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BLOCK POSTING 4 > RENAL PATHOLOGY > Flashcards

RENAL PATHOLOGY Flashcards

1
Q

What is the most common congenital renal anomaly?

A

Horseshoe kidney, where the kidneys are conjoined at the lower pole.

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2
Q

Where is a horseshoe kidney typically located?

A

In the lower abdomen, caught on the root of the inferior mesenteric artery.

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3
Q

What is renal agenesis?

A

Absence of kidney formation, which can be unilateral or bilateral.

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4
Q

What is the outcome of bilateral renal agenesis?

A

Oligohydramnios, Potter sequence (lung hypoplasia, flat face, limb defects), and incompatibility with life.

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5
Q

What characterizes dysplastic kidney?

A

Non-inherited congenital malformation with cysts and abnormal tissue such as cartilage.

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6
Q

How is polycystic kidney disease (PKD) inherited?

A

It can be autosomal recessive or autosomal dominant.

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7
Q

What are features of autosomal recessive PKD?

A

Presents in infants with renal failure, hypertension, Potter sequence, congenital hepatic fibrosis, and hepatic cysts.

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8
Q

What are features of autosomal dominant PKD?

A

Presents in young adults with hypertension, hematuria, renal failure, and associations with berry aneurysms, hepatic cysts, and mitral valve prolapse.

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9
Q

What is medullary cystic kidney disease?

A

An autosomal dominant defect causing cysts in the medullary collecting ducts, fibrosis, shrunken kidneys, and renal failure.

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10
Q

What are common risk factors for urinary tract infections (UTIs)?

A

Sexual intercourse, urinary stasis, and catheters.

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11
Q

What are the symptoms of cystitis?

A

Dysuria, urinary frequency, urgency, and suprapubic pain without systemic signs.

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12
Q

What are the common causes of cystitis?

A

E. coli (80%), Staphylococcus saprophyticus, Klebsiella pneumoniae, Proteus mirabilis, and Enterococcus faecalis.

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13
Q

What does sterile pyuria suggest?

A

Urethritis caused by Chlamydia trachomatis or Neisseria gonorrhoeae.

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14
Q

What are the symptoms of pyelonephritis?

A

Fever, flank pain, WBC casts, leukocytosis, and symptoms of cystitis.

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15
Q

What pathogens commonly cause pyelonephritis?

A

E. coli (90%), Klebsiella species, and Enterococcus faecalis.

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16
Q

What causes chronic pyelonephritis?

A

Recurrent acute pyelonephritis due to vesicoureteral reflux or obstruction.

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17
Q

What is characteristic of vesicoureteral reflux in chronic pyelonephritis?

A

Cortical scarring and blunted calyces at the upper and lower poles.

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18
Q

What is thyroidization of the kidney?

A

Atrophic tubules containing eosinophilic proteinaceous material resembling thyroid follicles.

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19
Q

What are waxy casts

A

and when are they seen?

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20
Q

What is the gold standard for diagnosing cystitis?

A

Urine culture with >100,000 colony-forming units.

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21
Q

What laboratory findings indicate cystitis?

A

Cloudy urine, >10 WBCs/high-power field, positive leukocyte esterase, and nitrites on dipstick.

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22
Q

What symptom is associated with Proteus mirabilis in cystitis?

A

Alkaline urine with an ammonia scent.

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23
Q

How does renal agenesis affect the remaining kidney in unilateral cases?

A

Leads to hypertrophy and increased risk of renal failure later in life.

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24
Q

What is the origin of the urinary system?

A

The urinary system develops from the intermediate mesoderm.

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25
Q

What are the three stages of kidney development?

A

Pronephros, mesonephros, and metanephros.

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26
Q

Which stage of kidney development is functional in the fetus?

A

The metanephros stage.

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27
Q

What is the pronephros?

A

The earliest stage of kidney development, which is nonfunctional and regresses by the 4th week of gestation.

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28
Q

What is the mesonephros?

A

A temporary kidney structure that functions during the early fetal period and contributes to the formation of the Wolffian duct.

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29
Q

What does the metanephros form?

