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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
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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
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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
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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
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hematuria(blood in urine)
oliguria (decreased urine function)
hypertension
mild protein in urine
Nephritic syndrome
- Acute Post-streptococcal glomerulonephritis
- rapidly progressive(crescentic) glomerulonephritits
- Goodpastures disease
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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
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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
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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
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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
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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
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diseases that affect the tubules and interstitium (3)
- acute pyelonephritis
- drug induced interstitial nephritis
- acute tubular necrosis
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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
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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
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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
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African american with hypertension, diabetes. Ischemic conditions because hyaline arteriolosclerosis to vessels
benign nephrosclerosis
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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
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Male with obstruction, pain, infection, hydronephrosis
kidney stones(renal calculi)
- calcium oxalate; with calcium phosphate; or uric acid
- staghorn calculi
- metabolic process, surgery, lithotripsy
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dilation rena pelvis and parenchymal atrophy from urine obstruction, sudden or slow developing
congenital or acquired(stones, tumors, neurogenic, preg related(only reversible))
Hydronephrosis
can be painless
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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
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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
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Male, 5th-6th decade, smoking, schistosomiasis infection, microscopic hematuria, flat papillary
transitional cell carcinoma, high recurrance
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