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42 Cards in this Set
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acute glomerulonephritis
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sudden, rapid onset hematuria (nephtritic means blood in urine generally)
variable GFR edema |
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rapidly progressive GN
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sudden onset, blood in urine nephritic
often progressed from acute glomerulonephritis severe, bad prognosis see crescent formation - due to enlarged openings in capillary -> cells, protein accumulation in bowman's space |
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nephrotic syndrome
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nephrOtic more characterized by proteinuria - see low albumin, hyperlipidemia, hypercoagulable state due to loss of antithrombin III
nephrItic more characterized by hematuria |
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asymptomatic urinary abnormalities
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patient has microscopic hematuria - no clinical symptoms, no proteinuria, normal sodium
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manifestations of glomerular disease (general)
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hematuria
proteinuria decreased GFR sodium excretion abnormalities -> edema, hypertension |
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chronic glomerulonephritis
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see small kidneys - indicative of longstanding problem
lots of protein or blood in urine endstage renal disease |
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silver stain can detect which glomerular diseases
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membranous glomerulopathy (stage II)
type I membranous proliferative glomerulonephropathy (MPGN) |
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subepitheilial glomerular humps is associated with
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post-strep glomerular nephritis
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focal vs diffuse
segmental vs global (glomerular disease) |
focal - less than 50% of glomeruli affected
diffuse - more than 50% of glomeruli affected segmental - only a small portion of glomerulus affected global - all portions of glomeruli is abnormal |
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RBC casts are indicative of
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nephritic syndrome
red blood cells in a tamm-horsefall protein cast - indicates glomerular origin |
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acute glomerularnephritis - SYSTEMIC diseases with LOW serum complement level (5)
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SLE
subacute bacterial endocarditis visceral abscess "shunt" nephritis cryoglobulinemia |
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acute glomerularnephritis - RENAL disease with LOW serum complement level (2)
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acute poststreptococcal glomerulonephritis
membranoproliferative glomerulo nephritis (type 1 and 2) |
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acute glomerularnephritis - SYSTEMIC diseases with NORMAL serum complement level (5)
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polyarteritis nodosa
hypersensitivity vasculitis wegener's granulomatosis henoch-schonlein purpura goodpasture syndrome |
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acute glomerularnephritis - RENAL disease with NORMAL serum complement (2)
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IgA nephropathy
idopathic rapidly progressive glomerulonephritis (anti-GBM disease, immune complex disease) |
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poststeptococcal GN
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children 2-6 years, adults over 40
group A strep infections - skin or pharyngeal - GN follows a LATENT PERIOD of ~10 days diffuse decreased C1q granular IF - IgG and C3 immune complex form electron microscopy shows subepithelial humps |
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membranoproliferative glomerulonephritis (MPGN) type 1 vs type 2
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type 1 - classical pathway of complement (low C4), "tram track" pattern on LM with silver stain, C3 and IgG granular pattern on IF, subendothelial deposits w/ mesangial cells interposed between GBM and endothelial cells
type 2 - alternate pathway (C4 normal), intensely stained GBM on LM, "dense election deposits" on EM, granular IF (C3 +/- IgG), |
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membranoproliferative glomerulonephritis (MPGN) etiology
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most are idiopathic
secondary causes: SLE, sjogrins, endocarditis, shunt nephritis, chronic hepatitis (often Hep C), sarcoidosis, sickle cell |
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membranoproliferative glomerulonephritis prognosis
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worse for nephrotic patients
treat the proteinuria with ACEI or ARB |
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lupus nephritis
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90% of patients are female
blacks more affected class IV is most common - bad renal disease - diffuse GN wire loop abnormality - thickening of capillary wall occurs 4 years of SLE onset ANA+ low complement |
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hypercellular glomerulous is indicative of nephrotic or nephritic disease
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nephritic
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glomerulonephritis associated with endocarditis
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see with staph aureus
bacterimia -> immune complex formation see other systemic effects before GN hematuria, nonnephrotic proteinuria treat with antiboitics |
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T/F the causes of RPGN are often similar to acute GN
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True
RPGN is essentially a severe form of acute GN but most often seen RPGN with goodpastures, SLE, Wergners, rest are idiopathic |
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What is the hallmark of RPGN?
