluorescence in a renal biopsy of a patient with minimal change disease?
A. No glomerular lesion and absence of immune deposits
B. Mesangial proliferation and IgA deposition
C. Glomerular sclerosis and C3 deposition
D. Crescent formation and IgG deposition

A

A. No glomerular lesion and absence of immune deposits

Rationale: MCD shows no glomerular lesions on light microscopy and is negative for immune deposits on immunofluorescence, though small amounts of IgM may occasionally be seen in the mesangium.

47
Q

What role does the APOL1 gene play in focal segmental glomerulosclerosis (FSGS)?
A. It promotes immune complex formation.
B. It encodes a circulating permeability factor.
C. Risk polymorphisms increase susceptibility to FSGS in African Americans.
D. It decreases glomerular filtration rate (GFR) directly.

A

C. Risk polymorphisms increase susceptibility to FSGS in African Americans.

Rationale: Variants in the APOL1 gene, which are more common among individuals of African ancestry, significantly increase the risk of developing FSGS and other kidney diseases, particularly in the setting of podocyte stress.

48
Q

Which of the following is a primary cause of membranous nephropathy?
A. Autoantibodies against M-type phospholipase A2 receptor (PLA2R)
B. Solid tumors (e.g., breast or lung cancer)
C. Infections such as hepatitis B or syphilis
D. Lupus or rheumatoid arthritis

A

A. Autoantibodies against M-type phospholipase A2 receptor (PLA2R)

Rationale: Approximately 70% of idiopathic membranous nephropathy cases are associated with autoantibodies targeting the M-type phospholipase A2 receptor on podocytes, making this a primary cause.

49
Q

What is the characteristic finding on renal biopsy in membranous nephropathy?
A. Uniform thickening of the basement membrane along capillary loops
B. Crescent formation in glomeruli
C. Mesangial proliferation
D. Fibrinoid necrosis

A

A. Uniform thickening of the basement membrane along capillary loops

Rationale: Light microscopy of renal biopsies in membranous nephropathy typically shows uniform thickening of the glomerular basement membrane along the peripheral capillary loops without significant cellular proliferation.

50
Q

Which complication is most commonly associated with membranous nephropathy compared to other nephrotic syndromes?
A. Acute kidney injury
B. Renal vein thrombosis
C. Hyperkalemia
D. Severe anemia

A

B. Renal vein thrombosis

Rationale: Membranous nephropathy has the highest reported incidences of thrombotic complications, including renal vein thrombosis, pulmonary embolism, and deep vein thrombosis, among all nephrotic syndromes.

51
Q

What is the single most common cause of chronic renal failure in the United States and worldwide?
A. Hypertensive nephrosclerosis
B. Polycystic kidney disease
C. Diabetic nephropathy
D. Chronic glomerulonephritis

A

C. Diabetic nephropathy

Rationale: Diabetic nephropathy is the leading cause of chronic renal failure globally, reflecting the rising prevalence of obesity and diabetes, particularly type 2 diabetes.

52
Q

What is an early morphologic change in diabetic nephropathy that appears within 1–2 years of clinical diabetes onset?
A. Mesangial expansion
B. Thickening of the glomerular basement membrane (GBM)
C. Nodular glomerulosclerosis
D. Crescent formation

A

B. Thickening of the glomerular basement membrane (GBM)

Rationale: Thickening of the GBM is an early and sensitive indicator of diabetic nephropathy that occurs within 1–2 years of diabetes onset. However, it does not strongly correlate with the presence of clinical nephropathy.

53
Q

Which autoimmune disease involves antibodies targeting the α3 NC1 domain of collagen IV?
A. Alport syndrome
B. Membranous nephropathy
C. Anti-glomerular basement membrane (anti-GBM) disease
D. Minimal change disease

A

C. Anti-glomerular basement membrane (anti-GBM) disease

Rationale: Anti-GBM disease is caused by autoantibodies directed against the α3 NC1 domain of type IV collagen in the glomerular basement membrane.

54
Q

What syndrome is commonly associated with anti-GBM disease?
A. Nephrotic syndrome
B. Goodpasture’s syndrome
C. Lupus nephritis
D. Henoch-Schönlein purpura

A

B. Goodpasture’s syndrome

Rationale: Goodpasture’s syndrome refers to the combination of anti-GBM disease with pulmonary-renal syndrome, characterized by rapidly progressive glomerulonephritis (RPGN) and pulmonary hemorrhage.