A

The permanent kidney, beginning development at 5 weeks of gestation.

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30
Q

What is the ureteric bud?

A

An outgrowth from the mesonephric duct that induces the formation of the metanephros.

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31
Q

What structures does the ureteric bud give rise to?

A

The ureter, renal pelvis, calyces, and collecting ducts.

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32
Q

What is the metanephric blastema?

A

A mass of mesenchymal tissue that forms the glomeruli, proximal tubules, and nephron loops.

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33
Q

What is renal agenesis?

A

A congenital absence of one or both kidneys due to failure of the ureteric bud to develop.

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34
Q

What causes Potter sequence?

A

Bilateral renal agenesis leading to oligohydramnios, lung hypoplasia, and facial and limb deformities.

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35
Q

What is a horseshoe kidney?

A

A congenital anomaly where the kidneys are fused at the lower poles and trapped by the inferior mesenteric artery.

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36
Q

What is the significance of the cloaca in development?

A

The cloaca is a common cavity that divides into the rectum and urogenital sinus during development.

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37
Q

What does the urogenital sinus form?

A

The bladder, urethra, and part of the reproductive tract.

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38
Q

What is the origin of the trigone of the bladder?

A

The trigone develops from the mesonephric ducts.

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39
Q

What are congenital anomalies of the ureter?

A

Duplicated ureter, ectopic ureter, and ureterocele.

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40
Q

What is a duplicated ureter?

A

A condition where two ureters drain a single kidney due to abnormal ureteric bud development.

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41
Q

What is an ectopic ureter?

A

A ureter that does not insert into the bladder normally, often draining into the urethra or vagina.

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42
Q

What is a urachal remnant?

A

A persistent remnant of the allantois that can form a urachal cyst, sinus, or fistula.

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43
Q

What is exstrophy of the bladder?

A

A congenital defect where the bladder is exposed on the surface of the body due to failure of the anterior abdominal wall to close.

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44
Q

What is the role of intermediate mesoderm in kidney development?

A

It forms the nephric structures, gonads, and parts of the adrenal glands.

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45
Q

What is the time frame for nephron formation?

A

Nephron formation begins at 9 weeks of gestation and is completed by 36 weeks.

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46
Q

What is the clinical significance of congenital renal anomalies?

A

They can lead to chronic kidney disease, hypertension, and urinary tract infections.

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47
Q

What are the main types of inflammatory renal diseases?

A

Glomerulonephritis, pyelonephritis, and tubulointerstitial nephritis.

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48
Q

What is glomerulonephritis?

A

Inflammation of the glomeruli, often due to immune complex deposition.

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49
Q

What are the clinical presentations of glomerulonephritis?

A

Hematuria, proteinuria, edema, and hypertension.

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50
Q

What is nephrotic syndrome?

A

A condition characterized by heavy proteinuria, hypoalbuminemia, hyperlipidemia, and edema.

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51
Q

What is nephritic syndrome?

A

A condition marked by hematuria, hypertension, and mild proteinuria.

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52
Q

What causes post-streptococcal glomerulonephritis (PSGN)?

A

Immune complex deposition following a streptococcal infection.

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53
Q

What is the characteristic histology of PSGN?

A

Subepithelial humps on electron microscopy and hypercellular glomeruli on light microscopy.

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54
Q

What is IgA nephropathy (Berger disease)?

A

IgA deposition in the mesangium causing hematuria and glomerular inflammation.

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55
Q

What is the main feature of rapidly progressive glomerulonephritis (RPGN)?

A

Crescents in Bowman’s space composed of fibrin and macrophages.

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56
Q

What are the three types of RPGN?

A

Type I: Anti-GBM disease, Type II: Immune complex-mediated, Type III: Pauci-immune (ANCA-associated).

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57
Q

What is Goodpasture syndrome?

A

An autoimmune disorder with anti-GBM antibodies causing glomerulonephritis and lung hemorrhage.

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58
Q

What is pyelonephritis?

A

Inflammation of the renal pelvis and parenchyma, typically due to bacterial infection.

