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27 Cards in this Set

  • Front
  • Back
Acute Nephritic Syndrome
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)
Rapidly Progressive Glomerulonephritis
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
Nephrotic syndrome
>3.5gm proteinuria/day
hypoalbuminemia
hyperlipidemia
lipiduria
Chronic renal failure
azotemia with uremia progressing for years
uremia
muscle twitches and cramps, fatigue, decreased mental acuity, N/V, hypertension secondary to hypervolemia, pruritis, pericarditis and occasionally uremia frost
ways for chronic renal failure to develop
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
Classic lab findings for CRF
hi creatinine
hi BUN
hi potassium
decreased RBC numbers
low calcium
metabolic acidosis
Imaging smaller than normal kidneys
Rapidly Progressive (crescentic) glomerulonephritis
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)
3 types of RPGN
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
Minimal Change disease (lipoid nephrosis, foot process disease)
risk age: 1-30, represents 4/5ths of childhood nephrotic syndromes; idiopathic 30% have recent history or URI
Biopsy findings: loss of foot processes
Membranous Glomerulonephritis
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
Focal Segmental Glomerulosclerosis
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
Membranoproliferative Glomerulonephritis (mesangiocapillar GN)
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
Acute proliferative Glomerulonephritis (acute post-streptococcal glomerulonephritis; acute post infectious glomerulonephritis)
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
Anti Glomerular Basement membrane disease (goodpastures syndrome)
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
IgA nephropathy (bergers disease)
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
diabetic Glomerulosclerosis (kimmelstiel-wilson syndrome)
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
Lupus Nephropathy (WHO Type IV)
wire loop lesions, diffuse proliferation (IgM, IgG, C3)
Goodpastures disease
linear basement membrane deposits, IgG and C3
Rapidly Progressive GN
wrinkled basement membrane and discontinuous BM (IgG, C3)
Diabetic nephropathy
thick BM and mesangial growth = nodular sclerosis
Post-Strep GN
"lumpy bumpy" subepithelial IgG and C3
Membranous GN
spike and dome, subepithelial IgG, C3
Minimal change disease
foot process loss
Alports syndrome
basement membrane splitting
Membranoproliferative GN
mesangial interposition ("tram Track"
Parts of the Glomerulus
Basement Membrane
Foot Processes
Bowmans space
epithelial cell
endothelial cell
mesangial matrix
mesangial cell