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CAQ-Nephrology study materials
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CAQ-Nephrology practice questions

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Question 1Glomerular and Tubulointerstitial Disease

A 6-year-old boy presents with periorbital edema, nephrotic-range proteinuria, and normal serum complement. Light microscopy of a renal biopsy is unremarkable. Which finding is most characteristic of the glomerular lesion?

  1. Diffuse podocyte foot process effacement on electron microscopy Correct answer.
  2. Tram-track double contours of the glomerular basement membrane
  3. Subepithelial immune complex humps on electron microscopy
  4. Mesangial deposits of IgA on immunofluorescence

Explanation

Minimal change disease is the most common cause of childhood nephrotic syndrome and produces no light-microscopic abnormality; electron microscopy shows widespread podocyte foot process effacement. Complement levels are typically normal, and immunofluorescence is negative.

Question 2Glomerular and Tubulointerstitial Disease

Two weeks after a pharyngeal streptococcal infection, a 7-year-old develops cola-colored urine, hypertension, and a low serum C3 level. Which renal biopsy finding is most expected?

  1. Subepithelial immune deposits containing anti-PLA2R antibody
  2. Linear IgG deposition along the glomerular basement membrane
  3. Mesangial IgA deposits
  4. Subepithelial immune complex humps Correct answer.

Explanation

Post-streptococcal glomerulonephritis is an immune-complex–mediated nephritis that follows streptococcal infection by one to three weeks. It classically causes low C3, hematuria, hypertension, and subepithelial humps on electron microscopy.

Question 3Glomerular and Tubulointerstitial Disease

A 30-year-old man has persistent isolated microscopic hematuria, normal renal function, no proteinuria, and a family history of hematuria. Renal biopsy shows uniform thinning of the glomerular basement membrane without immune deposits. What is the most likely diagnosis?

  1. Focal segmental glomerulosclerosis
  2. Thin basement membrane nephropathy Correct answer.
  3. IgA nephropathy
  4. Alport syndrome

Explanation

Thin basement membrane nephropathy is a benign familial condition characterized by isolated hematuria, normal kidney function, and diffuse GBM thinning on electron microscopy. Immune deposits are absent, and progression to kidney failure is uncommon.

Question 4Glomerular and Tubulointerstitial Disease

A 24-year-old man develops gross hematuria within two days of an upper respiratory infection, and his serum complement level is normal. Renal biopsy shows mesangial proliferation with IgA deposits. Which statement about this condition is correct?

  1. It is the most common primary glomerulonephritis. Correct answer.
  2. It uniformly responds to corticosteroid therapy.
  3. It is caused by circulating antibodies against the glomerular basement membrane.
  4. Serum C3 is typically low during episodes.

Explanation

IgA nephropathy is the most common primary glomerulonephritis in many populations, and its hallmark is mesangial IgA deposition with normal complement levels. Hematuria often follows mucosal infections within a few days, a shorter latency than post-streptococcal nephritis.

Question 5Glomerular and Tubulointerstitial Disease

A 55-year-old woman with nephrotic syndrome has a renal biopsy showing subepithelial immune deposits and spiked glomerular basement membrane. Which finding best supports primary membranous nephropathy over a secondary cause?

  1. Positive serum anti-PLA2R antibody Correct answer.
  2. Diffuse thickening of the glomerular basement membrane
  3. Nephrotic-range proteinuria
  4. Subepithelial deposits on electron microscopy

Explanation

Anti-PLA2R antibodies are found in the majority of primary membranous nephropathy and are uncommon in secondary forms. Secondary membranous nephropathy may instead accompany lupus, malignancy, or drugs.

Question 6Glomerular and Tubulointerstitial Disease

A 60-year-old man taking omeprazole and ibuprofen develops acute kidney injury, sterile pyuria, and peripheral eosinophilia. Renal biopsy shows interstitial inflammation with eosinophils. Which urinary finding is most consistent with this disorder?

  1. White blood cell casts Correct answer.
  2. Broad waxy casts
  3. Red blood cell casts
  4. Oval fat bodies

Explanation

Acute interstitial nephritis causes tubulointerstitial inflammation and is associated with sterile pyuria and white blood cell casts. Eosinophiluria and eosinophilia may support the diagnosis, although neither is specific.

Question 7Glomerular and Tubulointerstitial Disease

A 10-year-old boy has microscopic hematuria, sensorineural hearing loss, and anterior lenticonus. His maternal uncle developed kidney failure in his twenties. Which genetic defect is most likely responsible?

  1. NPHS1 mutation
  2. COL4A5 mutation Correct answer.
  3. APOL1 risk variants
  4. COL4A3 mutation

Explanation

Alport syndrome with hearing loss and lenticonus is most often X-linked and caused by COL4A5 mutations in type IV collagen. The maternal-uncle history fits X-linked inheritance, and COL4A3 mutations more often cause autosomal recessive disease.

Question 8Glomerular and Tubulointerstitial Disease

A 35-year-old man of West African ancestry presents with nephrotic syndrome and hypertension. Renal biopsy shows segmental glomerular sclerosis with collapse of some tufts and podocyte hyperplasia. Which factor is most strongly associated with this presentation?

