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.