GLOMERULAR DISEASES Flashcards

1
Q

What substance holds water intravascularly and intracellularly, preventing edema?

A

Albumin

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2
Q

What do dysmorphic red blood cells look like under a microscope?

A

Mickey Mouse

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3
Q

What does frothy or bubbly urine indicate?

A

Proteinuria

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4
Q

What is the threshold for detecting proteinuria on an ordinary urinalysis?

A

300 mg/day

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5
Q

What is one of the earliest signs of diabetic nephropathy?

A

Microalbuminuria

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6
Q

What type of casts are specific for glomerulonephritis?

A

Red blood cell casts

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7
Q

What type of casts are indicative of chronic kidney disease?

A

Waxy, broad casts

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8
Q

What is the gold standard for diagnosing glomerular diseases?

A

Renal biopsy

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9
Q

What stain is used to detect amyloid deposits in a kidney biopsy?

A

Congo red

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10
Q

How much proteinuria defines nephrotic syndrome?

A

> 3 g/day

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11
Q

What are the primary characteristics of nephrotic syndrome?

A

Proteinuria, hypoalbuminemia, edema, hyperlipidemia

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12
Q

What type of red blood cells are specific for nephritic syndrome?

A

Dysmorphic RBCs

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13
Q

What is a hallmark of nephritic syndrome seen in urine microscopy?

A

Red cell casts

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14
Q

What histologic feature in glomerular diseases indicates rapidly progressive or severe kidney disease?

A

Crescents

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15
Q

What type of glomerular injury is associated with nephrotic syndrome?

A

Podocyte injury

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16
Q

What type of glomerular injury is associated with nephritic syndrome?

A

Endothelial or mesangial cell injury

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17
Q

Which immune deposits are more nephrogenic: in-situ or circulating immune complexes?

A

In-situ immune deposits

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18
Q

What are the three final pathways of renal damage in glomerular diseases?

A

Interstitial nephritis, renal fibrosis, tubular atrophy

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19
Q

How do acute and chronic tubulointerstitial nephritis differ?

A

Acute is reversible (PMNs), chronic is irreversible (fibrosis, atrophy)

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20
Q

What is the purpose of the PAS stain in renal biopsies?

A

To stain carbohydrate moieties in the glomerular tuft and tubules

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21
Q

What does the presence of microalbuminuria signify in diabetic nephropathy?

A

An early sign of kidney damage below the detection threshold of dipsticks

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22
Q

What is the primary microscopic feature of Minimal Change Disease (MCD)?

A

Podocyte effacement seen on electron microscopy.

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23
Q

What percentage of nephrotic syndrome in children is caused by Minimal Change Disease (MCD)?

A

70-90% of nephrotic syndrome in childhood.

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24
Q

What first-line treatment is used for Minimal Change Disease (MCD) in children?

A

Prednisone 60 mg/m²/day for 4 to 6 weeks.

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25
Q

What are the common secondary associations of Minimal Change Disease (MCD)?

A

Hodgkin’s lymphoma, NSAID use, and allergies (e.g., food, dust).

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26
Q

What is the hallmark clinical feature of Focal Segmental Glomerulosclerosis (FSGS)?

A

Proteinuria, which may be nephrotic or non-nephrotic.

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27
Q

What is the collapsing variant of FSGS characterized by?

A

Segmental collapse of capillaries, hypertrophy of epithelial cells, and protein resorption droplets in podocytes.

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28
Q

What is a poor prognostic factor for FSGS?

A

Nephrotic-range proteinuria (>3 g/day).

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29
Q

What biopsy finding is diagnostic of Membranous Nephropathy (MN)?

A

Subepithelial immune complex deposits seen on electron microscopy.

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30
Q

What is the most common cause of chronic renal failure in diabetic patients?

A

Diabetic Nephropathy.

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31
Q

What are Kimmelstiel-Wilson nodules, and in which condition are they found?

A

Eosinophilic PAS-positive nodules, found in Diabetic Nephropathy.

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32
Q

What is the defining electron microscopy feature of Fibrillary Glomerulonephritis?

A

Randomly arranged nonbranching fibrils ~20 nm in diameter.

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33
Q

What stain is diagnostic of amyloidosis, and what characteristic does it show?

A

Congo red stain shows apple-green birefringence under polarized light.

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34
Q

What is the main treatment goal for AL Amyloidosis?

A

Decrease the production of monoclonal light chains.

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35
Q

What organ is most commonly affected by Amyloidosis?

A

Kidneys (in ~50% of cases).

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36
Q

What are the risk factors for Diabetic Nephropathy?

A

Hyperglycemia, hypertension, dyslipidemia, smoking, and family history of diabetes.