  1. Sickle cell trait
  2. COL4A5 mutation
  3. Anti-PLA2R antibodies
  4. APOL1 G1/G2 risk variants Correct answer.

Explanation

APOL1 G1 and G2 risk variants are strongly associated with HIV-associated and collapsing FSGS, particularly in individuals of West African ancestry. The collapsing variant shows tuft collapse and podocyte hyperplasia and tends to be aggressive.

Question 9Glomerular and Tubulointerstitial Disease

A 20-year-old woman has hematuria, proteinuria, a low C3 level, and a normal C4 level. Renal biopsy shows dominant C3 deposition in the mesangium and capillary walls without immunoglobulin. Which mechanism best explains this pattern?

  1. Dysregulation of the alternative complement pathway Correct answer.
  2. Autoantibodies directed against the glomerular basement membrane
  3. Classical pathway activation by immune complexes
  4. Lectin pathway activation triggered by IgA deposits

Explanation

Dominant C3 deposition with normal C4 and low C3 indicates C3 glomerulopathy, which results from alternative pathway dysregulation such as C3 nephritic factor. The absence of immunoglobulin deposits argues against immune-complex–mediated MPGN.

Question 10Glomerular and Tubulointerstitial Disease

A 40-year-old man presents with rapidly progressive kidney failure, hemoptysis, and linear IgG deposition along the glomerular basement membrane. Which diagnosis is most likely?

  1. IgA nephropathy
  2. Granulomatosis with polyangiitis
  3. Membranous nephropathy
  4. Anti-GBM antibody disease Correct answer.

Explanation

Linear IgG along the GBM with rapidly progressive nephritis and pulmonary hemorrhage defines anti-GBM disease, also called Goodpasture syndrome when lung involvement is present. Crescentic glomerulonephritis is the typical biopsy finding.

Question 11Glomerular and Tubulointerstitial Disease

A 29-year-old woman presents with malar rash, oral ulcers, arthralgia, and new hypertension. Urinalysis shows 3+ protein and red cell casts; serum C3 and C4 are low. Renal biopsy immunofluorescence demonstrates granular deposition of IgG, IgA, IgM, C3, and C1q along the glomerular capillary loops. Which diagnosis best fits these findings?

  1. IgA nephropathy
  2. Lupus nephritis Correct answer.
  3. Postinfectious glomerulonephritis
  4. Anti-GBM disease

Explanation

The combination of malar rash, oral ulcers, low C3 and C4, and 'full-house' granular immunofluorescence is characteristic of lupus nephritis. Postinfectious glomerulonephritis typically shows granular C3 and IgG with a low C3 but normal C4, while IgA nephropathy is IgA-dominant and anti-GBM disease produces linear IgG.

Question 12Glomerular and Tubulointerstitial Disease

A 64-year-old man with long-standing rheumatoid arthritis develops nephrotic-range proteinuria and progressive kidney failure. Renal biopsy shows amorphous eosinophilic deposits in the mesangium and capillary walls that stain with Congo red and show apple-green birefringence under polarized light. Which diagnosis is most likely?

  1. Fibrillary glomerulonephritis
  2. AL amyloidosis
  3. Light chain cast nephropathy
  4. AA amyloidosis Correct answer.

Explanation

AA amyloidosis complicates chronic inflammatory states such as rheumatoid arthritis and produces Congo red-positive deposits with apple-green birefringence. AL amyloidosis is driven by a plasma cell dyscrasia, while fibrillary glomerulonephritis is Congo red-negative and cast nephropathy affects tubules rather than producing mesangial amyloid.

Question 13Glomerular and Tubulointerstitial Disease

A 58-year-old woman with a 15-year history of type 2 diabetes and retinopathy has slowly increasing proteinuria and declining eGFR. Renal biopsy shows nodular mesangial expansion with eosinophilic Kimmelstiel-Wilson nodules and linear IgG staining along the glomerular basement membrane. Which diagnosis is most likely?

  1. Minimal change disease
  2. Amyloidosis
  3. Diabetic nephropathy Correct answer.
  4. Membranous nephropathy

Explanation

Long-standing diabetes with retinopathy, nodular mesangial expansion, and Kimmelstiel-Wilson nodules is classic for diabetic nephropathy. The linear IgG staining is nonspecific and does not indicate anti-GBM disease; membranous nephropathy shows subepithelial spikes, amyloidosis is Congo red-positive, and minimal change disease has normal light microscopy.

Question 14Glomerular and Tubulointerstitial Disease

A 67-year-old man presents with sinus pain, bloody nasal discharge, a rising serum creatinine, and diffuse alveolar hemorrhage. Renal biopsy shows crescentic glomerulonephritis with negative immunofluorescence for IgG, IgA, IgM, C3, and C1q. Which diagnosis is most likely?

  1. IgA nephropathy
  2. Granulomatosis with polyangiitis Correct answer.
  3. Anti-GBM disease
  4. Lupus nephritis

Explanation

Pauci-immune crescentic glomerulonephritis combined with upper and lower respiratory tract disease strongly suggests granulomatosis with polyangiitis, usually associated with PR3-ANCA. Anti-GBM disease shows linear IgG, IgA nephropathy shows IgA deposits, and lupus nephritis shows granular full-house immunofluorescence.