55
Q

Which of the following is a hallmark feature of anti-GBM disease on renal biopsy?
A. Mesangial proliferation
B. Linear deposition of IgG along the glomerular basement membrane
C. Immune complex deposition in the subepithelial space
D. Granular staining on immunofluorescence

A

B. Linear deposition of IgG along the glomerular basement membrane

Rationale: The hallmark of anti-GBM disease is linear IgG staining along the GBM on immunofluorescence microscopy, reflecting the binding of autoantibodies to the α3 NC1 domain of collagen IV.

56
Q

What pulmonary complication is often seen in Goodpasture’s syndrome?
A. Pulmonary edema
B. Pulmonary hemorrhage
C. Pleural effusion
D. Interstitial fibrosis

A

B. Pulmonary hemorrhage

Rationale: Goodpasture’s syndrome frequently includes pulmonary hemorrhage due to autoantibody-mediated damage to the alveolar basement membrane.

57
Q

Which of the following features is characteristic of Alport’s syndrome?
A. Granular IgG deposits in the glomerular basement membrane (GBM)
B. Thinning and splitting of the GBM
C. Crescent formation in glomeruli
D. Nodular glomerulosclerosis

A

B. Thinning and splitting of the GBM

Rationale: Alport’s syndrome is characterized by thinning and splitting of the GBM due to mutations in type IV collagen, leading to progressive renal disease.

58
Q

Which clinical finding is NOT typically associated with Alport’s syndrome?
A. Sensorineural deafness
B. Lenticonus of the anterior lens capsule
C. “Dot and fleck” retinopathy
D. Pulmonary hemorrhage

A

D. Pulmonary hemorrhage

Rationale: Pulmonary hemorrhage is not a feature of Alport’s syndrome. However, sensorineural deafness, anterior lenticonus, and “dot and fleck” retinopathy are characteristic extrarenal manifestations.

59
Q

What is the mode of inheritance in approximately 85% of Alport’s syndrome cases?
A. Autosomal recessive
B. Autosomal dominant
C. X-linked
D. Mitochondrial

A

C. X-linked

Rationale: The majority of Alport’s syndrome cases (85%) are X-linked, caused by mutations in the α5(IV) collagen chain on chromosome Xq22–24.

60
Q

Which genetic mutation is commonly associated with X-linked Alport’s syndrome?
A. Mutation in α1(IV) collagen
B. Mutation in α3(IV) collagen
C. Mutation in α5(IV) collagen
D. Mutation in α6(IV) collagen

A

C. Mutation in α5(IV) collagen

Rationale: X-linked Alport’s syndrome is caused by mutations in the gene encoding the α5(IV) collagen chain, critical for the integrity of the GBM.

61
Q

What structural abnormality is seen in the kidneys of patients with Alport’s syndrome under electron microscopy?
A. Linear deposition of IgG
B. Effacement of podocyte foot processes
C. Basket-weave appearance of the GBM
D. Dense immune deposits in the mesangium

A

C. Basket-weave appearance of the GBM

Rationale: The GBM in Alport’s syndrome shows a characteristic basket-weave appearance on electron microscopy due to irregular thickening, thinning, and lamellation.

62
Q

What is the primary clinical manifestation of thin basement membrane disease (TBMD)?
A. Proteinuria and hypertension
B. Microscopic hematuria
C. Rapidly progressive renal failure
D. Edema and nephrotic syndrome

A

B. Microscopic hematuria

Rationale: TBMD is characterized by persistent or intermittent microscopic hematuria. It is typically asymptomatic and not associated with proteinuria or significant renal dysfunction.

63
Q

What pattern of inheritance is most frequently observed in thin basement membrane disease?
A. Autosomal recessive
B. X-linked
C. Autosomal dominant
D. Mitochondrial

A

C. Autosomal dominant

Rationale: TBMD is typically inherited in an autosomal dominant pattern and often affects multiple family members, manifesting as benign familial hematuria.

64
Q

What renal biopsy finding is most characteristic of TBMD?
A. Basket-weave appearance of the GBM
B. Linear IgG deposition along the GBM
C. Diffuse thinning of the GBM
D. Subepithelial immune deposits

A

C. Diffuse thinning of the GBM

Rationale: The hallmark of TBMD on renal biopsy is diffuse thinning of the GBM, in contrast to the thickening or splitting observed in other glomerular diseases like Alport’s syndrome.