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37
Q

What is the first-line conservative therapy for Membranous Nephropathy (MN)?

A

RAAS blockade.

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38
Q

What is the median survival for patients with AA Amyloidosis?

A

Approximately 2 years.

39
Q

What are common infections associated with Minimal Change Disease (MCD)?

A

Viral and parasitic infections.

40
Q

Which variant of FSGS has a good prognosis and marked nephrosis?

A

Glomerular Tip Lesion Variant.

41
Q

How is microalbuminuria defined in Diabetic Nephropathy?

A

30-300 mg/24 hours or <30 mg/day.

42
Q

What is the pathognomonic sign of Diabetic Nephropathy on light microscopy?

A

Kimmelstiel-Wilson nodules.

43
Q

What are the features of nephrotic syndrome?

A

Proteinuria, hypoalbuminemia, hyperlipidemia, and edema.

44
Q

What percentage of nephrotic syndrome cases in adults is caused by Membranous Nephropathy?

A

Approximately 20%.

45
Q

Which drugs are used in steroid-resistant cases of Minimal Change Disease (MCD)?

A

Cyclosporine or Cyclophosphamide.

46
Q

What is the typical demographic for AL Amyloidosis?

A

Patients over 50 years old, with men affected twice as often as women.

47
Q

What is the classic presentation of Poststreptococcal Glomerulonephritis (PSGN)?

A

Tea-colored urine, hematuria, pyuria, RBC casts, edema, hypertension, and oliguric renal failure.

48
Q

What are the diagnostic markers for PSGN in the first week of symptoms?

A

Decreased CH50 and C3, normal C4; positive rheumatoid factor, cryoglobulins, circulating immune complexes, and ANCA-MPO; increased ASO titer, anti-DNAse, and antihyaluronidase antibodies.

49
Q

What is the typical prognosis for PSGN?

A

Good, with most children experiencing resolution of hematuria and proteinuria within 3-6 weeks. Persistent symptoms may indicate misdiagnosis or chronic PSGN.

50
Q

What is the pathognomonic gross appearance in Subacute Bacterial Endocarditis (SBE)-associated glomerulonephritis?

A

Subcapsular hemorrhages with a ‘flea-bitten’ appearance.

51
Q

What are the most common comorbidities in SBE-associated glomerulonephritis?

A

Valvular heart disease, IV drug use, Hepatitis C, and Diabetes Mellitus.

52
Q

What is the most common renal manifestation of Lupus Nephritis?

A

Proteinuria, often accompanied by hematuria, hypertension, and active urinary sediment with RBC casts.

53
Q

List the DOPAMINE RASH criteria for diagnosing systemic lupus erythematosus (SLE).

A

Discoid rash, Oral ulcers, Photosensitivity, Arthritis, Malar rash, Immunologic disorder, Neurologic disorder, Renal disorder, Antinuclear antibody, Serositis, Hematologic disorder.

54
Q

What are the main classifications of Lupus Nephritis based on biopsy findings?

A

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

55
Q

What are the two most common clinical presentations of IgA Nephropathy?

A

Recurrent episodes of macroscopic hematuria during or after an upper respiratory tract infection and persistent asymptomatic microscopic hematuria.

56
Q

What are the poor prognostic factors in Henoch-Schönlein Purpura (HSP)-associated nephritis?

A

Older age, acute nephritic presentation, severe nephrotic syndrome, and biopsy findings of glomerular fibrinoid necrosis or crescents.

57
Q

What is the triad of Wegener’s Granulomatosis (Granulomatosis with Polyangiitis)?

A

Vasculitis, granulomatous inflammation of the upper and lower respiratory tracts, and glomerulonephritis.

58
Q

What characterizes Anti-GBM Disease (Goodpasture’s Syndrome)?

A

Circulating antibodies targeting type IV collagen in the glomerular basement membrane, leading to pulmonary hemorrhage and glomerulonephritis.

59
Q

What are the treatment goals for severe Class IV Lupus Nephritis?

A

Aggressive immunosuppression with corticosteroids and cyclophosphamide or mycophenolate mofetil, followed by maintenance therapy.

60
Q

What are the risk factors for loss of renal function in IgA Nephropathy?

A

Hypertension, proteinuria, absence of macroscopic hematuria episodes, older age at onset, and extensive glomerulosclerosis or interstitial fibrosis.

61
Q

What are the classic tetrad of symptoms in Henoch-Schönlein Purpura (HSP)?

A

Dermal involvement (purpura), gastrointestinal disease, joint involvement, and glomerulonephritis.

62
Q

What is MPGN Type I commonly associated with?