Question 15Glomerular and Tubulointerstitial Disease

A 6-year-old boy develops palpable purpura over the buttocks and lower extremities, colicky abdominal pain, and hematuria two weeks after a viral upper respiratory illness. Serum complement levels are normal and the platelet count is normal. Which diagnosis is most likely?

  1. Poststreptococcal glomerulonephritis
  2. Thrombotic thrombocytopenic purpura
  3. IgA vasculitis (Henoch-Schönlein purpura) Correct answer.
  4. Hemolytic uremic syndrome

Explanation

Palpable purpura, abdominal pain, and hematuria with normal platelets and complement levels form the typical presentation of IgA vasculitis in children. Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome cause thrombocytopenia, while poststreptococcal glomerulonephritis typically lowers C3.

Question 16Glomerular and Tubulointerstitial Disease

A 52-year-old woman with chronic hepatitis C infection presents with palpable purpura, arthralgia, and nephrotic-range proteinuria. Serum C4 is markedly low and C3 is mildly low; cryoglobulins are positive. Renal biopsy shows membranoproliferative glomerulonephritis with intraluminal immune thrombi. Which process best explains these findings?

  1. Minimal change disease
  2. C3 glomerulopathy
  3. Cryoglobulinemic vasculitis causing MPGN Correct answer.
  4. Anti-GBM disease

Explanation

Chronic hepatitis C can cause mixed cryoglobulinemia, which activates the classical complement pathway, lowering C4 more than C3 and depositing immune complexes that produce an MPGN pattern with intraluminal thrombi. C3 glomerulopathy is characterized by isolated low C3 and dominant C3 deposition without cryoglobulins.

Question 17Glomerular and Tubulointerstitial Disease

A 61-year-old woman with bipolar disorder has polyuria, polydipsia, and a slowly rising creatinine after many years of maintenance therapy. Urinalysis shows no cells, no casts, and only trace protein. Renal biopsy shows interstitial fibrosis and tubular atrophy without significant glomerular disease. Which maintenance medication most likely explains the tubulointerstitial injury?

  1. Tenofovir
  2. Omeprazole
  3. Lithium therapy Correct answer.
  4. Ibuprofen

Explanation

Long-term lithium therapy causes chronic tubulointerstitial nephritis and nephrogenic diabetes insipidus, producing polyuria, bland urinalysis, and progressive fibrosis. Omeprazole and ibuprofen are more associated with acute interstitial nephritis, and tenofovir can cause proximal tubular injury.

Question 18Glomerular and Tubulointerstitial Disease

A 70-year-old man with anemia, hypercalcemia, and a monoclonal IgG spike develops acute kidney injury. Urine protein electrophoresis shows a monoclonal light chain, but the urine dipstick protein is only trace. Renal biopsy shows obstructed distal tubules filled with fractured, eosinophilic casts surrounded by giant cells. Which diagnosis is most likely?

  1. Membranous nephropathy
  2. Light chain cast nephropathy Correct answer.
  3. Acute interstitial nephritis
  4. AL amyloidosis

Explanation

Light chain cast nephropathy occurs when filtered monoclonal light chains obstruct distal tubules, producing fractured casts with a giant cell reaction; the urine dipstick may be misleadingly negative because it detects albumin poorly. AL amyloidosis produces Congo red-positive deposits, membranous nephropathy produces subepithelial deposits, and acute interstitial nephritis shows interstitial inflammation.

Question 19Glomerular and Tubulointerstitial Disease

A 34-year-old woman presents with microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury five days after a diarrheal illness. Peripheral smear shows schistocytes, and coagulation studies are normal. Renal biopsy shows fibrin thrombi in glomerular capillaries and arterioles without immune deposits. Which diagnosis is most likely?

  1. IgA nephropathy
  2. Hemolytic uremic syndrome Correct answer.
  3. Antiphospholipid syndrome
  4. Membranoproliferative glomerulonephritis

Explanation

Diarrhea-associated hemolytic uremic syndrome is caused by Shiga toxin-producing Escherichia coli and produces the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury with normal coagulation studies. Biopsy shows fibrin thrombi without immune deposits, unlike IgA nephropathy or MPGN.

Question 20Glomerular and Tubulointerstitial Disease

A 28-year-old man has episodes of burning pain in the hands and feet, decreased sweating, and clusters of small red-purple skin lesions around the umbilicus and groin. He also has proteinuria. Electron microscopy of the kidney shows numerous lamellated inclusions within podocytes. Which diagnosis is most likely?

  1. Fabry disease Correct answer.
  2. Niemann-Pick disease
  3. Minimal change disease
  4. Alport syndrome

Explanation

Fabry disease is an X-linked deficiency of alpha-galactosidase A that causes acroparesthesias, hypohidrosis, angiokeratomas, and proteinuria, with lamellated glycosphingolipid inclusions in podocytes. Alport syndrome causes hearing loss and lenticonus, Niemann-Pick disease causes hepatosplenomegaly and foam cells, and minimal change disease has normal glomerular ultrastructure.