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59
Q

What are the clinical features of acute pyelonephritis?

A

Flank pain, fever, dysuria, WBC casts, and leukocytosis.

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60
Q

What are risk factors for pyelonephritis?

A

Vesicoureteral reflux, urinary obstruction, and catheter use.

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61
Q

What is chronic pyelonephritis?

A

Chronic inflammation leading to interstitial fibrosis and tubular atrophy.

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62
Q

What are the hallmarks of chronic pyelonephritis?

A

Cortical scarring, blunted calyces, and thyroidization of the kidney.

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63
Q

What is tubulointerstitial nephritis?

A

Inflammation of the renal interstitium and tubules, often due to drugs or infections.

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64
Q

What drugs commonly cause tubulointerstitial nephritis?

A

NSAIDs, antibiotics (e.g., penicillin), and diuretics.

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65
Q

What are the clinical features of tubulointerstitial nephritis?

A

Fever, rash, eosinophilia, and hematuria after drug exposure.

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66
Q

What is the histological hallmark of tubulointerstitial nephritis?

A

Interstitial inflammation with eosinophils.

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67
Q

What is granulomatous interstitial nephritis?

A

A rare form of tubulointerstitial nephritis associated with sarcoidosis or tuberculosis.

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68
Q

What complications can arise from inflammatory renal diseases?

A

Chronic kidney disease, hypertension, and recurrent infections.

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69
Q

What are the diagnostic tools for inflammatory renal diseases?

A

Urinalysis, serum markers (e.g., creatinine), imaging, and renal biopsy.

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70
Q

What is the treatment for post-streptococcal glomerulonephritis?

A

Supportive care, including fluid management and antihypertensives.

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71
Q

How is pyelonephritis treated?

A

Antibiotics targeting common pathogens like E. coli.

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72
Q

What is glomerulonephritis?

A

Inflammation of the glomeruli caused by immune or non-immune mechanisms.

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73
Q

What are the clinical syndromes associated with glomerulonephritis?

A

Nephritic syndrome, nephrotic syndrome, and rapidly progressive glomerulonephritis (RPGN).

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74
Q

What is nephritic syndrome?

A

A condition characterized by hematuria, hypertension, proteinuria, and oliguria.

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75
Q

What is nephrotic syndrome?

A

A condition marked by proteinuria >3.5 g/day, hypoalbuminemia, hyperlipidemia, and edema.

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76
Q

What causes post-streptococcal glomerulonephritis (PSGN)?

A

Immune complex deposition following Group A streptococcal infection.

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77
Q

What are the histological features of PSGN?

A

Subepithelial humps on electron microscopy and hypercellular glomeruli on light microscopy.

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78
Q

What is IgA nephropathy (Berger disease)?

A

IgA deposition in the mesangium leading to episodic hematuria.

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79
Q

What systemic condition is associated with IgA nephropathy?

A

Henoch-Schönlein purpura, a systemic vasculitis.

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80
Q

What is the hallmark feature of rapidly progressive glomerulonephritis (RPGN)?

A

Crescent formation in Bowman’s space.

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81
Q

What are the three types of RPGN?

A

Type I: Anti-GBM disease, Type II: Immune complex-mediated, Type III: Pauci-immune (ANCA-associated).

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82
Q

What is Goodpasture syndrome?

A

An autoimmune disorder with anti-GBM antibodies affecting kidneys and lungs.

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83
Q

What is membranous nephropathy?

A

A nephrotic syndrome caused by subepithelial immune complex deposits leading to thickened glomerular capillary walls.

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84
Q

What is minimal change disease?

A

A nephrotic syndrome with podocyte effacement on electron microscopy, common in children.

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85
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

Segmental sclerosis and hyalinosis of glomeruli, often causing nephrotic syndrome.

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86
Q

What is membranoproliferative glomerulonephritis (MPGN)?

A

A glomerular disease with mesangial proliferation and immune complex deposition.

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87
Q

What are the types of MPGN?

A

Type I: Subendothelial deposits, Type II: Dense deposit disease (intramembranous deposits).

