Renal Pathology Flashcards
ADPKD: describe
autosomal dominant polycystic kidney disease, it’s adult onset, CLINICALLY: hematuria, flank pain, UTI, renal stones, HTN, chronic renal failure beginning at 40-60 y/o, cysts are spherical and uniformly distributed, chromosome 16, PKD1 mutations
ARPKD
autosomal recessive polycystic kidney disease, manifests in children and is often fatal, enlarged, cystic kidneys at birth, cysts are from collecting ducts and form a sunburst pattern, chromosome 6, PKHD1 mutations
Distinguish the clinicopathologic features between acute and chronic renal failure
Acute is rapid onset of oliguria or anuria with azotemia while chronic is the end stage of all chronic renal diseases and results in uremia—fatigue, neuropathy, anorexia, Vit D deficiency, nausea, and more.
Discriminate between the clinicopathologic features and pathogenesis of nephrotic and nephritic syndrome
Nephritic syndrome is damage to the glomeruli resulting in mild proteinuria and hematuria. Nephrotic syndrome is also glomerular damage but is more severe, with a proteinuria of 3.5 g/day or more and systemic edema, hypoalbuminemia, and hyperlipidemia. The main difference between the two is the amount of proteinemia; the rest of the symptoms can be equally bad.
Outline the generalities of Primary glomerulonephritis
is when the kidney is the primary organ involved, whereas secondary is when systemic disease causes the damage. Primary is usually caused by hypersensitivity reactions. Antigen can be from the GBM itself (glomerular basement membrane) or circulate from blood and get trapped in glomerulus.
What are the two types of glomerulonephritis (GN) progression?
once GFR reaches 30-50% the kidney will steadily approach end-stage renal failure (ESRF). There’s 2 types of progression: focal segmental glomerulosclerosis and tubulointerstital fibrosis. In the former, undamaged glomeruli undergo compensatory hypertrophy, but this hypertrophy eventually leads to sclerosis and their failure. This causes a cycle as other glomeruli then repeat this trend. Tubulointerstitial fibrosis is the progression of ischemia causing interstitial inflammation and fibrosis.
Post infectious, aka acute, nephritis
common in children, usually post-streptococcal (Group A, strains 1, 4, 12, B hemolytic) 1-4 weeks post infection, Ig-mediated, histo: diffuse GN and proliferation and leukocytic infiltrate
Rapidly progressive glomerulonephritis (RPGN)
has 3 types. Type 1 is mediated by anti-GBM Ig’s, linear IgG deposit on immune staining, idiopathic, may be a part of Goodpasture syndrome. Type 2 is immune complex mediated, and Type 3 is pauci-immune (not immune mediated) and caused by ANCAs (anti-neutrophil cytoplasmic antibodies), histo: proliferation, crescents
Membranous glomerulopathy
common cause of adult nephrotic syndrome, insidious onset, usually idiopathic, in situ Ig mediated, histo: diffuse capillary wall thickening, GBM granular staining (vice linear) on immunochemical stain
Minimal change disease
most often cause of nephrotic syndrome in children, beteween 2-6 y.o, idiopathic/maybe podocyte injury, responds very well to corticosteroids, good prognosis, histo: looks pretty normal except for lipid in tubules
Focal segmental glomerulosclerosis
nephrotic, can be idiopathic primary disease or secondary to a bunch of stuff like drug abuse, caused by visceral epithelial damage, can also be caused by HIV, Histo: focal and segmental sclerosis and hyalination
Membranoproliferative nephritis
nephrotic, immune-complex mediated, usually adolescence or young adulthood, Histo: GBM thickening of both capillary loops and mesangial cells, mesangial proliferation
IgA nephropathy
most common type of GN worldwide, recurrent proteinuria and/or hematuria often following an infection, idiopathic, Histo: pretty normal except for a bit of focal proliferative GN, mesangial cell widening
what titer can you do for acute nephritis?
anti-streptolysin O titer (ASOT)
bid difference between nephritic and nephrotic syndrome?
Nephritic has hematuria, nephrotic doesn’t. Also, nephrotic leaks more protein (>3.5 g/day)
