renal disease II Flashcards
Acute Pyelonephritis
AKA: tubulointerstitial nephritis
suppurative inflammation in the renal pelvis, tubules and interstitium caused by bacterial infection
-neutrophil infiltration, clustering in the tubular lumens
-sudden onset of pain at the costovertebral angle
Drug induced interstitial nephritis
caused by AB, NSAIDS and duiretics
pathogenesis of drug induced interstitial nephritis
hypersensitive, drug binds to tubular or interstitial cells and act as a hapten with an immunogenic response (eosinophils and PMNs)
-glomeruli NOT involved
clinical drug induced intersitial nephritis
rapid onset ( 2 to 40 days) fever, eosinophilia, renal dysfunciton with HEMATURIA but no real protenuria
pathologic findings of drug induced interstitial nephrtis
interstitial mononuclear cell infiltration and edema, eosinophils, non-nectroitizing granulomas, dilation of tubules, necrosis of epithelium
drug induced interstitial nephritis prognosis
generally good, full recovery (6 - 8 weeks) with removal of the drug and corticosteroids
Acute tubular necrosis
clinical and path condition where renal funciton declines rapidly with evidence of tubular epithelial damage/necrosis from ischemia (shock) or toxin
-acute kidney injury - oliguria (1/4-1/2 normal pee), electroylte imbalance and decreased GFR
what causes acute tubular necrosis
severe trauma, ischemia, septicemia, toxins
features of acute tubular necrosis
dilation of tubules, edema, necrosis of tubular epithelium
- focal pathology with ischemic injury
- diffuse injury from a toxin
tx of acute tub necrosis
supporative care, dialysis
prognosis is the absence of preexisting kidney disease fully recover, harder when other kindey disease present
-regeneration of tubular epithelium in a few weeks
Arterionephrosclerosis
thickening and sclerosis of renal arteries associated with benign hypertension
apolipoprotein L1 gene deficiency - malignant form
pathology of arterionephrosclerosis
- grossly small kidney / atrophic (granular), thin cortex
- hylaine arteriosclerosis and fivroelastic hyperplasia in mm. arteries (benign form)
- hyperplasia artherioslcerosis (malignant form)
- tubular atrophy and fibrosis
- global sclerosis of glomeruli
contributing factors arterionephrosclerosis
- malignant hypertension (200/120) assoc with the malignant hyperplastic arteriosclerosis form
- diabetes
clinical arterionephrosclerosis
cranial pressure, proteinuria, ischemia leading to acute kidney injury
thrombotic microangiopathies
TTp (thrombotic thrombosytopenia purpura) and hemolytic uremic syndrome (HUS)
-widespread microthrombi in capillaries with RBC damage (schistocytes)
HUS
endothelial cell injury leads to comsumption of platelets and activation
- mainly from shiga toxin of e. coli
- often occurs in children
TTP
acquired or inherited defect of ADAMTS (plasma protease) - degrades vWF, activates platelets
difference in HUS and TTP
HUS predominately kidney, TTP can affect other organs (widespread)
Urolithiasis
aka renal stones
- result in urinary tract obstruciton, ulceration and urothelial bleeding
- small stones to ureters and produce flank pain (serious)
- large stones remain in the pelvis and may be manifested by hematuria and superimposed infection
pathology urolithiasis
stones are unilarteral 80% of the time within calyces and pelvis (maybe bladder)
staghorn calculi
large stones will form a cast of the pelvis and calyceal system
types of stones
calcium (increased pee calcium), magnesium ammonium phosphate (infection with proteus or staph pre-disposes and alkaline pee)and uric acid (gout, leukemia or acidic urine)
Hydronephrosis
dilation of renal pelvis/calyces with parenchymal atrophy becasue of obstruction
causes of hydronephrosis
renal stones, UTI, enlarged prostate, neoplasms, meurogenic bladder, pregnancy