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88
Q

What is Alport syndrome?

A

A genetic disorder caused by mutations in type IV collagen, leading to hematuria, hearing loss, and ocular abnormalities.

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89
Q

What is thin basement membrane disease?

A

A hereditary condition causing isolated hematuria with thin glomerular basement membranes.

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90
Q

What is lupus nephritis?

A

Renal involvement in systemic lupus erythematosus (SLE), classified into six classes.

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91
Q

What is the most severe form of lupus nephritis?

A

Class IV: Diffuse proliferative glomerulonephritis.

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92
Q

What is ANCA-associated glomerulonephritis?

A

Pauci-immune glomerulonephritis associated with anti-neutrophil cytoplasmic antibodies.

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93
Q

What is the treatment for Goodpasture syndrome?

A

Plasmapheresis and immunosuppression.

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94
Q

What causes diabetic nephropathy?

A

Non-enzymatic glycosylation of glomerular basement membranes leading to proteinuria and glomerulosclerosis.

95
Q

What are Kimmelstiel-Wilson nodules?

A

Eosinophilic nodular glomerulosclerosis seen in diabetic nephropathy.

96
Q

What are the complications of nephrotic syndrome?

A

Hypercoagulability, infections, and chronic kidney disease.

97
Q

What diagnostic tools are used for glomerulonephritis?

A

Urinalysis, renal biopsy, and serological tests (e.g., ANCA, anti-GBM, complement levels).

98
Q

What is the hallmark finding in minimal change disease under light microscopy?

A

Normal glomeruli despite heavy proteinuria.

99
Q

What are the primary glomerular diseases?

A

Diseases affecting the glomeruli directly, such as minimal change disease, FSGS, and membranous nephropathy.

100
Q

What are secondary glomerular diseases?

A

Diseases where glomerular damage occurs due to systemic conditions like diabetes, lupus, or infections.

101
Q

What triggers IgA nephropathy episodes?

A

Infections like respiratory or gastrointestinal infections.

102
Q

What type of hypersensitivity reaction is post-streptococcal glomerulonephritis?

A

Type III hypersensitivity reaction due to immune complex deposition.

103
Q

What is the typical presentation of lupus nephritis?

A

Proteinuria, hematuria, hypertension, and nephritic or nephrotic syndrome.

104
Q

What are the classes of lupus nephritis?

A

Class I: Minimal mesangial, Class II: Mesangial proliferative, Class III: Focal proliferative, Class IV: Diffuse proliferative, Class V: Membranous, Class VI: Advanced sclerosing.

105
Q

What type of deposits are seen in membranous nephropathy?

A

Subepithelial immune complex deposits.

106
Q

What is the most common cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis (FSGS).

107
Q

What conditions are associated with focal segmental glomerulosclerosis?

A

HIV, heroin use, and sickle cell disease.

108
Q

What is the characteristic histological finding in membranoproliferative glomerulonephritis?

A

Tram-track appearance due to mesangial interposition.

109
Q

What antibodies are associated with Type III RPGN?

A

Anti-neutrophil cytoplasmic antibodies (ANCAs), including c-ANCA and p-ANCA.

110
Q

What is the treatment for rapidly progressive glomerulonephritis (RPGN)?

A

Immunosuppression with corticosteroids and cyclophosphamide.

111
Q

What genetic mutation causes Alport syndrome?

A

Mutations in the COL4A3, COL4A4, or COL4A5 genes affecting type IV collagen.

112
Q

What are the clinical features of Alport syndrome?

A

Hematuria, sensorineural hearing loss, and ocular abnormalities like lenticonus.

113
Q

What is the key finding in diabetic nephropathy on light microscopy?

A

Mesangial expansion and nodular glomerulosclerosis (Kimmelstiel-Wilson nodules).

114
Q

What is crescent formation in glomerulonephritis?

A

Accumulation of fibrin and macrophages in Bowman’s space, seen in RPGN.

115
Q

What are common triggers for membranous nephropathy?

A

Hepatitis B or C, autoimmune diseases, and drugs like NSAIDs and gold.