Question 21Glomerular and Tubulointerstitial Disease

A 63-year-old man with long-standing multiple myeloma presents with nephrotic-range proteinuria and progressive edema. Renal biopsy shows amorphous eosinophilic mesangial deposits that stain with Congo red and demonstrate apple-green birefringence under polarized light. Which protein most commonly forms these deposits in AL amyloidosis?

  1. Fibrinogen A alpha chain
  2. Serum amyloid A protein
  3. Monoclonal immunoglobulin light chains Correct answer.
  4. Transthyretin

Explanation

AL amyloidosis is caused by tissue deposition of monoclonal immunoglobulin light chains, most often lambda type, produced by a plasma cell clone. Congo red staining with apple-green birefringence is characteristic of amyloid fibrils. Serum amyloid A causes AA amyloidosis, whereas transthyretin and fibrinogen A alpha chain cause hereditary amyloidoses.

Question 22Glomerular and Tubulointerstitial Disease

A 38-year-old man with untreated HIV infection has a CD4 count of 90 cells/mm3, a high HIV viral load, nephrotic-range proteinuria, and rising creatinine. Renal biopsy shows collapsing focal segmental glomerulosclerosis with tubulointerstitial inflammation. Which factor best explains the strong predisposition to this lesion in patients of West African ancestry?

  1. Complement factor H mutation
  2. APOL1 high-risk variants Correct answer.
  3. HLA-B27
  4. ACE insertion/deletion polymorphism

Explanation

HIV-associated nephropathy typically presents as collapsing focal segmental glomerulosclerosis, and the risk is strongly linked to the APOL1 G1 and G2 high-risk variants common in West African populations. These variants also predispose to other forms of APOL1-associated kidney disease. HIV viral proteins and direct viral infection contribute to podocyte injury.

Question 23Glomerular and Tubulointerstitial Disease

A 52-year-old woman with dry eyes and dry mouth has chronic kidney disease, serum potassium 2.9 mmol/L, and a non-anion gap metabolic acidosis. Urinalysis shows no significant proteinuria or hematuria. Which renal lesion best explains these findings?

  1. Nephrogenic diabetes insipidus
  2. Distal renal tubular acidosis from tubulointerstitial nephritis Correct answer.
  3. Type 4 renal tubular acidosis from hypoaldosteronism
  4. Proximal renal tubular acidosis from Fanconi syndrome

Explanation

Sjögren syndrome commonly causes tubulointerstitial nephritis, which can impair distal hydrogen ion secretion and produce distal renal tubular acidosis. Distal RTA causes a non-anion gap metabolic acidosis with hypokalemia, and the urinary sediment is often bland. Proximal RTA would be accompanied by glycosuria, phosphaturia, and aminoaciduria.

Question 24Glomerular and Tubulointerstitial Disease

A 47-year-old man with fever, a new heart murmur, and multiple blood cultures growing Staphylococcus aureus develops hematuria, proteinuria, a low C3 level, and rising creatinine. Renal biopsy shows diffuse proliferative glomerulonephritis with subepithelial humps. Which mechanism best explains the glomerular injury?

  1. Anti-glomerular basement membrane antibodies
  2. Glomerular deposition of circulating immune complexes Correct answer.
  3. ANCA-mediated neutrophil activation
  4. Direct bacterial invasion of glomerular capillaries

Explanation

Endocarditis-associated glomerulonephritis is an infection-related immune complex glomerulonephritis. Circulating immune complexes containing bacterial antigens deposit in glomeruli, activate complement, and produce a proliferative pattern with subepithelial humps and low C3. Treating the infection is central to management.

Question 25Glomerular and Tubulointerstitial Disease

A 66-year-old woman with metastatic melanoma started ipilimumab plus nivolumab 8 weeks ago. Serum creatinine has risen from 0.9 to 2.4 mg/dL, urinalysis shows sterile pyuria with white blood cell casts, and she has no rash, fever, or eosinophilia. Which next step is most appropriate?

  1. Start broad-spectrum antibiotics
  2. Begin therapeutic plasma exchange
  3. Hold immunotherapy and start high-dose glucocorticoids Correct answer.
  4. Continue immunotherapy and monitor creatinine

Explanation

Checkpoint inhibitor-associated acute interstitial nephritis is treated by withholding the offending agent and giving corticosteroids, especially when kidney function is significantly impaired. White blood cell casts support tubulointerstitial inflammation. The classic fever, rash, and eosinophilia triad is often absent.

Question 26Glomerular and Tubulointerstitial Disease

A 54-year-old kidney transplant recipient 7 months after transplantation has creatinine rising from 1.3 to 2.1 mg/dL. Urinalysis is bland, BK viral load is 12,000 copies/mL, and biopsy shows viral cytopathic changes in tubular epithelial cells with SV40 positivity. Which management is most appropriate?

  1. Start oral acyclovir
  2. Increase immunosuppression
  3. Proceed with transplant nephrectomy
  4. Reduce immunosuppression Correct answer.

