urologic problems: glomerular disease Flashcards
azotemia
increase BUN and Cr in urine
glomerular filtration rate (GFR)
blood test to check kidney function –> blood filtered per hour
calculated of blood metabolic panel
glomerular disorders
glomerulonephritis
nephrotic syndrome
glomerulonephritis
a variety of conditions that cause inflammation of glomeruli
-primarily an immune response
-focal or diffused
-affects BOTH kidneys equally
**3rd leading cause of kidney failure in US (25% of ESRD cases)
where does the damage of glomerulonephritis occur?
glomerulus - delicate network of arterioles within the Bowman’s capsule
tubules - massive consumer of oxygen
glomerular disorders
alterations in glomerular capillary
glomerulus layers
capillary membranes have 3 layers:
1. endothelium
2. basement membrane
3. podocytes (special epithelial cells)
primary vs. secondary glomerulonephritis
primary - isolated to kidneys
secondary - caused by systemic disease
type II immune complex
reactions occur on the cell surface and result in direct cell death or malfunction
type III immune complex
immune complexes are deposited into tissues and the resulting inflammation damages the tissues
what are the 2 type of glomerulonephritis injuries?
- antibodies attach to antigens of the glomerular basement membrane (“anti-GBM antibodies”) –> 5%
- antibodies react with circulating antigens and are deposited as immune complex in the GBM –> 90%
what do BOTH types of glomerulonephritis have in common?
-accumulation of antigens, antibodies, and complement
-complement activation results in tissue injury
acute glomerulonephritis characterized by…
ABRUPT ONSET
HARP
H- hematuria
A- azotemia
R- retention (sodium & water retention; leads to oliguria, edema and HTN)
P- proteinuria
triggers of acute glomerulonephritis
post-infectious:
-post-streptococcal infection
-non-streptococcal infection (bacterial, viral, parasitic)
primary disease
(ex: Berger disease)
multisystem disease:
(ex: goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis)
anti-GBM antibodies
acute glomerulonephritis patho
- trigger
- immune complexs form
- complement activated
- release of mediators
- tissue injury
- hematuria, proteinuria, decreased GFR
chronic glomerulonephritis
longer term complication build up of scar tissue – scar tissue can’t filter/produce urine effectively
*inflammatory process
*can lasts months - years
clinical manifestations of chronic glomerulonephritis
similar to acute –>
HARP
H- hematuria
A- azotemia
R- retention (sodium & water retention; leads to oliguria, edema and HTN)
P- proteinuria
*dependent of severity of damage to kidney’s
prognosis of chronic glomerulonephritis
slow progressive destruction of glomerular tissue
ENDS with ESRD and REQUIRES dialysis
pharmacotherapy for glomerulonephritis
corticosteroids (predisone) - reduce inflammation
diuretics - reduce swelling
immunosuppressants
anti-hypertensives (ACE or ARB)
other treatment (aside from meds)
dialysis
diet (less PRO, salt, potassium)
common S/S of glomerulonephritis
hematuria (coffee colored urine)
oliguria (<400mL/day)
fluid retention (edema, HTN)
labs
- elevated BUN, Cr (>20:1 BUN:Cr ratio)
-++proteinuria
-hypoproteinemia
glomerulopathy: DM
diabetic neuropathy
-major complication
-underlying pathology (gross thickening of GBM–> poor filtration)
END RESULT:
glomerulopathy: HTN
hypertensive glomerular disease
-decreased renal perfusion
-sclerotic glomerular changes
nephrotic syndrome
the glomerulus is too permeable to plasma proteins
elimination > 3 grams of protein per day
cause of nephrotic syndrome
glomerulonephritis
DM
nephrotic syndrome PATHO
increased glomerular permeability –> proteinuria –> hypoalbuminemia
clinical manifestations of nephrotic syndrome
edema
HTN
hyperlipidemia
hyper coagulation (DVT, PE) – loss of antithrombin III and plasminogen
antithrombin III fxn
keeps balance between clots and free flowing blood
plasminogen
percursor to plasmin which helps breakdown clots that do form
