Path 3-6

  1. Basis for glomerular disease
    Rarely congenital

    Aquired to by systemic conditions: diabetes, hypertension, Systemic lupus erythematosus

    Immune basis: Circulating AB, Ag-AB complexes, inflammatory response
  2. Protein and lipid loss in urine, low protein in serum, high lipid in serum, and severe edema because of upset in oncotic pressure
    nephrotic syndrome:

    minimal change disease and focal segmental glomerulosclerosis
  3. child, may be using due to NSAID use but usually idiopathic

    protein loss in urine, no microscopic changes
    Minimal change disease; nephrotic syndrome

    podocytes effaced and leaky

    children respond to steroid therapy, adults are resistant
  4. Young adults and children, often associated with HIV, heroin use, igA nephropathy and maladaption of nephron loss

    damage to podocyte initiates to global sclerosis. nonfavorable prognosis, renal insufficiency, can reoccur post transplant
    Focal segmental glomerulosclerosis: nephrotic syndrome
  5. hematuria(blood in urine)
    oliguria (decreased urine function)
    mild protein in urine
    Nephritic syndrome

    • Acute Post-streptococcal glomerulonephritis
    • rapidly progressive(crescentic) glomerulonephritits
    • Goodpastures disease
  6. Children 3-14
    Infection 1-4 weeks after group A streptococcal pharyngitis or impetigo
    Immune complex causes large sub-epithelial humps-deposits and enlarged hyper-cellular glomeruli
    symptoms: abrupt smokey pee, edema, oliguria, fever nausea
    Acute post streptococcal glomerulonephritis :nephritic disease

    • fully recovering good prognosis in children
    • less favorable in adults
  7. A clinical syndrome present in the 4th and 5th decades. There is a presence of crescents around the nephron which can lead to rapid and progressive loss of renal function. Immune mediated.
    rapidly progressive(crescentric) glomerulonephritis; nephritic disease
  8. IgG and C3 are linearly deposited along the glomerular basement membrane(circulating Ab). No deposits are evident on EM but in some cases pulmonary alveolar capillary basement membranes are attacked and mey lead to pulmonary hemorrhage and renal failure.
    Good-pasture's syndrome, Anti-GBM disease; nephritic disease

    treat with plasmapheresis to remove circulating anti GBM antibodies
  9. Children and young adults, Abnormal amounts of IgA deposits post viral infections of upper respiratory tract. Favor mesangial deposition and complement activation leading to glomerular damage. Blood in urine.
    IgA neuropathy- Berger's Disease

    most common primary glomerulonephritis worldwide

    usually benign but recurrance post transplant is frequent
  10. Important cause of end stage renal failure in young to middle age adults.

    Slow development discovered late with protein in urine or edema
    transient nephrotic or nephritic syndrome

    hypertension, shrunken kidneys, global glomerulosclerosis with interstitial fibrosis and tubular atrophy
    chronic glomerulonephritis

    poor prognosis, need transplant and/or dialysis
  11. diseases that affect the tubules and interstitium (3)
    • acute pyelonephritis
    • drug induced interstitial nephritis
    • acute tubular necrosis
  12. Usually caused by e.coli bacterial infection

    pus inflammation of kidney and renal pelvis
    PMNs infiltrate tubules

    common in women, flank pain, frequent urination with pain

    kidneys enlarged and swollen with yellowish abscesses
    acute pyelonephritis

    predisposed by bacteria and urethra because of urethral instrumentation or obstruction of urine flow

    antibiotic treatment
  13. Hypersensitivity reaction to penicillins, nsaids, thiazide diuretics that cause eosinophilia, rash, hematuria, leukocyturia, oliguria, creatine in serum, interstitial edema
    drug induced interstitial nephritis, stop using drug
  14. Sepsis, ischemia or toxins can cause destruction of the renal tubules at any age.

    acute suppression renal function(oliguria, anuria) and rise in serum creatine

    swollen kidneys with pale cortex and red medulla
    Acute tubular nephropathy(necrosis)

    • denudation, flattening, loss of brush border on tubular epithelium
    • antifreeze
    • reversible, dialysis
  15. African american with hypertension, diabetes. Ischemic conditions because hyaline arteriolosclerosis to vessels
    benign nephrosclerosis
  16. Young adult with Inherited gene defect chromosome 16 with protein called polycystin-1.

    enlarged kidney, hematuria, proteinuria, eventually renal failure
    Autosomal dominant polycystic kidney disease, sure with transplant, dialysis
  17. Male with obstruction, pain, infection, hydronephrosis
    kidney stones(renal calculi)

    • calcium oxalate; with calcium phosphate; or uric acid
    • staghorn calculi
    • metabolic process, surgery, lithotripsy
  18. dilation rena pelvis and parenchymal atrophy from urine obstruction, sudden or slow developing

    congenital or acquired(stones, tumors, neurogenic, preg related(only reversible))

    can be painless
  19. 2.5-3.5 yo, chromosome 11 defect, triphasic: epithelial, stromal, and blastemal
    Wilms tumor, most common kidney tumor and cancer of childhoon derived from embryonic renal tissue
  20. 5th-6th decade smoker with adenocarcinoma from renal tubule

    golden yellow tumor, may metastasize widely, zones hemorrhage and nephrosis, hematuria, flank pain, palatable mass
    renal cell carcinoma

    radical nephrectomy
  21. Male, 5th-6th decade, smoking, schistosomiasis infection, microscopic hematuria, flat papillary
    transitional cell carcinoma, high recurrance
Card Set
Path 3-6
Pathology of Kidney