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crescent formation in glomerulous
EM shows characteristic breaks in glomerular basement membrane |
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idiopathic RPGN
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more common in spring and summer
mean age 58 more females can be associated with pulmonary infiltrates 3 types: 1. anti-GBM with linear staining (not goodpastures) 2. immune complex with granular stain 3. pauci-immune RPGN with few deposits see crescents and breaks in glomerular basement membrane on EM normal complement anti GBM+ in type 1 and good pastures ANCA+ |
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goodpastures syndrome
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TRIAD:
GN anti-GBM antibodies pulmonary hemorrhage antigen is alpha3 chain of type IV collagen linear staining pattern due to direct attack by antibodies pulmonary hemorrhage first, renal disease later |
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wergners granulomatosis
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Triad:
upper respiratory tract lower respiratory tract kidneys look for granulomatous vasculitis C-ANCA |
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nephrotic syndrome
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proteinuria
hyperlipidemia edema hypercoagulable states due to loss of Antithrombin III |
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tubular proteinemia
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small proteins that get through the glomerular basement membrane FAIL to be reabsorbed in the tubule
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glomerular proteinemia
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bigger proteins get through the glomerular basement membrane
either due to loss of negative charge of GBM or due to increased pore size |
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primary causes of nephrotic syndrome
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membranous
minimal change focal glomerular sclerosis (FGS) membranous proliferative glomerular nephritis (MPGN) |
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secondary causes of nephrotic syndrome
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diabetes
SLE amyloid multiple myeloma |
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membranous glomerulonephritis
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most common primary cause of nephrotic syndrome in adults
stage 1 - capilary wall thickening stage 2 - "spikes" seen on silverstain stage 3 - GBM material around deposit Stage 4 - deposts are electron lucent on EM subepithelial deposits BUT: differentiated from poststrep GN due to LACK OF SUBEPITHELIAL HUMPS |
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what diseases is silverstain useful for detecting the presence of for in glomerularnephritis
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stage 2 membranous glomerulonephropathy
Type 1 MPGN |
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minimal change disease
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most common primary cause of nephrotic syndrome
causes: idiopathic mostly hodgkin disease NSAIDS only morpholgical change detected will be fused/effaced foot processes on EM (but this is not specific for minimal change disease) |
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focal segmental glomerulosclerosis
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males and blacks more affected
focal (<50% glomerulous affected), segmental (only parts of glomerulous affected) IgM can see a contracted glomerulous and prominent bowman's space most idiopatic 2ndary: HIV, nephron ablation, obesity, heroin |
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treatment of nephrotic syndromes
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worse proteinuria is corrolated with worse outomces
ACEI and ARBs reduce proteinuria |
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diabetic nephropathy
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#1 cause of endstage renal disease
mostly type 1 diabetics see: large kidneys basement membrane thickening diffuse intercapillary sclerosis nodular intercapillary sclerosis (kimmelsteil-wilson lesion) hylinization of affterent and efferent see concurrent diabetic retinopathy (both are microvascular complications) want to catch before stage IV |
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kimmerlsteil wilson lesion
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nodular intercapillary sclerosis seen in diabetic nephropathy
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glomerular amyloidosis
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extracellular deposition of proteins with beta pleated sheet
types: primary - Ig framents secondary - AA protein hereditary - prealbumin dialysis - beta2 microglobulin most likely see nephrotic syndrome with secondary amyloidosis, some with primary renal disease rare with hereditary amyloidosis mesangium expansions congo red stain -> green birefringince |
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IgA nephropathy (berger's disease)
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most common primary glomeulonpehritis worldwide
most are 16-35yo usually due to inhaled or ingested antigen (but don't know specific) IgA circulate form immune complex in glomeruli (look for >50% serum IgA) mesangial expansion (IF pattern), see IgA microscopic hematuria, but gross hematuria after exertion or infections similar renal disease with systemic manifestation is Henoch-Schonlein papura most idiopathic association with chronic liver disease, celiac disease, dermatitis herpetiformis, ankylosing spondylitis |
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Alport Syndrome
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inheritied (often X-linked) - mutation often in alpha5 type IV collagen
renal and auditory issues look for splitting of lamina densa hematuria - males affected more renal transplantation may cause anti-GBM antibodies |
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thin basement membrane nephropathy
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benign familial hematuria
common 5-9% of population alpha3 or alpha4 chains of type IV collagen they have a THIN basement membrane they have microscopic hematuria - don't see gross hematuria, most dont have proteinuria |