Explanation

BK polyomavirus nephropathy is managed primarily by reducing immunosuppression so that the host immune response can control viral replication. There is no consistently effective antiviral therapy for BK nephropathy, and reducing immunosuppression improves outcomes when done before irreversible fibrosis develops. Graft nephrectomy is reserved for a nonviable or rejected graft.

Question 27Glomerular and Tubulointerstitial Disease

A 58-year-old man has painless obstructive jaundice, an enlarged pancreas, and slowly rising creatinine. Serum IgG4 is elevated, and renal biopsy shows a dense lymphoplasmacytic infiltrate with storiform fibrosis and numerous IgG4-positive plasma cells. Which renal diagnosis is most likely?

  1. NSAID-induced acute interstitial nephritis
  2. IgG4-related tubulointerstitial nephritis Correct answer.
  3. Light chain cast nephropathy
  4. Granulomatosis with polyangiitis

Explanation

IgG4-related disease commonly involves the pancreas and biliary tree and can cause a tubulointerstitial nephritis with storiform fibrosis and IgG4-positive plasma cells. Serum IgG4 is often elevated, though it is not specific by itself. Glucocorticoids are the mainstay of treatment.

Question 28Glomerular and Tubulointerstitial Disease

A 61-year-old woman with short bowel syndrome after extensive intestinal resection develops rising creatinine. Urine microscopy shows numerous envelope-shaped calcium oxalate crystals, and renal biopsy shows crystals within tubules with surrounding interstitial inflammation. Which mechanism best explains her kidney disease?

  1. Uric acid nephropathy
  2. Cystinuria
  3. Hypercalcemia-induced nephrocalcinosis
  4. Enteric hyperoxaluria Correct answer.

Explanation

Extensive small bowel resection causes fat malabsorption; unabsorbed fatty acids bind dietary calcium, leaving more free oxalate to be absorbed in the colon. The resulting enteric hyperoxaluria causes calcium oxalate crystal deposition in tubules and can lead to chronic kidney disease. Treatment includes a low-oxalate diet, calcium supplementation with meals, and correction of volume depletion.

Question 29Glomerular and Tubulointerstitial Disease

A 57-year-old woman has proteinuria of 4.5 g/day, hematuria, hypertension, and slowly rising creatinine. Serologies for hepatitis, ANCA, and anti-GBM are negative. Renal biopsy shows mesangial and capillary wall deposits that are Congo red negative, stain for IgG and C3, and contain randomly oriented nonbranching fibrils 15 to 20 nm in diameter on electron microscopy. Which diagnosis is most likely?

  1. Light chain deposition disease
  2. Cryoglobulinemic glomerulonephritis
  3. AL amyloidosis
  4. Fibrillary glomerulonephritis Correct answer.

Explanation

Fibrillary glomerulonephritis is characterized by Congo red-negative randomly oriented fibrils that are thicker than amyloid fibrils, typically 15 to 20 nm, with IgG and C3 deposition. It commonly presents with proteinuria, hematuria, hypertension, and progressive kidney disease. Amyloid fibrils are thinner, Congo red positive, and show apple-green birefringence.

Question 30Glomerular and Tubulointerstitial Disease

A 64-year-old man with bone pain, anemia, and a serum monoclonal kappa free light chain has glycosuria, phosphaturia, aminoaciduria, and a serum phosphate of 2.0 mg/dL. Creatinine is only mildly elevated. Renal biopsy shows proximal tubular cells containing intracytoplasmic crystalline inclusions that stain for kappa. Which diagnosis is most likely?

  1. AL amyloidosis
  2. Tenofovir-induced Fanconi syndrome
  3. Myeloma cast nephropathy
  4. Light chain proximal tubulopathy Correct answer.

Explanation

Light chain proximal tubulopathy is caused by monoclonal light chain deposition or crystallization within proximal tubular cells, producing a Fanconi syndrome with glycosuria, phosphaturia, and aminoaciduria. Kidney function may be only mildly reduced early in the course. The crystalline intracytoplasmic kappa inclusions are characteristic.

Question 31Glomerular and Tubulointerstitial Disease

A 24-year-old man presents with a 2-week history of periorbital and leg edema. Blood pressure is 118/72 mmHg, serum albumin is 2.1 g/dL, and urine protein is 9.8 g/day. Complement levels are normal, and light microscopy of a kidney biopsy is unremarkable. Which electron microscopy finding is most characteristic?

  1. Double-contour basement membranes
  2. Diffuse foot-process effacement Correct answer.
  3. Mesangial deposits of IgA
  4. Subepithelial immune-complex humps

Explanation

Minimal change disease produces nephrotic syndrome with normal light microscopy and no immune deposits. Electron microscopy shows widespread podocyte foot-process effacement, which explains the selective proteinuria. Subepithelial humps, tram-track membranes, and mesangial IgA deposits indicate other glomerular diseases.

Question 32Glomerular and Tubulointerstitial Disease

An 8-year-old girl develops cola-colored urine and hypertension 12 days after a sore throat. Complement C3 is low and C4 is normal. Which biopsy finding best supports the likely diagnosis?

