glomerular problems (W3) Flashcards
what is the functional unit of the kidney?
the nephron
glomerulonephritis
a variety of conditions that cause the inflammation of glomeruli
can be focal or diffuse
affects both/either or
3rd leading cause of kidney failure, about 1/4 of ESRD cases
primarily an immune-mediated response
where does damage occur?
glomerulus- delicate network of arterioles within bowmans capsule
tubules- massive oxygen consumer
glomerular d/o
alterations in glomerular capillary
glomerulus (3 layers of the capillary membrane)
- endothelium layer
- basement membrane
- podocytes (special epithelial cells)
how to classify glomerulonephritis
etiology:
primary- isolated to kidneys
secondary- caused by systemic disease
damage to glomeruli:
focal- only some glomeruli
local- an area of glomeruli
disease progression
clinical presentation
type 2
occurs on the cell surface and results in direct cell death/malfunction
type 3
immune complexes are deposited into tissues and the resulting inflammation destroys tissues
type 2 and 3- what do they have in common?
immune complexes
two types of injury
- AB attack to antigens of the glomerular basement membrane, direct attack via “anti-GBM AB” (> 5%)
- antibodies react with circulating antigens that are deposited in the GBM (> 90%)
both types of injury- what do they have in common?
- accumulation of antigens, AB, complement
- complement activation results in tissue injury
- inflammation
acute glomerulonephritis
abrupt onset
“HARP”
H- hematuria, blood in urine
A- azotemia, buildup of wast products
R- retention, sodium/water/oliguria/leads to htn and edema
P- proteinuria, protein in urine
AG triggers
post-infection: strep/non-strep/bacterial/viral/parasitic
primary disease: berger disease
multisystem disease: good pasture syndrome, systemic lupus (SLE), vasculititis
anti-GBM AB
think about the disease good pasture syndrome
similar to lungs
hemoptysis
results in renal and respiratory problems
acute glomerulonephritis pathogenesis
- trigger
- immune complex formation
- complement activation
- release mediators
- tissue injury
- hematuria, proteinuria, decreaed GFR
chronic glomerulonephritis
LT inflammaton- weeks to months
buildup of scar tissue, results in non-functional kidney
similar s/s of acute
progression- s/s renal failure
slow
eventually ESRD- dialysis
pharm
corticosteroids
diuretics
immunosuppressants
anti-hypertensives
other treatment
dialysis
diet (< protein, salt, potassium)
S/S of glomerular problems
hematuria- coffee/cola-colored
oliguria
fluid retention
labs (increased BUN/creatinine- ratio 20:1, positive protein in the urine, hypoproteinemia, low albumin)
loss of albumin
hypoproteinemia
glomerulopathy
diabetes
hypertension
diabetic glomerulopathy
major complication
gross thickening of GBM
hypertension glomerulopathy
decreased renal perfussion
scarring
sclerotic glomerular changes
nephrotic syndrome
damage causes glomeruli to be too permeable to plasma proteins, eliminates > 3 grams of protein each day
etiology:
1. glomerulonephritis
2. diabetes
patho of nephrotic syndrome
increased glomeruli permeability
proteinuria
hypo-abluminemia
nephrotic syndrome- clinical manifestations
edema (decreased albumin)
hypertension (compensates)
liver (hyperlipidemia, hypercoagulation because of loss of antithrombin 3 and plasminogen)
why does edema occur in nephrotic syndrome?
due to decrease in serum osmotic pressure caused by loss of serum albumin
