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27 Cards in this Set
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Acute Nephritic Syndrome
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Hematuria
Azotemia (thus hi creatinine and BUN) Variable proteinuria Oliguria (decreased urine volume production because glomerulus is not able to adequately carry out filtration processes) Edema Hypertension (from fluid retention and activation or RAAS) |
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Rapidly Progressive Glomerulonephritis
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Acute nephritis (is the severest form of nephritic syndrome)
Proteinuria Acute Renal failure (with complete or near complete glomerular failure) severe oliguria severe edema hypertension marked azotemia |
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Nephrotic syndrome
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>3.5gm proteinuria/day
hypoalbuminemia hyperlipidemia lipiduria |
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Chronic renal failure
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azotemia with uremia progressing for years
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uremia
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muscle twitches and cramps, fatigue, decreased mental acuity, N/V, hypertension secondary to hypervolemia, pruritis, pericarditis and occasionally uremia frost
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ways for chronic renal failure to develop
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glomerulonephritis
any other severe and/or prolonged insult to the kidney (kidney stones), other causes of obstructive uropathy (tumor), pyelonephritis, PCD, and reflux neuropathy all will eventually result in azotemia with uremia |
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Classic lab findings for CRF
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hi creatinine
hi BUN hi potassium decreased RBC numbers low calcium metabolic acidosis Imaging smaller than normal kidneys |
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Rapidly Progressive (crescentic) glomerulonephritis
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all involve severse glomerular injury and are a severe form of acute nephritic syndrome
without treatment, will cause death from renal failure in weeks to months always has crescents (proliferation of epithelium of Bowman's capsule that surrounds glomerulus) |
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3 types of RPGN
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1: antibody-mediated cytotoxicity
causes: idiopathic, goodpastures 2. immune complex disease causes: idiopathic, SLE, Henoch-Schonlein, post-infectious 3: pseudo-immune - +ANCA disorders causes: idiopathic, wegeners, microscopic polyangiitis, and occasionally, advanced, terminal polyarteritis nodosa |
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Minimal Change disease (lipoid nephrosis, foot process disease)
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risk age: 1-30, represents 4/5ths of childhood nephrotic syndromes; idiopathic 30% have recent history or URI
Biopsy findings: loss of foot processes |
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Membranous Glomerulonephritis
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Risk age: 30s-50s; is the most common adult nephrotic disorder
usually idiopathic, although it can also be seen in association with colon or lung carcinoma, chronic infections, heavy metal exposure, and drugs microscopic hematuria common complication is renal vein thrombosis Pathology and biopsy findings: thickened basement membranes with subepithelial depositis of IgG and C3 complement in a "spike and dome" pattern Progresses to chronic renal failure and then end-stage renal disease in several years |
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Focal Segmental Glomerulosclerosis
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Risk age: less than 35; idiopathic, although can be due to chronic urethral reflux or heroin abuse
Nephrotic syndrome with hematuria, hypertension, and/or renal insufficiency Pathology and biopsy findings: sclerosis (scarring) of the glomerulus in a focal and segmental pattern; this progresses to be a diffuse and global pattern that then causes CRF |
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Membranoproliferative Glomerulonephritis (mesangiocapillar GN)
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risk age: 5-30, small predilection for females
is a result of immune complex deposition in glomerulus is closely associated ith URI, chronic infections (hep C), heroin abuse, certain cancers, SLE and other autoimmune disorders can initially demonstrate a nephritic syndrome, but the glomerular damage results in a nephrotic syndrome Pathology and biopsy findings: mesangial cell proliferation with capillary basement membrane thickening and splitting, plus subendothelial deposits of C3 complement; shows "tram track" patterns Labs: decreased complement levels usually progresses to chronic renal failure, most patients with ESRD within 10 years |
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Acute proliferative Glomerulonephritis (acute post-streptococcal glomerulonephritis; acute post infectious glomerulonephritis)
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Risk is highest at 3-14 years, and declines with age
occurs after a group a strep infection (often strep pyoderma or impetigo in southern us or a pharyngitis in northern us states) results from immune complex deposition onto glomerulus, resulting in imflammation nephritic syndrome labs show + ASO titer and decreased C3 complement Pathology and biopsy findings: mesangial proliferation with subepithelial deposits of IgG and C3 complement in a coarsely granular "lumpy bumpy" or "hump"-like pattern is usually self limited with an excellent prognosis |
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Anti Glomerular Basement membrane disease (goodpastures syndrome)
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risk age: 11-39, with a strong predilection for males
is due to antiglomerular basement membrane antibodies (anti-GBM) deposited antibodies activate complement system and damage membranes, causing severe inflammation Hemoptysis is common since pulmonary basement membranes often undergo coincident or subsequent antibody attack Nephritis, and usually progresses to rapidly progressive glomerulonephritis Pathology and biopsy findings: mesangial proliferation and linear deposition of IgG and C3 on basement membrane. Crescents in those who progress to RPGN Most progress to ESRD within months to years |
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IgA nephropathy (bergers disease)
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risk age 11-29, strong predilection for males
is due to immune complex depostition, composed primarily of IgA, activation of complement system causes glomerular damage and inflammation represents the most common overall primary glomerular disease usually follows viral URI, non-specific viral syndrome, gi syndrome, or other acute pronounced infectious episode Pathology and Biopsy: focal and segmental glomerular mesangial proliferation with IgA immune complex deposits. Labs show increased serum IgA Usually a benign disease, but 1/5 do go on to develop chronic renal failure |
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diabetic Glomerulosclerosis (kimmelstiel-wilson syndrome)
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risk age: any age with development about 20 years after onset of DM type 1 and 2
most common overall secondary glomerular disease (and represents a 'secondary' glomerular disease since it occurs secondary to DM) often demonstrates both nephrotic and nephritic syndrome features microalbuminuria is an early laboratory finding pathology and biopsy: grossly there are small kidneys, microscopically there is diffuse glomerulosclerosis (marked thickening of glomerular capillary basement membranes; known as diffuse diabetic glomerulosclerosis) this later becomes nodular due to nodules of mesangial proliferation (nodular diabetic glomerulosclerosis, kimmelsteil-wilson disease) Gradually progresses to CRF and ESRD |
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Lupus Nephropathy (WHO Type IV)
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wire loop lesions, diffuse proliferation (IgM, IgG, C3)
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Goodpastures disease
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linear basement membrane deposits, IgG and C3
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Rapidly Progressive GN
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wrinkled basement membrane and discontinuous BM (IgG, C3)
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Diabetic nephropathy
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thick BM and mesangial growth = nodular sclerosis
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Post-Strep GN
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"lumpy bumpy" subepithelial IgG and C3
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Membranous GN
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spike and dome, subepithelial IgG, C3
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Minimal change disease
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foot process loss
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Alports syndrome
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basement membrane splitting
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Membranoproliferative GN
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mesangial interposition ("tram Track"
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Parts of the Glomerulus
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Basement Membrane
Foot Processes Bowmans space epithelial cell endothelial cell mesangial matrix mesangial cell |