module 12 glomerular disorders / AKI Flashcards
glomerulopathies
alter glomerular capillary structure and function
damage mediated by immune or inflammatory processes
hereditary and environmental factors
- metabolic, infectious, hemodynamic, toxic, genetic, trauma
-> hematuria, proteinuria, abnormal casts, dec. DFR, edema, HTN
Classical s/s: proteinuria
classification of glomerular disorders (8)
Primary: only the kidney is involved
Secondary: results from other disease, conditions, medication
- goodpasture syndrome
- systemic lupus erythematosus
- diabetic nephropathy
Diffuse: all glomeruli
Focal: some but not all glomeruli
Global: affecting all parts of glomerulus
Segmental: only specific parts of glomerulus
Membranous: thickening of glomerular capillary walls, basement membrane
Sclerotic: scarring
sites of deposition in glomerular disorders
mesangial
subendothelial
subepitheilal
nephrotic syndrome
necrosis
characterized by protein loss >3 to 3.5 grams in 2 hours
more severe, more protein loss
nephritic syndrome
inflammation
mild to moderate proteinuria
hematuria and RBC casts present in sediment
glomerulonephritis
assortment of immune mediated conditions -> inflammation
Primary: autoimmune
Secondary: autoimmune, metabolic, malignant, infectious
acute glomerulonephritis
abrupt onset of hematuria, proteinuria, oliguria, azotemia, edema, HTN
- wide variety of triggers initiate inflammatory response
Post- infectious: follows infection
- impentigo
- strep
- viruses
Antibody-antigen complexes deposition -> glomerular damage/inflammation
acute glomerulonephritis s/s
smoke/coffee urine (hematuria) RBC casts (nephritic syndrome) proteinuria dec. GFR edema HTN oliguria inc. serum creatinine and BUN
acute glomerulonephritis flow chart
initiating trigger
- > immune complex deposition
- > complement activation
- > macrophages and neutrophil attraction, coagulation cascade activated
- > lysosomal enzymes attack glomerulus
- > inc. membrane permeability
- > dec. GFR, proteinuria, hematuria
acute glomerulonephritis flow chart vasoactive side
initiating trigger
- > local vasoactive chemicals
- > dec. capillary perfusion
- > dec. GFR
- > inc. serum creatinine, azotemia, oliguria, edema
crescentic glomerulonephritis/ rapidly progressive
characteristic lesions: proliferative, crescent shaped deposits of epithelial cells, fibrin, and macrophages in bowman’s capsule
- podocytes progressively lose differentiation
- acute onset hematuria, proteinuria, and RBC casts followed by swift dec . in renal function
20-50 y/o
crescentic glomerulonephritis categories
idiopathic or following 4
- complication of acute/subacute infection
- compilation of multi-system disease
- drug exposure
- primary disorder in absence of systemic disease
common associated infections w/ crescentic glomerulonephritis
post-strep glomerulonephritis infective endocarditis lupus Henoch-Schonlein purpura Systemic necrotizing vasculitis Goodpasture syndrome
chronic glomerulonephritis
glomerular diseases with progressive course -> CKD
persistant proteinuria with our without hematuria
slowly dec. renal function
proliferative and membranous lesions present
sclerotic injury -> ongoing fibrotic changes
tubulointerstitial damage
nephrons atrophy - small nonfunctional kidneys
CKD -> ESRD requiring dialysis or transplant
nephrotic syndrome
d/t inc. glomerular permeability to proteins
proteinuria -> hypoalbuminemia
-> generalized edema, dec. blood osmotic pressure
Inc. in liver activity -> hyperlipidemia, and hypercoagulability