116
Q

What is dense deposit disease (Type II MPGN)?

A

A condition with dense intramembranous deposits caused by complement dysregulation.

117
Q

What laboratory finding is common in ANCA-associated vasculitis?

A

Elevated c-ANCA or p-ANCA levels.

118
Q

What is the treatment for IgA nephropathy?

A

ACE inhibitors, steroids, and fish oil for proteinuria and inflammation.

119
Q

What infections are associated with membranoproliferative glomerulonephritis?

A

Hepatitis B and C infections.

120
Q

What is fibrillary glomerulonephritis?

A

A rare glomerular disease with fibrillary deposits that stain negative for Congo red.

121
Q

What is cryoglobulinemic glomerulonephritis?

A

A glomerular disease caused by cryoglobulin deposition, often associated with hepatitis C.

122
Q

What are the complications of RPGN if untreated?

A

End-stage renal disease and dialysis dependency.

123
Q

What is the significance of low complement levels in glomerulonephritis?

A

Seen in immune complex-mediated diseases like PSGN, lupus nephritis, and cryoglobulinemia.

124
Q

What is the primary diagnostic test for glomerular diseases?

A

Renal biopsy for histology, immunofluorescence, and electron microscopy.

125
Q

What percentage of people are born with significant urinary system malformations?

A

About 10%.

126
Q

What accounts for 20% of chronic kidney disease in children?

A

Renal dysplasias and hypoplasias.

127
Q

What is bilateral renal agenesis associated with?

A

Stillbirth, hypoplastic lungs, and limb defects; incompatible with life.

128
Q

What happens in unilateral renal agenesis?

A

The solitary kidney undergoes compensatory hypertrophy and can sustain life.

129
Q

What is renal hypoplasia?

A

A kidney with fewer lobes and pyramids, often causing early renal failure if bilateral.

130
Q

What is multicystic dysplasia?

A

A developmental anomaly with cysts, ducts, and abnormal mesenchyme in the kidney.

131
Q

Where are ectopic kidneys located?

A

Above the pelvic brim or within the pelvis.

132
Q

What is a horseshoe kidney?

A

A congenital anomaly where the kidneys are fused, usually at the lower poles.

133
Q

What causes cystic kidney diseases?

A

Defects in the cilia-centrosome complex of tubular epithelial cells.

134
Q

What are the features of simple renal cysts?

A

1-5 cm in diameter, clear fluid, confined to the renal cortex.

135
Q

What is acquired cystic kidney disease?

A

Multiple cysts in end-stage renal disease patients on long-term dialysis.

136
Q

What increases in acquired cystic kidney disease?

A

Risk of renal neoplasms, over 100 times higher than the general population.

137
Q

What is autosomal dominant polycystic kidney disease (ADPKD)?

A

A genetic disorder with multiple cysts in both kidneys, often causing renal failure.

138
Q

What gene is mutated in 85-90% of ADPKD cases?

A

PKD1 on chromosome 16.

139
Q

What does polycystin-1 do?

A

Functions in the primary cilium of tubular cells, related to mechanosensing and calcium influx.

140
Q

What is the difference between PKD1 and PKD2 mutations in ADPKD?

A

PKD1 mutations lead to faster progression, while PKD2 mutations are slower.

141
Q

What is the morphology of ADPKD kidneys?

A

Enlarged kidneys filled with fluid-filled cysts, replacing normal parenchyma.

142
Q

What is autosomal recessive polycystic kidney disease (ARPKD)?

A

A childhood disorder with small cysts and PKHD1 gene mutations.

143
Q

What protein is affected in ARPKD?

A

Fibrocystin, found in cilia of tubular epithelial cells.

144
Q

What are common complications of ARPKD?

A

Liver fibrosis and early renal failure.

145
Q

What is minimal-change disease?

A

A nephrotic syndrome with podocyte effacement and excellent steroid response.

146
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

Sclerosis of some glomeruli, often causing nephrotic syndrome.

147
Q

What is the cause of acute postinfectious glomerulonephritis?

A

Immune complexes after infections like streptococcus, staphylococcus, or viral illnesses.