  1. Linear IgG staining along the glomerular basement membrane
  2. Subepithelial immune-complex humps Correct answer.
  3. Segmental sclerosis with hyalinosis
  4. Pauci-immune crescent formation

Explanation

Post-streptococcal glomerulonephritis typically follows pharyngitis by 1 to 3 weeks and causes low C3 with normal C4. Biopsy shows granular subepithelial immune-complex deposits, often called humps. Linear IgG, segmental sclerosis, and pauci-immune crescents point to anti-GBM disease, FSGS, and ANCA vasculitis, respectively.

Question 33Glomerular and Tubulointerstitial Disease

A 16-year-old boy has persistent microscopic hematuria, progressive sensorineural hearing loss, and a maternal uncle with kidney failure. Kidney biopsy shows alternating thinning and thickening of the glomerular basement membrane, and immunofluorescence is negative. Which diagnosis is most likely?

  1. X-linked Alport syndrome Correct answer.
  2. Autosomal dominant polycystic kidney disease
  3. IgA nephropathy
  4. Thin basement membrane nephropathy

Explanation

X-linked Alport syndrome results from COL4A5 mutations and causes hematuria, sensorineural deafness, and progressive kidney disease with a characteristic family history. Biopsy shows irregular thinning, thickening, and splitting of the glomerular basement membrane without immune deposits. Thin basement membrane nephropathy is benign and does not cause deafness.

Question 34Glomerular and Tubulointerstitial Disease

A 45-year-old man has nephrotic syndrome, normal complement levels, and a positive anti-PLA2R antibody. Kidney biopsy shows subepithelial immune deposits. Which additional biopsy finding is most characteristic of this disease?

  1. Subepithelial deposits with GBM spikes Correct answer.
  2. Mesangial hypercellularity with IgA deposits
  3. Subendothelial deposits with tram-track appearance
  4. Crescents in most glomeruli

Explanation

Primary membranous nephropathy is associated with anti-PLA2R antibodies and causes subepithelial immune deposits. Silver staining shows basement membrane spikes growing between deposits. Tram tracks, mesangial IgA, and extensive crescents indicate different glomerular diseases.

Question 35Glomerular and Tubulointerstitial Disease

A 68-year-old woman has fatigue, weight loss, foot drop, and a serum creatinine of 3.1 mg/dL. Urinalysis shows dysmorphic red cells and red-cell casts. MPO-ANCA is positive, anti-GBM is negative, and complement levels are normal. Which biopsy pattern is most likely?

  1. Mesangial C3 deposits only
  2. Pauci-immune crescentic glomerulonephritis Correct answer.
  3. Linear IgG along the glomerular basement membrane
  4. Granular subepithelial immune deposits

Explanation

Microscopic polyangiitis is an ANCA-associated vasculitis that commonly causes pauci-immune crescentic glomerulonephritis. Positive MPO-ANCA with active urine sediment and a mononeuritis multiplex presentation supports this diagnosis. Linear IgG, subepithelial deposits, and isolated C3 deposits indicate other forms of glomerular injury.

Question 36Glomerular and Tubulointerstitial Disease

A 57-year-old woman started omeprazole 6 weeks ago for reflux. She now has fatigue, a creatinine rise from 0.9 to 2.4 mg/dL, sterile pyuria, and white-cell casts. Urine eosinophils are present. Which biopsy finding best supports the diagnosis?

  1. Amyloid deposition in arterioles
  2. Foam cells in the interstitium
  3. Crescentic glomerulonephritis
  4. Interstitial infiltrate with eosinophils Correct answer.

Explanation

Drug-induced acute interstitial nephritis classically presents with a rising creatinine, sterile pyuria, white-cell casts, and eosinophiluria after exposure to a medication such as a proton-pump inhibitor. Biopsy shows interstitial inflammation rich in lymphocytes and eosinophils. Crescentic, amyloid, and prominent foam-cell patterns indicate other diagnoses.

Question 37Glomerular and Tubulointerstitial Disease

A 22-year-old man develops hematuria, hypertension, and edema after a mild upper respiratory illness. C3 is low, C4 is normal, and antinuclear antibodies are negative. Kidney biopsy shows isolated C3 deposition in mesangium and capillary walls with no immunoglobulin. Which diagnosis is most likely?

  1. Post-infectious glomerulonephritis
  2. IgA nephropathy
  3. Membranous nephropathy
  4. C3 glomerulonephritis Correct answer.

Explanation

C3 glomerulonephritis results from alternative complement pathway dysregulation and shows dominant C3 deposition with little or no immunoglobulin. Low C3 with normal C4 fits alternative pathway activation. Post-infectious glomerulonephritis can also lower C3, but biopsy usually shows immunoglobulin and subepithelial humps.

Question 38Glomerular and Tubulointerstitial Disease

A 38-year-old man with class III obesity has 3.8 g/day proteinuria and a creatinine of 1.3 mg/dL. Kidney biopsy shows focal segmental sclerosis with glomerulomegaly and hyalinosis, and electron microscopy shows only segmental foot-process effacement. Which initial management is most appropriate?

  1. Rituximab infusion weekly for 4 weeks
  2. Cyclophosphamide plus plasmapheresis
  3. High-dose prednisone for 8 to 16 weeks
  4. Weight loss plus ACE inhibitor or ARB Correct answer.

