Chapter 11 Glomerulonephritis Flashcards
What is immune-mediated glomerulonephritis?
A progressive inflammation and injury of the glomeruli caused by humoral and cellular immunity, leading to increased permeability to proteins through the podocyte gaps.
What is the pathologic basis of glomerulonephritis?
Deposition of antibody to the glomerular basement membrane.
What chronic infections favor the production of antigen-antibody immune-complexes in glomerulonephritis?
Leptospira pomona, equine infectious anemia virus, and Streptococcus spp.
What are the consequences of antibody deposition in the glomerular subendothelial space, mesangium, or basement membrane?
Attraction of neutrophils and complement, recruitment of macrophages and lymphocytes, and propagation of inflammation.
What causes tissue damage in glomerulonephritis?
Activated-complement cell destruction, activity of metalloproteases, and reactive oxygen species.
What are the effects of increased production of platelet activating factor (PAF), thromboxane A2, renin, and angiotensin II during renal injury?
Intravascular coagulation, glomerular injury, mesangial fibrosis, sclerosis, and glomerular hypertension.
How is glomerulonephritis classified in human medicine?
Asymptomatic proteinuria, nephrotic syndrome, acute nephritic syndrome, and chronic renal failure.
What are the hallmark clinical signs of glomerulonephritis in horses?
Proteinuria and hematuria, with consequent rapid weight loss, hypoproteinemia (particularly albumin), and tissue edema.
What systemic effects can develop secondary to glomerulonephritis in horses?
Hyperlipidemia and hypercholesteremia due to hepatic lipoprotein production.
What is the immunologic mechanism behind glomerulonephritis?
Deposition of antibodies and immune-complexes in the glomerular basement membrane and mesangium.
What types of histological lesions are associated with glomerulonephritis?
Mesangioproliferative lesions, non-proliferative (membranous) lesions, and combination membranoproliferative lesions.
What can immunofluorescence identify in glomerulonephritis?
Presence of antibody on the glomerular basement membrane, with a linear pattern suggesting direct antibody deposition and a granular pattern suggesting immune-complex deposition.
What is the role of cryoglobulins in glomerulonephritis?
They form immune-complexes that deposit in glomeruli, causing inflammation and tissue damage.
What are common clinical signs of glomerulonephritis in horses?
Proteinuria, hematuria, edema, weight loss, hypoproteinemia, hyperlipidemia, and hypercholesteremia.
What are the common blood work findings in horses with glomerulonephritis?
Neutrophilia, hyperglobulinemia, hyperfibrinogenemia, hypoproteinemia, and hypercholesteremia.
What is the role of urinalysis in diagnosing glomerulonephritis?
Detecting proteinuria and lipiduria, with a urine protein:creatinine ratio higher than 2.0 supporting glomerular protein loss.
What diagnostic methods are used to evaluate glomerulonephritis?
Kidney ultrasonography, renal biopsy, histology, electron microscopy, immunofluorescence, and serologic testing for streptococcal M-protein.
What is the primary treatment for glomerulonephritis?
Immunosuppressive therapy, combined with antimicrobials if there is an underlying infection.
What drugs are used in the treatment of glomerulonephritis?
Dexamethasone, prednisolone, low-dose aspirin, and angiotensin-converting enzyme (ACE) inhibitors like enalapril.
What is the recommended dietary modification for horses with glomerulonephritis?
Reduced protein intake to 1.3 g/kg/day using late-growth grass hay and 12% protein senior feed.
What is the prognosis for horses with glomerulonephritis?
Poor, with potential for disease progression and recurrence despite treatment.
What are the histological features of mesangioproliferative glomerulonephritis?
Increased cellularity of the glomerular tufts, expansion of the mesangial matrix, synechiae to the Bowman’s capsule, sclerosis, and atrophy.
What are the potential complications of glomerulonephritis in horses?
Chronic renal failure, severe protein loss, edema, and secondary infections.
What are the immunologic isotypes involved in glomerulonephritis?
IgG, IgM, and IgA.
What is the role of cyclophosphamide in human glomerulonephritis treatment?
Used in combination with glucocorticoids and occasionally plasmapheresis to control severe cases.
What is the clinical significance of low levels of antithrombin III in glomerulonephritis?
Indicates a hypercoagulable state, increasing the risk of thrombotic events.
What are common etiologies of glomerulonephritis in horses?
Chronic infections, direct antibody production to endothelial epitopes, and idiopathic causes.
What is the significance of systemic hypertension in glomerulonephritis?
Indicates glomerular hypertension due to mesangial proliferation and capillary thrombosis.
What are the potential systemic effects of increased production of vasoactive compounds in glomerulonephritis?
Promotes intravascular coagulation, glomerular injury, and systemic hypertension.
What is the role of renal biopsy in diagnosing glomerulonephritis?
Provides information on the type and severity of the disease, guiding treatment decisions.
What is the significance of hyperlipidemia in glomerulonephritis?
Secondary to hepatic lipoprotein production, compensating for low plasma oncotic pressure and urinary loss of regulatory proteins.
What is the importance of early diagnosis and treatment in glomerulonephritis?
Prevents progression to chronic renal failure and reduces the risk of severe complications.
What are the typical histopathological findings in glomerulonephritis?
Mesangial cell proliferation, expansion of mesangial matrix, synechiae to Bowman’s capsule, sclerosis, and thickening of capillary basement membranes.
What is the role of electron microscopy in diagnosing glomerulonephritis?
Identifies electron-dense deposits and other ultrastructural changes in the glomeruli.
What are the clinical indications for initiating immunosuppressive therapy in glomerulonephritis?
Presence of proteinuria, hematuria, and clinical signs of kidney damage.
What are the potential adverse effects of long-term immunosuppressive therapy?
Increased risk of infections, gastrointestinal issues, and drug toxicity.
What is the role of low-dose aspirin in managing glomerulonephritis?
Reduces hypercoagulability and risk of thrombotic events.
What are the potential complications of uncontrolled glomerulonephritis?
Chronic renal failure, severe protein loss, and systemic hypertension.
What are the key diagnostic criteria for glomerulonephritis in horses?
Proteinuria, hematuria, hypoproteinemia, and histopathological findings from kidney biopsy.
What is the role of ACE inhibitors in managing glomerulonephritis?
Helps control systemic and glomerular hypertension, reducing proteinuria and progression of kidney damage.
What are the potential benefits of dietary protein restriction in glomerulonephritis?
Reduces the workload on the kidneys and helps manage proteinuria.
What are the common clinical signs of acute nephritic syndrome in horses with glomerulonephritis?
Sudden onset of proteinuria, hematuria, and azotemia (acute renal failure).
What is the significance of identifying specific etiologies in glomerulonephritis?
Guides targeted treatment and improves the likelihood of managing the disease effectively.
What are the common causes of asymptomatic proteinuria in glomerulonephritis?
Other systemic diseases that may accompany glomerulonephritis.
What is the role of immunofluorescence in diagnosing glomerulonephritis?
Identifies antibody and complement deposition patterns, providing insights into the underlying immunologic mechanisms.
What are the common laboratory findings in horses with chronic glomerulonephritis?
Persistent proteinuria, hypoproteinemia, hyperlipidemia, and occasional azotemia.
What is the impact of mesangial proliferation on glomerular function?
Leads to glomerular hypertension, reduced filtration, and increased protein loss.