148
Q

What is the hallmark of acute pyelonephritis?

A

Liquefactive necrosis and abscess formation in the renal parenchyma.

149
Q

What predisposes to papillary necrosis in pyelonephritis?

A

Diabetes, urinary tract obstruction, and sickle cell anemia.

150
Q

What are the two forms of chronic pyelonephritis?

A

Chronic obstructive pyelonephritis and reflux nephropathy.

151
Q

What is vesicoureteral reflux?

A

Abnormal urine backflow from the bladder into the ureters and kidneys.

152
Q

What is the pathogenesis of ascending UTIs?

A

Bacteria colonize the urethra, bladder, and ascend via the ureters to infect the kidney.

153
Q

What is the morphology of chronic pyelonephritis?

A

Scarring, calyceal deformity, and interstitial fibrosis with tubular atrophy.

154
Q

What characterizes nephrotic syndrome?

A

Proteinuria (>3.5 g/day), hypoalbuminemia, edema, hyperlipidemia, and hypercoagulability.

155
Q

What causes the hypercoagulable state in nephrotic syndrome?

A

Loss of antithrombin III in the urine.

156
Q

What is minimal change disease (MCD)?

A

The most common cause of nephrotic syndrome in children, characterized by effacement of podocyte foot processes.

157
Q

What is the typical response of MCD to steroids?

A

Excellent response due to T-cell-mediated cytokine damage.

158
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous nephropathy.

159
Q

What are the histological features of membranous nephropathy?

A

Thickened glomerular basement membrane and subepithelial immune complex deposits (‘spike and dome’ appearance).

160
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

Segmental sclerosis of some glomeruli, often associated with HIV and sickle cell disease.

161
Q

What is the hallmark of diabetic nephropathy?

A

Kimmelstiel-Wilson nodules in the mesangium.

162
Q

What slows the progression of diabetic nephropathy?

A

ACE inhibitors, which reduce glomerular hyperfiltration.

163
Q

What is the characteristic histology in systemic amyloidosis?

A

Amyloid deposits in the mesangium showing apple-green birefringence with Congo red staining.

164
Q

What are key features of nephritic syndrome?

A

Hematuria, oliguria, azotemia, hypertension, and RBC casts.

165
Q

What is poststreptococcal glomerulonephritis (PSGN)?

A

A nephritic syndrome following a group A streptococcal infection, marked by subepithelial humps on EM.

166
Q

What is the key histology of rapidly progressive glomerulonephritis (RPGN)?

A

Crescents in Bowman’s space made of fibrin and macrophages.

167
Q

What distinguishes Goodpasture syndrome in RPGN?

A

Linear IF pattern due to anti-GBM antibodies affecting kidneys and lungs.

168
Q

What causes IgA nephropathy (Berger disease)?

A

IgA immune complex deposition in the mesangium, often after mucosal infections.

169
Q

What is Alport syndrome?

A

An inherited defect in type IV collagen causing hematuria, hearing loss, and ocular disturbances.

170
Q

What are the subtypes of membranoproliferative glomerulonephritis (MPGN)?

A

Type I (subendothelial deposits) and Type II (dense deposit disease).

171
Q

What is the role of C3 nephritic factor in MPGN?

A

Stabilizes C3 convertase, leading to complement overactivation and low C3 levels.

172
Q

What is the primary cause of nephritic syndrome in SLE?

A

Diffuse proliferative glomerulonephritis (subendothelial immune complex deposits).

173
Q

What infections can cause postinfectious glomerulonephritis?

A

Group A streptococcus, pneumococcus, staphylococcus, and certain viral infections.

174
Q

What are renal papillary adenomas?

A

Small benign adenomas (<0.5 cm) arising from renal tubular epithelium, commonly found in the renal cortex.

175
Q

What is the clinical importance of angiomyolipomas?

A

They may spontaneously hemorrhage and are associated with tuberous sclerosis.

176
Q

What is a distinguishing feature of oncocytomas?

A

A central stellate scar seen on imaging.

177
Q

What is the most significant risk factor for renal cell carcinoma?

