Glomerular diseases Flashcards
Glomerulonephritis
variety of conditions causing inflammation in the glomeruli
- focal or diffuse
- mostly an immune process
- often leads to dialysis
- 3rd leading cause of kid fail in U.S.
Glomerulonephritis patho
Type 2 and 3 injury
- antibodies attach to antigens of GBM (anti-GBM antibodies) and cause direct cell death (type 2) OR react with circulating antigens and deposit in GBM as immune complexes that destroy tissues (type 3)
Glomerulus
network of arterioles w/i Bowman’s capsule
- all blood flows thru it; in thru afferent artery, out thru efferent
How does the glomerulus work?
Pressure difference of afferent and efferent arteries push toxins and fluids out vessels thru capillaries in the GBM to filter and add them to urine
What gases are needed for the glomerulus to work?
20% of the body’s CO of oxygen
Podocytes
help with urine production
Layers of the capillary membranes
- endothelium
- basement membrane
- podocytes (special epithelial cells)
Fluid travels thru the nephron and particles are excreted and reabsorbed to get final concentration of urine
Similarity in type 2 and 3 hypersensitivity reaction
Both accumulate antigens, antibodies, and complement (inflammatory process) - complement activation causes injury to the GBM
Acute glomerulonephritis CM
SUDDEN ONSET - HARP
- Hematuria
- Azotemia (high waste products in the blood)
- Retention of Na and water (oliguria, edema, HTN)
- Proteinuria from damaged GBM
Acute glomerulonephritis
Abrupt onset; often hospital patients
Triggers of Acute glomerulonephritis
- after strep and infection - bodily antibodies attack GBM bc think it is a foreign antigen?
- Primary Berger disease
- multisystem disease like Goodpasture sx, lupus, vasculitis
Berger disease
antibody IgA builds up kidney, inflames glom
Goodpasture sx
anti-GBM antibodies (type 2) attack lungs and GBM (bc of similar structure) causing hemoptysis (major sign), respiratory probs, renal problems
Acute glom patho
Trigger - immune complex forms - complement activated (inflammatory process)- release mediators - GBM (tissue) injury - sx (hemoptysis and proteinuria) and dec GFR
Chronic glom
Develop scar tissue over months and years–kidneys fxn less
- sx depend on severity but are similar to acute
- slow progressive destruction to ESRD
Nephrotic syndrome
glomerulus too permeable to plasma proteins causing spills of protein (often albumin) into blood that start to pass thru as tissue weakens into urine (proteinuria) then get 3rd spacing from lack of protein
Causes of nephrotic syndrome
uncontrolled DM, GLOMERULONEPHRITIS
How to diagnose nephrotic syndrome
24h urine - over 3g/day protein
CM of nephrotic syndrome
Edema, HTN (RAS activated to get more volume–HTN and inc kidney perfusion), liver problems, HLD, hypercoag (PE & DVT), proteinuria and hematuria
Why does nephrotic syndrome cause hypercoag?
antithrombin 3 and plasminogen are some of the proteins lost in the blood, can’t b/d clots w/o plasminogen
DM complication of nephropathy
Diabetic nephropathy specific to glomerulus; gross thickening of GBM causes build up toxins and less urine and ESRD
HTN and glomerular disease
inc pressure on BVs causes dec renal perfusion and sclerotic glomerular changes (scarring)
Where does damage occur with glomerulonephritis?
Glomerulus and tubules (big consumer of oxygen)
Which hypersensitivity is more common with glomerulonephritis?
Type 3
Glomerulopathy
Diabetic and HTN complications of glomerulonephritis
Glomerulopathy CM
Hematuria, oliguria (<400 mL/day), fluid retention, inc BUN:Cr ratio, proteinuria, low albumin (hypoproteinemia)
