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
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.
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.
treat with plasmapheresis to remove circulating anti GBM antibodies
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
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
poor prognosis, need transplant and/or dialysis
diseases that affect the tubules and interstitium (3)
drug induced interstitial nephritis
acute tubular necrosis
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
predisposed by bacteria and urethra because of urethral instrumentation or obstruction of urine flow
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
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
African american with hypertension, diabetes. Ischemic conditions because hyaline arteriolosclerosis to vessels
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
Male with obstruction, pain, infection, hydronephrosis
kidney stones(renal calculi)
calcium oxalate; with calcium phosphate; or uric acid
metabolic process, surgery, lithotripsy
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
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
5th-6th decade smoker with adenocarcinoma from renal tubule
golden yellow tumor, may metastasize widely, zones hemorrhage and nephrosis, hematuria, flank pain, palatable mass