A

Tobacco use.

178
Q

What are the three major types of renal cell carcinoma?

A

Clear cell carcinoma, papillary carcinoma, and chromophobe carcinoma.

179
Q

What is the genetic mutation commonly found in clear cell carcinoma?

A

Loss of VHL gene sequences on chromosome 3.

180
Q

What are the cytogenetic features of papillary carcinoma?

A

Trisomies 7 and 17 and loss of Y in male sporadic cases.

181
Q

What is the prognosis of chromophobe carcinoma compared to other renal cancers?

A

It has an excellent prognosis compared to clear cell and papillary carcinoma.

182
Q

What is Xp11 translocation carcinoma?

A

A subtype of renal cell carcinoma defined by TFE3 gene translocations, often occurring in young patients.

183
Q

What is the origin of collecting duct carcinoma?

A

Arises from collecting duct cells in the renal medulla.

184
Q

What is a common morphological feature of clear cell carcinoma?

A

Yellow appearance due to lipid accumulations in tumor cells.

185
Q

What characteristic behavior is associated with renal cell carcinoma?

A

Tendency to invade the renal vein and metastasize widely before causing local symptoms.

186
Q

What is the most common solid renal cancer in children?

A

Wilms tumor.

187
Q

What are urothelial carcinomas of the renal pelvis?

A

Tumors arising from the urothelium, ranging from benign papillomas to invasive carcinomas.

188
Q

What syndromes are associated with hereditary renal cell carcinoma?

A

Von Hippel-Lindau (VHL) syndrome and hereditary papillary carcinoma.

189
Q

What is the primary mechanism of immune-mediated glomerulonephritis?

A

Immune complex deposition leading to complement activation and neutrophil recruitment.

190
Q

What distinguishes nephritic syndrome from nephrotic syndrome?

A

Nephritic syndrome features inflammation and hematuria, while nephrotic syndrome involves severe proteinuria and edema.

191
Q

What is the main pathological feature of diffuse proliferative glomerulonephritis?

A

Diffuse hypercellularity and subendothelial immune complex deposits.

192
Q

What systemic condition is associated with membranous nephropathy?

A

Systemic lupus erythematosus (SLE).

193
Q

What triggers IgA nephropathy episodes?

A

Mucosal infections, such as respiratory or gastrointestinal infections.

194
Q

What is the characteristic finding in Alport syndrome on electron microscopy?

A

Basket-weave appearance of the glomerular basement membrane.

195
Q

How is post-streptococcal glomerulonephritis confirmed?

A

Presence of anti-streptolysin O (ASO) titers or anti-DNAse B antibodies.

196
Q

What is the most common cause of end-stage renal disease in diabetic patients?

A

Diabetic nephropathy.

197
Q

What role do ANCA antibodies play in glomerulonephritis?

A

They are associated with pauci-immune glomerulonephritis and vasculitis.

198
Q

What distinguishes Type I from Type II membranoproliferative glomerulonephritis?

A

Type I involves subendothelial deposits, while Type II (dense deposit disease) involves intramembranous deposits.

199
Q

What causes the ‘tram-track’ appearance in membranoproliferative glomerulonephritis?

A

Mesangial cell proliferation and splitting of the glomerular basement membrane.

200
Q

What is the significance of ‘humps’ in post-streptococcal glomerulonephritis?

A

They represent subepithelial immune complex deposits.

201
Q

What are the major complications of nephrotic syndrome?

A

Hypercoagulability, infections, and progression to chronic kidney disease.

202
Q

What laboratory findings indicate RPGN?

A

Crescents on biopsy, hematuria, proteinuria, and rapidly declining renal function.

203
Q

What distinguishes Churg-Strauss syndrome from other ANCA-associated vasculitides?

A

The presence of eosinophilia and asthma.

204
Q

What is the first-line treatment for crescentic glomerulonephritis?

A

High-dose corticosteroids and immunosuppressants like cyclophosphamide.

205
Q

What distinguishes primary from secondary glomerulonephritis?

