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Acute Post-streptococcal Glomerulonephritis
Nephritic Syndrome
LM: Diffuse and enlarged glomeruli with neutrophil infiltration
EM: Subepithelial immune complex deposit
IF: Granular

Hematuria 1-3 wks following Grop A  streptococcal infection.  Periorbital edema (sodium retention); Peripheral edema can occasionally be more extensive but it is related to sodium retention not hypoalbuninemia
Usually transient HTN
Resolves spontaneously; supportive tx
Rapidly progressive cresenteric glomerulonephritis
Nephritic Syndrome
LM: Crescent moon shape
EM: no electron-dense deposits
IF: Crescent moon shape or it can appears linear
Crescent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages
Associated with the following:
-  Goodpasture's syndrome: Type II hypersensitivity; antibodies to GBM. Male dominant disease with hematuria and hemoptysis due to lung involvement. IF- linear
-  Wegner's granulomatosis: c-ANCA
-  Microscopic polyarteritis: p-ANCA
Goodpasture Syndrome
Rapidly progressive (crescentric) GM
Type II hypersensitivity; antibodies to GBM. Male dominant disease with hematuria and hemoptysis due to lung involvement. IF- linear
Wegner's Granulomatosis
c-ANCA
Microscopic polyarteritis
p-ANCA
Diffuse proliferative glomerulonephritis
Diffuse proliferative GN is the most common subtype of glomerular disease in SLE (other types have a nephrotic presentation)
Most common cause of death in SLE
DNA-anti-DNA immune complex activate classical complement pathway
"Wire-looping" of capillaries (corresponds to subendothelial immune complex deposits) 
IF: Granular 
Berger's disease (IgA glomerulopathy)
Most common nephropathy
Majority are nephritic
Affects children and adults
Often presents/flares with a URI or acute gastroenteritis
Increased mucosal synthesis and decrease clearance of IgA; increased serum of IgA
LM and IF: granular deposits in mesangium
Alport's Syndrome
Nephritic syndrome
X-Linked Recessive disorder
Mutation in Type IV collagen leading to split basement membrane
Includes nerve disorders, ocular disorders, and deafness
Nephritic Syndrome
Inflammatory Process
Glomerular injury primarily due to neutrophils
Associated with:
RBC casts
Azotemia with a BUN:Cr ratio > 15
Oligouria: due to decreased GFR from inflammed glomeruli but tubular function is intact
Hematuria
HTN: due to Na+ retention)
Proteinuria (<3.5g/day)
Nephrotic syndrome
Glomerular injury is due to cytokines and not to neutrophils
Cytokines damage podocytes causing them to fuse together and destroys the negative charge of the GBM
Associated with:
Proteinuria (>3.5g/day)
Generalized pitting edema and ascities (due to hypoalbunmenia)- increased risk of developing spontaneous peritonitis due to Strep. pneumoniae
HTN
Fatty cast with maltese cross and oval fat bodies----Lipiduria
Minimal Change Disease
Nephrotic syndrome
Most common nephrotic syndrome in children (Girls> Boys)
Often preceded by respiratory infection or routine immunization
T-cell cytokines causes GBM to lose negative charge
Secondary cause: Hodgkin lymphoma
Selective proteinuria- albumin not globins
Normotensive unlike most nephrotic syndrome
LM: Normal glomeruli
IF: negative
EM: Foot process effacement; fusion of podocytes and no deposits
Tx: Responsive to corticosteroid
Focal segmental glomerulosclerosis
Most common glomerular disease in patients with HIV and IV heroin abuse
LM: segmental sclerosis and hyalinosis
EM: focal damage to visceral epithelial cells
IF: negative
Diffuse membranous glomerulopathy
Most common cause of nephrotic syndrome in adults
Caused by drugs (e.g. captopril and gold therapy), infection (HBV, P. malariae, syphilus), SLE (nephrotic presentation), carcinomas
LM: diffuse capillar and GBM thickening
EM: Silver staining shows "spike and dome" pattern beneath visceral epithelial cells
IF: granular
Tx: corticosteroid might slow progression
Membrano-proliferative glomerulonephritis
Type I: Associated with HBV>HCV; EM-"tram track appearance" due to GBM splitting
Type II: Associated with C3 nephritic factor, which is an autoantibody that binds to C3 convertase and prevents degradation of C3 convertase causing sustained activation of C3 resulting in low levels of C3.EM-"dense deposit 
Diabetic glomerulonephropathy
Nephrotic syndrome
DM Type I > DM Type II (Most common cause of chronic renal failure)
Nonenzymatic glycosylation (NEG) of GBM leads to increased permeability and thickening.  Also affects tubular basement membrane.
NEG of efferent arterioles leads to increased GFR and hence increased mesangial expansion
Osmotic damage to glomerular capillary endothelial cells due to sorbitol
LM: Mesangial expansion; GBM thickening, nodular glomerulosclerosis (Kimmelstiel- Wilson disease)
IF: nonspecific
Renal amyloidosis
LM: Congo red stain, apple-green birefringence
Associated with:
Multiple Myeloma
Chronic conditions
TB
RA
Casts
Formed in tubular lumen in the kidney
Composed of matrix protein within which are trapped cells, debris, or protein leaking through the glomeruli
Hyaline casts
Non-specific
Acellular ghost-like cast containing protein
RBC cast
Nephritic type of GN, ischemia, or malignant HTN
WBC casts
Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
Granular ("muddy brown") or Renal Tubular cell cast
Sign of acute tubular necrosis
Waxy casts
Refractile, acellular cast
Advanced renal disease/ Chronic renal failure
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