Glomerular disease Flashcards
Mechanisms of Glomerular Disease
Immunocomplex deposition (circulate then deposit in glomerulus, activates complement resulting in neutrophil chemotaxis)
Antibodies against GBM or glomerular antigens
Cytokine production by inflammatory cells
glomerular disease presentation
Loss of GFR, Hematuria, proteinuria
Nephrotic vs nephritic
Nephrotic syndrome: proteinuria > 3.5 g/day
Hypoalbuminemia
Edema (loss of plasma oncotic pressure vs Na/H20 retention)
Hyperlipidemia (increased hepatic protein production)
Lipiduria
Hypercoagulability (loss of proteins C and S)
Nephritis: mild proteinuria, hematuria (RBC, RBC casts, dysmorphic RBCs), hypertension, Edema
IgA nephropathy
Most common glomerulonephritis
pts between age 10-50
Hematuria is most prominent feature (50-60% episodic gross hematuria, 30% persistent microhematuria, 10% acute GN or nephrotic syndrome)
Proteinuria if present is generally mild
Many cases are subclinical
Dysuria and loin pain may accompany hematuria (frequently occurs in conjuction with an upper respiratory infection (synpharyngitic hematuria)
HTN may be present in patients with more advanced disease
henoch-schölein purpura
systemic disorder characterized by IgA, depostition in multiple organs
Multiple manifestions: Skin (characteristic non blanching purpura on legs and buttocks), joints (transient arthralgias), GIT, kidney (hematuria, proteinuria, rarely progressive renal failure
Post infectious GN
Post Streptococcal GN classic example
7-14 days after pharyngitis, 14-28 days after skin infection
Anti-GBM/ goodpastures syndrome
Males>females
May present as a pulmonary renal syndrome
Hemoptysis, pulmonary infiltrates, GN, due to circulating anti GBM antibody
Linear IgG and C3 on kidney biopsy IF
Pauci immune GN
Crescenteric GN with little deposition of immune reactancts, idiopathic or associated with Anti neutrophil cytoplasmic antibody (ANCA vasculitis)
Nphtrotic glomerular disease
Primary renal disease (membranous nephropathy, focal segmental glomerulosclerosis minimal change disease, in children- 80% will have minimal change
Secondary to DM, SLE, amyloidosis, infections, drugs
Renal biopsy
treatment: acei or ARB, statins, diuretics, salt restriction to improve edema
Minimal change disease: NSAIDS, hodkinns lymphomas, infections
membranous nephropathy
Most common cause of nephrotic syndrome in whites
HBC, SLE
Neoplasms
Diffuse thickening of GBM
Focal segmental glomerulosclerosis
nephrotic glomerulosclerosis (FSGS) HTn
HIV