Chapter 11 Glomerulonephritis Flashcards

1
Q

What is immune-mediated glomerulonephritis?

A

A progressive inflammation and injury of the glomeruli caused by humoral and cellular immunity, leading to increased permeability to proteins through the podocyte gaps.

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2
Q

What is the pathologic basis of glomerulonephritis?

A

Deposition of antibody to the glomerular basement membrane.

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3
Q

What chronic infections favor the production of antigen-antibody immune-complexes in glomerulonephritis?

A

Leptospira pomona, equine infectious anemia virus, and Streptococcus spp.

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4
Q

What are the consequences of antibody deposition in the glomerular subendothelial space, mesangium, or basement membrane?

A

Attraction of neutrophils and complement, recruitment of macrophages and lymphocytes, and propagation of inflammation.

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5
Q

What causes tissue damage in glomerulonephritis?

A

Activated-complement cell destruction, activity of metalloproteases, and reactive oxygen species.

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6
Q

What are the effects of increased production of platelet activating factor (PAF), thromboxane A2, renin, and angiotensin II during renal injury?

A

Intravascular coagulation, glomerular injury, mesangial fibrosis, sclerosis, and glomerular hypertension.

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7
Q

How is glomerulonephritis classified in human medicine?

A

Asymptomatic proteinuria, nephrotic syndrome, acute nephritic syndrome, and chronic renal failure.

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8
Q

What are the hallmark clinical signs of glomerulonephritis in horses?

A

Proteinuria and hematuria, with consequent rapid weight loss, hypoproteinemia (particularly albumin), and tissue edema.

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9
Q

What systemic effects can develop secondary to glomerulonephritis in horses?

A

Hyperlipidemia and hypercholesteremia due to hepatic lipoprotein production.

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10
Q

What is the immunologic mechanism behind glomerulonephritis?

A

Deposition of antibodies and immune-complexes in the glomerular basement membrane and mesangium.

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11
Q

What types of histological lesions are associated with glomerulonephritis?

A

Mesangioproliferative lesions, non-proliferative (membranous) lesions, and combination membranoproliferative lesions.

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12
Q

What can immunofluorescence identify in glomerulonephritis?

A

Presence of antibody on the glomerular basement membrane, with a linear pattern suggesting direct antibody deposition and a granular pattern suggesting immune-complex deposition.

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13
Q

What is the role of cryoglobulins in glomerulonephritis?

A

They form immune-complexes that deposit in glomeruli, causing inflammation and tissue damage.

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14
Q

What are common clinical signs of glomerulonephritis in horses?

A

Proteinuria, hematuria, edema, weight loss, hypoproteinemia, hyperlipidemia, and hypercholesteremia.

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15
Q

What are the common blood work findings in horses with glomerulonephritis?

A

Neutrophilia, hyperglobulinemia, hyperfibrinogenemia, hypoproteinemia, and hypercholesteremia.

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16
Q

What is the role of urinalysis in diagnosing glomerulonephritis?

A

Detecting proteinuria and lipiduria, with a urine protein:creatinine ratio higher than 2.0 supporting glomerular protein loss.

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17
Q

What diagnostic methods are used to evaluate glomerulonephritis?

A

Kidney ultrasonography, renal biopsy, histology, electron microscopy, immunofluorescence, and serologic testing for streptococcal M-protein.

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18
Q

What is the primary treatment for glomerulonephritis?

A

Immunosuppressive therapy, combined with antimicrobials if there is an underlying infection.

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19
Q

What drugs are used in the treatment of glomerulonephritis?

A

Dexamethasone, prednisolone, low-dose aspirin, and angiotensin-converting enzyme (ACE) inhibitors like enalapril.

20
Q

What is the recommended dietary modification for horses with glomerulonephritis?

A

Reduced protein intake to 1.3 g/kg/day using late-growth grass hay and 12% protein senior feed.

21
Q

What is the prognosis for horses with glomerulonephritis?

A

Poor, with potential for disease progression and recurrence despite treatment.

22
Q

What are the histological features of mesangioproliferative glomerulonephritis?

A

Increased cellularity of the glomerular tufts, expansion of the mesangial matrix, synechiae to the Bowman’s capsule, sclerosis, and atrophy.

