Tubulointerstitial/Vascular/Chronic Kidney disease Flashcards
cast nephropathy in multiple myeloma due to
factors favoring intratubular percipitation and cast formation (3)
due to excessive production and urinary excretion of light chains
factors: hypercalcemia
volume depletion
nephrotoxins
2 findings in chronic kidney disease, due to uremic toxin buildup
coagulopathy > platelet dysfunction
sensorimotor neropathy
cortical infarct morpholhy
renal artery occlusion > extensive parenchymal infarction
smaller branch - wedge shaped infarct, pale with yperremic baorder and coagulation necrosis, hemorrhage+acute inflam at edge
later fibrosis
predisposing conditions pyelonephritis
urinary obstruction
UT instrumentation
vesicoureteral reflux
pregancy
diabetes
often occurs after artial angiography
histopathologic evidence of clefts in vascular lumen
causes both acute and progressive kidney dysfunction
aheroembolic dieseases
mechanism of secondary hyperparathyroidism in chronic kidney disease
decreased renal synth of 1,25-dihyrdroxy D3 AND decreased phosphate excretion lead to:
hypocalcemia
hyperphosphatemia
renal osteodystrophy
treatment myeloma cast nephropathy
hydration and urinary alkalinization to prevent tubular obstruction by casts
chemo or stem cell transplant
kidney transplant at what point?
GFR
typical bacteria of pyelonephritis
gram neg bacilli
renal artery stensosis from atherosclerosis morpholohy
proximal stenosis
excentric plaque with intimal fibrosis, cell debris, lipid+foam cells
medial and adventitial fibrosis
plaque may hemorrhage or disect
calcification
presenting features multiple myeloma
>40
renal insuffciency+proteinuria
hx of bone pain and fractures
hypercalcemia
monoclonal light chains in blood/urine
thrombotic microangiopathy characterized by (3)
thrombosis in capillaries+arterioles (microangiopathic hemolytic anemia, thromboytopenia, renal failure)
Hemolytic uremic syndrome
thrombot thrmbocytopenic purpura
mechanism of HTN in renal artery stenosis
not enough pressure to kidney > increased renin production due to perceived hypotension
causes acute interstitial nephritis
drug hypersensitivity (PCN, NSAIDs. sulfonamides, rifampin)
infection
autoimmune - SLE, sjogrens
suspect renal artery stenosis in:
elderly or late onset HTN
difficult to control HTN
abdominal or flank bruit
renal failure after starting ACEi
anemia in chronic kidney disease results from ___
occurs at which point?
decreased EPO production
occurs below GFR of 60ml/min
characterized by interstitial and tubular inflammation and the precense of bacteria on urine culture
often due to ascending UTI
pyelonephritis
2 main casuses renovacualr hypertension
atherosclerosis
fibromuscular dysplasia
(also trauma, dissection, extrinsic compression from neoplasms)
acute inflammation of kidney due to bacterial infection
(usually via bacterial route or hematogenous route)
acute pyelonephritis
charactreized by fractured tubular casts with either lambda or kappa light chain predominance
myeloma cast neuropatyh
physical exam symptoms of chromic in chronic kidney disease
lethary/fatigue
day-night sleep reversal
anoerixia, nausea, vomitng
pruritis
restless leg syndrome
uremic pericarditis
comorbid infection related to thrombotic microangiopathy Hemolytic uremic syndrome
E coli 0157:H7
mechanism of metabolic acidosis presenting in chronic kidney disease
decreased secretion of ammonium and retention of phosphate and sulfates
morphologic features myeloma cast nephropathy
LM: crystalline, **fractured casts **in tubules with associated cellular reaction
IF: light chain predominance
EM: electron dense fractured casts
characteized by interstitial infalmmation with eosinophil predomiance, eosinophilia, eosinophiluria,
often caused by drugs
acute interstitial nephritis
renal artery stenosis stemming from fibromuscular dysplasia morphology
younger women
alternating thinned media and thicken fibromuscular ridges
string of beads
middle to distal artery
chronic renal failure in multiple myeloma results from (3)
direct tubular toxicity of light chains
tubular obstruction by casts
interstitial inflammation
measure of ESRD
GFR
to slow progression of chronic kidney disease
control HTN
reduce proteinuria
control blood sugar
smoking cessation
(and other disease specific therapy0
morphological features acute interstitial nephritis
inflammation+edema of interstitium+tubules (spraing of glomeruli and vessels)
lymphocytes, plasma cells, eosinophils
possible granulomas
along with renal failure, other manifestations of atheroembolic disease event
bowel infarct
digital infarct
stroke
(eosinophils in blood or urine)
pathogenesis thromobotic microangiopatyh
endothelial injury and activation > intravscualr thrombosis
or
platelet aggregation > vascular obstruction and constriction
presentation acute interstitial nephritis
**hypersensitivity signs key: **fever, arthalgias, macuopapular rash
peripheral blood eosinophilia,
eosinophils in urine
urine: WBCs WBC casts, RBCs
morphology renal malignant hypertension
mucoid intimal thickening of arteries
glomerular capillary wringling
gbm duplication
treatment renal artery stenosis
surgical revacularization
angioplasty and stenting
consequences of chronic kidney disease (3)
Anemia
HTN
secondary hyperparathyroidism
morphology hypertensive nephrosclerosis
gross: normal-small size, finely granualr subcapsular surface
LM: subcapsu;lar glomerular scleorisis,
tubular atrophy,
interstitial fibrosis
arteriolar hyaline
chemotactic for eosinophils seen in atheroemboli eosinophilia
C5a activation
