• large, irregularly-spaced subeepithelial deposits
• Endothelial cell edema
• Neutrophils
• Some cellular proliferation leading to apperance of hypercellularity on H&E
• Coarse granularity on immunofloresence
• usually nephritic syndrome

1. Post-streptococcal glomerulonephritis
2. bacterial endocarditis
3. deep staphylococcal infections
4. infected AV shunts
5. systemic lupus

most common cause of diffuse proliferative glomerulonephritis

• produces nephritic syndrome in kids about 2 wks following a respiratory or skin infection
• caused by circulating immune complexes

• Results when glomeruli are damaged severly enough to allow fibrin to enter Bowman's spaces
• Involved rapid loss of renal function with nephritic syndrome
• will see fibrin crescents microscopically

Etiology: Anti-GBM disease (ex. goodpastures, Masugi's)

• Pt. makes antibodies against an antigen uniformly distributed along the glomerular basement membrane (GBM)

anti-GBM disease with rapidly progressive glomerularnephritis and lung hemorrhages

• the auto-antibody deposits on lung and glomerular BMs

• linear immunofluorescence
• fibrin forms the basis for the crescents of RPGN
• ex. Goodpasture's

Etiology: Severe Immune Complex Disease

• ex: severe post-strep or other bacterial-based gomerulonephritis

Etiology: Vasculitis syndromes

• ex. Wegener's granulomatosis, Polyarteritis, Churg-Strauss, RA with vasculitis
• produce segmental necrotizing glomerulonephritis with crescents

• Deposits primarily in the mesangium, with some proliferation of the mesangial cells
• IgA is the most common deposited immunoglobulin
• immunoflouresence = "tree in winter"
• causes asymptomatic hematuria

1. IgA disease
2. Lupus II and III
3. Zuni disease
4. any other mild disease

• most common cause of nephrotic syndrome in adults (foamy urine - proteinuria)
• electron microscopy shows uniform, evenly-spaced sub-epithelial immune deposits
• immunofluorescence = finely granular pattern
• GBM grows around the deposits and forms spikes

1. mostly idiopathic
2. Lupus V
3. Hep B/C
4. NSAIDs
5. drugs

• most common cause of nephrotic syndrome in children
• EM reveals fused foot processes
• heavy proteinuria due to loss of polyanions from the GBM

• causes nephrotic syndrome in children and adults
• pts have proteinuria, oliguria, hypertension and chronic renal failure
• loss of foot processes plus focal-segmental sclerosis

1. Idiopathic
2. AIDS nephropathy
3. heorin
4. reflux
5. hyperfiltration from any cause

• mesangial cells proliferate and send cell processes between basement membrane and endothelials cells
• leads to tram track appearance due to the split GBM
• immunofluorescence = coarse granularity
• usually causes nephritic-nephrotic syndrome

Many causes

- idiopathic cases have C3 nephritic factor, and autoantibody which stabilizes C3 convertase

• most common in young people
• begins with asymptomatic hematuria or nephrotic syndrome
• Deposit is C3 but usually noo Ig
• immunofluorescence = "worms" - C3 stain only
• dense deposits

• commonest serious glomerular disease
• 'Berger's disease'
• pts have gross hematuria and high BP
• light microscopy = mesangial and focal-segmental proliferation and sclerosis
• serum IgA elevated

• purpuric dermal lesions on lower extremities and buttocks
• abdominal pain and GI bleeding
• nonmigratory arthralgias
• renal abnormalities

• major cause of chronic renal failure
• light microscopy = hyaline obliteration of glomeruli, lost tubules, thickened vessel walls

Mesangial immune complex deposits with mesangial cell proliferation.

Diffuse glomerulonephritis

-massive mesangial, subepithelial and/or subendothelial immune complex deposits with diffuse proliferation and sometimes necrosis of glomeruli

• you will see anything but anti-GBM
• wire loops - subendothelial mega-deposits
• immunofluorescence = coarse granularity in mixed chunks
• Hematuria or nephritic syndrome or RPGN

caused by deposition of ciculating bacterial antigen-antibody complexes

• lesions range from focal GN to diffuse proliferative GN and on
• pts have hematuria, proteinuria and even RPGN

• most common cause of end stage renal disease
• diffuse glomerulosclerosis - hyperfiltration, thickened GBM (w/ increased mesangial matrix = nodular glomerulosclerosis)
• both afferent and efferent arteriold hyalinze in diabetes

• first deposited in the mesangium
• pts get nephrotic syndrome

due to mutated alpha-chain of collagen

• basket-weave basement membrane, renal failure and hearing loss

refers to the presence of marginally-soluble proteins in blood that in cold or local hemoconcentration of a glomerulus

• hallmark = pseudo-thrombus

• lethal
• kidneys look normal grossly but have extreme hypoplasia of the proximal tubules
• unborn children have oligohydramnios and pulmonary hypoplasia

persistence of primitive mesenchyme, which may produce cartilage, undifferentiated mesenchyme, and immature collecting tubules

• results from failure of glomeruli to drain into the ureter during embryonic life

• dilated distal portions of collecting ducts superficially resemble cysts
• stones can form in the dilated ducts leading to chronic back pain

• "nephronophthisis"
• a group of diseases with cysts at the corticomedullary junction
• severe damage to cortex

• A name for the kidneys in people who have been kept alive for a long time on dialysis
• kidneys are useless numbbins

• harmless
• develop after small kidney infarcts

Kidneys unable to reabsorb some or all the good things

• glucose, PO4, Ca++, cysteine, amino acids, Wilsons (copper), lead

• the designation for all forms of acute renal failure caused by damage to tubular epithelial cells
• Early: necrotic cells - oliguria, hyperkalemia danger
• Later: regeneration - diuresis, potassium wasting
• Throughout: isosthenuria
• Causes: kidney poison, NSAIDs, brief hypoperfusion

• kidney failure that develops in patients with liver failure, without anatomic changes in the kidney
• often due to use of diuretics

• microscopically - 2 or more neutrophils in the tubule
• pain at costovertebral angle
• E.coli most common bug
• Papillary necrosis is a complication in diabetics

• any chronic renal infection, or
• severe scarring from one or more healed kidney infections - usually around the calyces and pelvis
• microscopic = normal glomeruli with messed up tubules. Fibrosis around glomerulus or BC
• casts in tubular remnants

• caused by proteus infection and some problem with cGMP
• located around pelvis
• lipid-laden macrophages make the kidney look yellow (mimics RCC microscopically)

• seen in transplants and immunosuppressed
• pathologists look for decoy cells

Analgesic Nephritis due to

• Phenacetin users
• diabetics

• pt develops fever, skin rash, eosinophilia, hematuria, proteinuria, steirle pyura and/or eosinophiluria
• methicillin is the best-know offending drug
• sulfa drugs are other causes

• vessels hyalinize in a string of beads pattern

Extensive metastatic calcification of the kidney tubules causing inflammation or obstruction

-inability to concentrate urine b/c loop of henle is damaged first

causes acute renal shutdown

-can be cause by something as simple as a phosphate enema

• hallmark = big clear vacuoles in the proximal tubules

-tubules plugged with free light chains

-pts often get amyloidosis