Explanation

Obesity-related secondary FSGS produces glomerulomegaly, hyalinosis, and only segmental foot-process effacement. It does not respond to immunosuppression; management targets weight loss and uses ACE inhibitors or ARBs to reduce proteinuria and slow progression. High-dose steroids, cyclophosphamide, and rituximab are used for selected primary glomerular diseases.

Question 39Glomerular and Tubulointerstitial Disease

A 25-year-old man presents with hemoptysis and acute kidney injury. Anti-GBM antibodies are positive, and kidney biopsy shows linear IgG staining along the glomerular basement membrane. Which antigen is the principal target of these autoantibodies?

  1. Phospholipase A2 receptor on podocytes
  2. Myeloperoxidase in neutrophil granules
  3. Alpha-3 NC1 domain of collagen IV Correct answer.
  4. Complement factor H in plasma

Explanation

Anti-GBM disease is caused by autoantibodies against the noncollagenous 1 domain of the alpha-3 chain of type IV collagen. Binding produces linear IgG along the glomerular basement membrane and crescentic glomerulonephritis, often with pulmonary hemorrhage. PLA2R, myeloperoxidase, and factor H are targets in other kidney or complement disorders.

Question 40Glomerular and Tubulointerstitial Disease

A 70-year-old woman has a 10-year history of chronic back pain treated with a combination analgesic containing phenacetin. She has slowly rising creatinine, difficulty concentrating urine, and sterile pyuria. CT shows papillary necrosis. Which process best explains her kidney disease?

  1. Granular subendothelial immune-complex deposition
  2. Medullary ischemia from prostaglandin inhibition Correct answer.
  3. Crescentic injury triggered by anti-GBM antibodies
  4. Amyloid fibril accumulation in the medulla

Explanation

Analgesic nephropathy causes chronic tubulointerstitial injury and papillary necrosis, especially with prolonged combination analgesic use including phenacetin. Prostaglandin inhibition reduces medullary blood flow and produces ischemia, fibrosis, and papillary damage. Immune-complex deposition, amyloidosis, and anti-GBM crescents cause different patterns of kidney injury.

Question 41Fluid, Electrolyte, and Acid-Base Disorders

A 68-year-old man with small cell lung cancer has serum sodium 118 mEq/L and appears clinically euvolemic. Serum osmolality is 250 mOsm/kg, urine osmolality 480 mOsm/kg, and urine sodium 55 mEq/L on a normal salt diet. He takes no diuretics, and thyroid and adrenal testing are normal. Which cause of hyponatremia is most likely?

  1. Hypovolemic hyponatremia from diuretic use
  2. SIADH from ectopic ADH production by the tumor Correct answer.
  3. Primary polydipsia with appropriately dilute urine
  4. Hypervolemic hyponatremia of decompensated heart failure

Explanation

Euvolemic hypotonic hyponatremia with urine osmolality above 100 mOsm/kg and urine sodium above 40 mEq/L, in a patient with normal thyroid and adrenal function and no diuretics, defines SIADH. The concentrated urine reflects continued ADH effect despite serum hypotonicity, as occurs with ectopic ADH from small cell lung cancer.

Question 42Fluid, Electrolyte, and Acid-Base Disorders

A patient with advanced CKD has a serum potassium of 7.2 mEq/L and a widened QRS complex on the ECG. Which therapy should be given first?

  1. Administer intravenous insulin with dextrose
  2. Administer oral sodium polystyrene sulfonate
  3. Administer intravenous calcium gluconate Correct answer.
  4. Administer nebulized albuterol

Explanation

A widened QRS indicates hyperkalemic cardiac membrane instability, and intravenous calcium is the immediate treatment because it restores the myocardial threshold potential without lowering serum potassium. Potassium-lowering measures are then given to shift potassium into cells and later remove it from the body.

Question 43Fluid, Electrolyte, and Acid-Base Disorders

A hospitalized patient has arterial pH 7.22, bicarbonate 8 mEq/L, sodium 140 mEq/L, chloride 110 mEq/L, and a normal serum albumin. Which acid-base disturbance is present?

  1. High-anion-gap acidosis with concurrent metabolic alkalosis
  2. Pure high-anion-gap metabolic acidosis
  3. Pure normal-anion-gap metabolic acidosis
  4. Mixed high- and normal-anion-gap acidosis Correct answer.

Explanation

The anion gap is 140 minus 110 minus 8, or 22 mEq/L, so the delta gap is about 10 above a normal value of 12 while bicarbonate has fallen by 16 mEq/L. A delta ratio below 1 means bicarbonate is lower than the high-anion-gap acidosis alone would explain, indicating a superimposed normal-anion-gap acidosis such as diarrhea or renal tubular acidosis.

Question 44Fluid, Electrolyte, and Acid-Base Disorders

A 70-kg man with poor oral intake has a serum sodium of 160 mEq/L and no ongoing losses. Using total body water estimated at 60% of body weight and a target sodium of 140 mEq/L, what is his approximate free-water deficit?