A

Primary affects the glomeruli directly, while secondary results from systemic conditions like lupus or diabetes.

206
Q

What is the characteristic urine finding in nephritic syndrome?

A

RBC casts and dysmorphic red blood cells.

207
Q

What is the pathophysiological mechanism in Goodpasture syndrome?

A

Anti-GBM antibodies targeting type IV collagen in glomerular and alveolar basement membranes.

208
Q

What is the role of complement levels in glomerulonephritis diagnosis?

A

Low complement levels are seen in immune complex-mediated diseases like PSGN and lupus nephritis.

209
Q

What is glomerulonephritis?

A

Inflammation of the glomeruli, often due to immune-mediated damage.

210
Q

What are the two broad categories of glomerulonephritis?

A

Nephritic syndrome and nephrotic syndrome.

211
Q

What are the clinical features of nephritic syndrome?

A

Hematuria, hypertension, oliguria, and proteinuria (<3.5 g/day).

212
Q

What are the clinical features of nephrotic syndrome?

A

Proteinuria (>3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia.

213
Q

What is post-streptococcal glomerulonephritis (PSGN)?

A

A nephritic syndrome caused by immune complex deposition after Group A Streptococcal infection.

214
Q

What is the characteristic finding in PSGN on electron microscopy?

A

Subepithelial humps of immune complexes.

215
Q

What is rapidly progressive glomerulonephritis (RPGN)?

A

A severe glomerulonephritis with crescent formation in Bowman’s space, leading to rapid renal failure.

216
Q

What are the three immunofluorescence patterns in RPGN?

A

Linear (anti-GBM disease), granular (immune complex deposition), and negative (pauci-immune).

217
Q

What is Goodpasture syndrome?

A

An anti-GBM disease causing hematuria and hemoptysis due to antibodies against collagen in the basement membrane.

218
Q

What is the most common cause of nephritic syndrome in SLE?

A

Diffuse proliferative glomerulonephritis.

219
Q

What is IgA nephropathy (Berger disease)?

A

IgA immune complex deposition in the mesangium, causing episodic hematuria.

220
Q

What is Alport syndrome?

A

An inherited defect in type IV collagen causing hematuria, hearing loss, and ocular abnormalities.

221
Q

What is membranous nephropathy?

A

A nephrotic syndrome with subepithelial immune complex deposits, leading to a ‘spike and dome’ appearance.

222
Q

What is minimal change disease?

A

A nephrotic syndrome common in children, characterized by podocyte effacement on electron microscopy.

223
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

Segmental glomerular scarring often associated with HIV, heroin use, or sickle cell disease.

224
Q

What is membranoproliferative glomerulonephritis (MPGN)?

A

A glomerular disease with a ‘tram-track’ appearance due to mesangial proliferation and immune deposits.

225
Q

What are the two types of MPGN based on deposit location?

A

Type I (subendothelial deposits) and Type II (dense deposit disease).

226
Q

What is the hallmark feature of diabetic nephropathy?

A

Kimmelstiel-Wilson nodules and hyaline arteriolosclerosis.

227
Q

What is the treatment for nephrotic syndrome due to minimal change disease?

A

Corticosteroids, with excellent response in most cases.

228
Q

What is the role of ACE inhibitors in diabetic nephropathy?

A

They reduce glomerular hyperfiltration and slow disease progression.

229
Q

What is systemic amyloidosis in the context of nephrotic syndrome?

A

Amyloid deposits in the mesangium leading to nephrotic syndrome, showing apple-green birefringence on Congo red staining.

230
Q

What infections are associated with membranoproliferative glomerulonephritis?

A

Hepatitis B and C.

231
Q

What is pauci-immune glomerulonephritis?

A

A type of RPGN associated with ANCA-related vasculitis, showing no immune complex deposition on IF.

232
Q

What are the complications of untreated RPGN?

A

Chronic kidney disease and end-stage renal failure.

233
Q

What is the pathophysiology of crescent formation in RPGN?

A

Fibrin and macrophages accumulate in Bowman’s space, causing rapid glomerular damage.

BLOCK POSTING 4 (8 decks)

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