A

Persistent Hepatitis C infections, autoimmune diseases (e.g., lupus), cryoglobulinemia, or neoplastic disease.

63
Q

What age group is most commonly affected by MPGN Type I?

A

Children aged 8-16 years.

64
Q

What gender is affected equally by MPGN Type I?

A

Male = Female.

65
Q

What characterizes MPGN Type I on renal biopsy?

A

Mesangial proliferation with lobular segmentation, mesangial interposition between capillary basement membrane and endothelial cells, producing a double contour or ‘tram-tracking.’

66
Q

What are the clinical features of MPGN Type I?

A

Nephrotic range proteinuria, hematuria, pyuria, hypertension, and nephritic picture with RPGN.

67
Q

What is the prognosis of MPGN Type I 10 years after diagnosis?

A

50% of patients develop ESRD.

68
Q

What is the treatment for MPGN Type I?

A

RAAS inhibitors, glucocorticoids, anticoagulation, and treatment of underlying conditions like hepatitis or neoplasia.

69
Q

What are poor prognostic factors in MPGN Type I?

A

Hypertension, nephrotic syndrome, and renal insufficiency.

70
Q

What is a key feature of MPGN Type II?

A

Low serum C3 with dense thickening of the GBM containing ribbons of dense deposits.

71
Q

What age group is most commonly affected by MPGN Type II?

A

Children and young adults.

72
Q

What are common clinical features of MPGN Type II?

A

Hematuria, proteinuria, hypertension (mild or severe), and kidney dysfunction.

73
Q

What is a poor prognostic factor for Dense Deposit Disease in MPGN Type II?

A

The prognosis is worse in adults than in children.

74
Q

What is the main treatment for MPGN Type II?

A

Inhibition of angiotensin II (e.g., RAAS inhibitors).

75
Q

What is the inheritance pattern of Alport’s Syndrome?

A

Usually X-linked.

76
Q

What are the clinical features of Alport’s Syndrome?

A

Persistent microscopic hematuria, episodic gross hematuria, mild proteinuria, chronic glomerulosclerosis, sensorineural deafness, and ocular abnormalities.

77
Q

What is the treatment strategy for Alport’s Syndrome?

A

Proteinuria reduction, aggressive control of hypertension (e.g., ACEI), and renal replacement therapy.

78
Q

What are the clinical features of Thin Basement Membrane Nephropathy?

A

Persistent or recurrent hematuria, typically not associated with proteinuria, hypertension, or loss of renal function.

79
Q

What are the characteristic features of Nail-Patella Syndrome?

A

Tetrad of anomalies: nail dysplasia, patellar aplasia, elbow and iliac horn abnormalities.

80
Q

What are common features of Hypertensive Nephropathy?

A

Systemic hypertension causing arteriosclerosis, chronic nephrosclerosis, and interstitial fibrosis.

81
Q

What is the treatment for Hypertensive Nephrosclerosis?

A

RAAS inhibitors, combination therapy (e.g., ACEI + HCTZ), and strict blood pressure control (<130/80 in CKD or DM).

82
Q

What is the main pathology in Cholesterol Emboli?

A

Irregular emboli trapped in microcirculation causing ischemic damage and inflammation.

83
Q

What is the characteristic renal lesion in Sickle Cell Disease?

A

FSGS, interstitial nephritis, renal infarction, and hyposthenuria.

84
Q

What are the two major conditions causing Thrombotic Microangiopathies?

A

TTP and HUS.

85
Q

What is the recommended treatment for TTP and HUS?

A

Plasmapheresis.

86
Q

What is the defining renal feature of Antiphospholipid Antibody Syndrome (APAS)?

A

Proteinuria, active urinary sediment, hypertension, and progressive renal dysfunction.

87
Q

What is the mainstay treatment for APAS with recurrent thrombosis?

A

Heparin followed by warfarin (target INR >3).

88
Q

What is the renal pathology associated with HIV?

A

HIV-associated nephropathy (HIVAN) with FSGS (collapsing type).

89
Q

What is the treatment for HIV-associated nephropathy?

A

ACEI and HIV medications to reduce proteinuria.

90
Q

What is the most common glomerular lesion in Hepatitis B?

A

Membranous glomerulonephritis (MGN) in children and MPGN in adults.

91
Q

What is the typical renal manifestation of Syphilis?

A

Nephrotic syndrome due to MGN with subepithelial immune deposits.

92
Q

What is the characteristic renal lesion in Leprosy?

A

FSGS, mesangioproliferative GN, or renal amyloidosis.

93
Q

What is the renal pathology caused by P. malariae malaria?

A

Severe mesangioproliferative GN with subendothelial and mesangial deposits.