  1. 6 L Correct answer.
  2. 9 L
  3. 12 L
  4. 3 L

Explanation

Total body water is estimated as 0.6 times 70, or 42 L, and the free-water deficit equals total body water multiplied by (sodium/140 minus 1), which is 42 times (160/140 minus 1), or about 6 L. This estimates the water needed to return the sodium to 140 mEq/L before accounting for ongoing losses and the sodium content of replacement fluids.

Question 45Fluid, Electrolyte, and Acid-Base Disorders

After five days of vomiting, a patient has arterial pH 7.52, bicarbonate 34 mEq/L, urine chloride 8 mEq/L, and urine sodium 10 mEq/L. Which classification and initial therapy is correct?

  1. Saline-resistant alkalosis; treat with acetazolamide
  2. Renal tubular acidosis; treat with potassium citrate
  3. Saline-responsive alkalosis; treat with 0.9% saline Correct answer.
  4. Saline-resistant alkalosis; treat with spironolactone

Explanation

A urine chloride below 20 mEq/L during metabolic alkalosis indicates chloride depletion and a volume-responsive state, as seen with vomiting, and it corrects with sodium chloride administration. Saline-resistant alkalosis instead shows a urine chloride above 40 mEq/L and suggests mineralocorticoid excess or continued diuretic effect.

Question 46Fluid, Electrolyte, and Acid-Base Disorders

A 34-year-old has metabolic acidosis with bicarbonate 14 mEq/L, potassium 2.9 mEq/L, urine pH 6.9, and nephrocalcinosis on imaging, with no diarrhea. Which diagnosis best fits?

  1. Proximal (type 2) renal tubular acidosis
  2. Diarrhea-induced normal-anion-gap acidosis
  3. Distal (type 1) renal tubular acidosis Correct answer.
  4. Diabetic ketoacidosis

Explanation

Inability to lower urine pH below 5.5 during systemic metabolic acidosis indicates impaired distal hydrogen secretion, the hallmark of type 1 distal renal tubular acidosis, which also causes hypokalemia and nephrocalcinosis. Type 2 proximal renal tubular acidosis can lower urine pH below 5.5 once bicarbonate is sufficiently depleted and often shows Fanconi syndrome.

Question 47Fluid, Electrolyte, and Acid-Base Disorders

A patient with CKD stage 4 has serum phosphate 6.9 mg/dL and a normal corrected calcium of 9.1 mg/dL. Which intervention is most appropriate?

  1. Take calcium carbonate on an empty stomach
  2. Start oral aluminum hydroxide for long-term use
  3. Restrict dietary phosphate to below 400 mg/day
  4. Take calcium acetate with each meal Correct answer.

Explanation

Calcium acetate is a phosphate binder taken with meals, binding dietary phosphate in the gut and limiting absorption, which is the initial approach when serum calcium is not elevated. Aluminum-based binders are avoided long term because of accumulation and toxicity, and extreme phosphate restriction risks protein-energy malnutrition.

Question 48Fluid, Electrolyte, and Acid-Base Disorders

A patient taking furosemide has serum potassium 2.7 mEq/L and magnesium 1.2 mg/dL. Potassium replacement alone fails to raise the potassium. Which explanation is most accurate?

  1. Hypomagnesemia alkalinizes the urine and shifts K into cells
  2. Hypomagnesemia blocks aldosterone synthesis and sodium delivery
  3. Hypomagnesemia impairs intestinal potassium absorption
  4. Renal K wasting persists until magnesium is repleted Correct answer.

Explanation

Magnesium depletion increases distal potassium secretion through renal outer medullary potassium channels and depletes intracellular potassium stores, so hypokalemia is refractory until magnesium is replaced. Furosemide-induced hypomagnesemia should therefore be treated with magnesium alongside potassium.

Question 49Fluid, Electrolyte, and Acid-Base Disorders

A patient with chronic hyponatremia and serum sodium 108 mEq/L has a witnessed seizure. Which rate of sodium correction is safest during the first 24 hours?

  1. 16 to 20 mEq/L
  2. 6 to 8 mEq/L Correct answer.
  3. 10 to 12 mEq/L
  4. Raise sodium to 135 mEq/L within 12 hours

Explanation

Chronic hyponatremia allows brain volume adaptation, so overrapid correction risks osmotic demyelination; correction is therefore limited to roughly 6 to 8 mEq/L in the first 24 hours in high-risk patients such as those with sodium below 105 mEq/L or seizures. If the limit is exceeded, desmopressin with free water can be used to re-lower the sodium.

Question 50Fluid, Electrolyte, and Acid-Base Disorders

A patient with chronic liver disease is chronically hyperventilating. Arterial pH is 7.50 and PaCO2 is 28 mmHg. Which serum bicarbonate value is most consistent with chronic rather than acute respiratory alkalosis?

  1. 24 mEq/L
  2. 22 mEq/L
  3. 26 mEq/L
  4. 19 mEq/L Correct answer.

Explanation

In acute respiratory alkalosis, bicarbonate falls by about 2 mEq/L for every 10-mmHg fall in PaCO2, which would give roughly 22 mEq/L here. Chronic respiratory alkalosis permits renal compensation of about 4 to 5 mEq/L per 10 mmHg, so a bicarbonate near 19 mEq/L indicates the chronic form.