glomerular disorders Flashcards
glomerulonephritis
Affects both kidneys equally
Definition: A variety of conditions that cause inflammation of glomeruli
Can be focal or diffuse
3rd leading cause of kidney failure in the U.S.
About ¼ of the ESRD cases
Primarily an IMMUNE-mediated process
where does the damage occur?
glomerulus
tubules - massive consumer of oxygen
afferent - blood going in
efferent - blood going out
layers of the glomerulus
Capillary membranes have 3 layers: Endothelium Basement membrane (GBM) Podocytes (special epithelial cells) - begins production of urine
how to classify glomerulonephritis?
etiology
- Primary – isolated to the kidney
- Secondary – caused by systemic disease
Damage to glomeruli?
Diffuse
Focal – only some glomeruli
Local – an area of the glomerulus
Disease progression
Clinical presentation
type 2 vs type 3 hypersensitivity rxn
both forms can have:
accumulation of antigens, antibodies, and complement
complement activation results in tissue injury
Type II- reactions occur on the cell surface and result in direct cell death or malfunction
- anti-GBM antibodies example
- can cause lung issues
Type III- immune complexes are deposited into tissues and the resultinginflammation damages the tissue
acute glomerulonephritis
**abrupt onset
Abrupt onset of glomerulonephritis Characterized by H.A.R.P. Hematuria Azotemia Retention - Sodium & water retention - *Oliguria - Leads to HTN and edema Proteinuria
Acute Glomerulonephritis: Triggers
Post-Infectious
- Poststreptococcal infection
- Nonstreptococcal infection
- Bacterial, viral, parasitic
- response and see GBM as bad
Primary Disease
- E.g., Berger disease
Multisystem Disease - autoimmune
- E.g., Goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis
anti-GBM antibodies - good pasture syndrome
Type 2 sensitivity
attacks GBM of kindey and lungs
- causes cough up blood and increase respiratory distress
acute glomerulonephritis - pathogenesis
- trigger - infection
- immune complexes form
- type 2 and type 3 sensitivities
- complement activated
- release mediators
- tissue injury
- type 2: direct cell death
- type 3: complement inflammation
- hematuria, proteinuria, decreased GFR
chronic gomerulonephritis
long-term for multiple months of inflammation, increased scar tissue, decreased urine production/output
same s/s as acute, also renal failure
prognosis:
slow progression
end stage kidney disease (ESKD) - require dialysis
pharmacology - tx the underlying issues
Corticosteroids such as prednisone
Diuretics
Immunosuppressants
Anti-hypertensives – ACE or ARB
Other Treatment
Dialysis
Diet - decrease protein, Na, and K
common presenting s/s
Hematuria - Coffee/cola colored urine, rusty Oliguria - Less than 400 mL/day or 30 ml/hr Fluid retention - Generalized edema, HTN Labs - Elevated BUN and creatinine (greater than 20:1 BUN: Creatinine ratio)
++ Protein in urine
Hypoproteinemia
decreased albumin
Glomerulopathy: Diabetes and Hypertension
Diabetic nephropathy
- Major complication
- Underlying Pathology
- Gross thickening of GBM - DECREASE filter of
particles
End result? - thickening
Hypertensive Glomerular Disease Underlying Pathology * renal perfusion Sclerotic glomerular changes ***SCARRING
nephrotic syndrome
**24 hr urine and measure amount
Definition:
The glomerulus is too permeable to plasma proteins
Elimination of >3 grams of protein per day
Etiology:
Glomerulonephritis
Diabetes mellitus
nephrotic syndrome - pathogenesis
increased glomerular permeability
proteinuria
hypoalbuminemia