23
Q

What are the potential complications of glomerulonephritis in horses?

A

Chronic renal failure, severe protein loss, edema, and secondary infections.

24
Q

What are the immunologic isotypes involved in glomerulonephritis?

A

IgG, IgM, and IgA.

25
Q

What is the role of cyclophosphamide in human glomerulonephritis treatment?

A

Used in combination with glucocorticoids and occasionally plasmapheresis to control severe cases.

26
Q

What is the clinical significance of low levels of antithrombin III in glomerulonephritis?

A

Indicates a hypercoagulable state, increasing the risk of thrombotic events.

27
Q

What are common etiologies of glomerulonephritis in horses?

A

Chronic infections, direct antibody production to endothelial epitopes, and idiopathic causes.

28
Q

What is the significance of systemic hypertension in glomerulonephritis?

A

Indicates glomerular hypertension due to mesangial proliferation and capillary thrombosis.

29
Q

What are the potential systemic effects of increased production of vasoactive compounds in glomerulonephritis?

A

Promotes intravascular coagulation, glomerular injury, and systemic hypertension.

30
Q

What is the role of renal biopsy in diagnosing glomerulonephritis?

A

Provides information on the type and severity of the disease, guiding treatment decisions.

31
Q

What is the significance of hyperlipidemia in glomerulonephritis?

A

Secondary to hepatic lipoprotein production, compensating for low plasma oncotic pressure and urinary loss of regulatory proteins.

32
Q

What is the importance of early diagnosis and treatment in glomerulonephritis?

A

Prevents progression to chronic renal failure and reduces the risk of severe complications.

33
Q

What are the typical histopathological findings in glomerulonephritis?

A

Mesangial cell proliferation, expansion of mesangial matrix, synechiae to Bowman’s capsule, sclerosis, and thickening of capillary basement membranes.

34
Q

What is the role of electron microscopy in diagnosing glomerulonephritis?

A

Identifies electron-dense deposits and other ultrastructural changes in the glomeruli.

35
Q

What are the clinical indications for initiating immunosuppressive therapy in glomerulonephritis?

A

Presence of proteinuria, hematuria, and clinical signs of kidney damage.

36
Q

What are the potential adverse effects of long-term immunosuppressive therapy?

A

Increased risk of infections, gastrointestinal issues, and drug toxicity.

37
Q

What is the role of low-dose aspirin in managing glomerulonephritis?

A

Reduces hypercoagulability and risk of thrombotic events.

38
Q

What are the potential complications of uncontrolled glomerulonephritis?

A

Chronic renal failure, severe protein loss, and systemic hypertension.

39
Q

What are the key diagnostic criteria for glomerulonephritis in horses?

A

Proteinuria, hematuria, hypoproteinemia, and histopathological findings from kidney biopsy.

40
Q

What is the role of ACE inhibitors in managing glomerulonephritis?

A

Helps control systemic and glomerular hypertension, reducing proteinuria and progression of kidney damage.

41
Q

What are the potential benefits of dietary protein restriction in glomerulonephritis?

A

Reduces the workload on the kidneys and helps manage proteinuria.

42
Q

What are the common clinical signs of acute nephritic syndrome in horses with glomerulonephritis?

A

Sudden onset of proteinuria, hematuria, and azotemia (acute renal failure).

43
Q

What is the significance of identifying specific etiologies in glomerulonephritis?

A

Guides targeted treatment and improves the likelihood of managing the disease effectively.

44
Q

What are the common causes of asymptomatic proteinuria in glomerulonephritis?

A

Other systemic diseases that may accompany glomerulonephritis.

45
Q

What is the role of immunofluorescence in diagnosing glomerulonephritis?

A

Identifies antibody and complement deposition patterns, providing insights into the underlying immunologic mechanisms.

46
Q

What are the common laboratory findings in horses with chronic glomerulonephritis?

A

Persistent proteinuria, hypoproteinemia, hyperlipidemia, and occasional azotemia.

47
Q

What is the impact of mesangial proliferation on glomerular function?

A

Leads to glomerular hypertension, reduced filtration, and increased protein loss.