TMA/TI/Diuretics/Cyst Flashcards
thrombocytopenia, hemolytic anemia and dysfunction of affected organs
Thrombotic microangiopathy
renal dominant disease
hemolytic uremic syndrome
Predominant neurological involvement
ttp
severe adamts13 deficienct
ttp
most sensitive marker of hemopysis due to cell lysis and tissue ischemia
elevated ldh
pathological features of tma - blood
schistocytes
glomerular capillary wall thickening with thrombi
Acute hus
initial treatment of choice in TTP
Plasma exchange
recombinized humanized monoclonal antibody that functionally blocks C5, 1st line treatment for children
Eculizumab
predominant pathogen in stec-hus
E coli 0157
classical prodromal feature of stec-hus
Bloody diarrhea
Principal effector mediating tubulointerstitial fibrosis
fibroblasts
final common pathway leading to eskd
Fibrosis
abrupt deterioration in renal function and characterized by inflammation and edema in the renal interstitium
Acute interstitial nephritis
1/3 of cases of drug related ain are caused by
antibiotics
pathology of infection causing ain
Direct injury
medications used
hallmark pathology of ain
Infiltration of inflammatory cells with associated edema usually sparing glomeruli and blood vessels
epithelial cell degenration resembling patchy tubular necrosis with some disruption of the tbm
Tubulitis
dress syndrome
drug rash
eosinophilia
systemic symptoms
40% of drug induced ain
rising serum crea level but little or no evidence of glomerular or arterial disease, no prerenal factors, no obstruction + clinical hx of exposure to a high risk drug
ain
provide confirmatory evidence of AIN
Urine eosinophils
gold standard dx of ain
Renal biopsy
lymphocytic infiltrates in the peritubular areas of the interstitium usually with edema
ain
management of ain
withdrawal of factor, supportive care
time when medication should be discontinued that recovery is expected
within 2 weeks
dose of steroids in ain
prednisone 1mkd po for 2-3 weeks followed by tapering over 3-4 weeks
given to patients who fail to respond to a 2 week course of steroid therapy in ain
cyclophosphamide 4 week 2mkd
immunosuppresive agent used in granulomatosis interstitial nephritis
Mycophenopate mofetil
used in patients with circulating anti-tbm and anti-gbm antibodies
Plasmapharesis
worse prognosis in ain
increasing ageb
biopsy of diffuse disease + interstitial fibrosis
amount of analgesic to vayse analgesic nephropathy
6 tablets daily for > 3 years
decreased renal size, bumpy contours and papillary calcification
analgesic nephropathy
identified risk factor in lithium for ain
Duration of therapy
most powerful predictor of ultimate progression to eskd in lithium as cause of ain
> 2.5 mg/dL
Tx for lead nephropathy
Chronic edta chelation
Bone pain (itai-itai or ouch ouch disease) + osteopenia + renal failure
cadmium
hypertension and frequent gout in Ain
Lead
presenting feature of sarcoidosis
Nephrolithiasis
common cause of chronic renal failure in sarcoidosis
nephrocalcinosis
pathogenesis in sarcoidosis
disordered ca metabolism (hypercalcemia or hypercalciuria)
noncasseating granulomas of giant cells, histiocyyes and lymphocytes; focal lymphocytic infiltrates and periglomerular fibrosis, no immune deposits
Sarcoidosis
tx for patients with sarcoidosis who could not tolerate corticosteroids and effective in decrasing vitamin D and calcium
Ketoconazole
renal failure caused by tubulointerstitial nephritis associated with uveitis
Tinu syndrome
Tx for tinu syndrome
Steroids
most profibrogenic and tubulotoxic fatty acids
oleate and linoleatr
most susceptible to luminal attack by C5b-9
Renal tubular epithelial cells
marker of tissue fibroblasts
fibroblasts specific protein I
most numerous cells in ain
lymphocytes (CD4+ Tcells)
inhibits procimal bicarbonate and Na cl reabsorption at the proximal tubule
Carbonic anhydrase inhibitor
inhibits sodium water reabsorption proximal tubule
osmotic diuretics
inhibits nkcc at medullary and cortical thick ascending limb
Loop diuretics
inhibits ncc at distal tubule
Thiazide diuretics
enac and mineralocorticoid blocker at connecting and collecting tubules
distal K sparing diuretics
prototypic osmotic diuretic
mannitol
level of albumin that enhances furosdemide metabolism but decreases tubular secretion of active diuretic
Low serum albumin
enhance thiazide binding and tubular action
mineralocorticoids, glucocorticoids and estrogens
actions of thiazide and thiazide like
increase water excretion of Na K Cl Mg; reduce Ca
prevent amphotericin induced hypoK and hypoMg
Amiloride
First line agent fir ECV expansion in cirrhotic ascites
spironolactone + furosemide (100/40)
natriuretic antihypertensive; inhibit nacl reabsorption in the proximal tubule and diluting segment, inc in gfr
Adenosine type 1 receptor antagonist: Aminophylline
recombinant form of b type natriuretic peptide causes natriuresis and relaxation of smooth muscle cell
nesiritide
observation that diuretics no longer produce a negative Na balance
Diuretic braking phenomenon
how to overcome diuretic braking
diuretic Na restriction or addition of a second diuretic
strategies to overcome diuretic braking
- restrict dietary salt to prevent postdiuretic salt retention
- another class of diuretic
- multiple daily dosing or diuretic with prolonged action
- Do not stop abruptly
- Prevent or reverse diuretic induced metabolic alkalosis
inadequate clearance of edema despite a full dose of diuretic
Diuretic resistance
mainstay therapy for acute decompensated heart failure
vasodilator and diuretic therapy
first line treatment in chronic heart failure
Diuretics and ace/arbs
Second: bblocker
3rd: Mra or hydralazine-isdn
final: digoxin, icd
diuretic that impair carbohydrate tolerance and precipitate dm
Hyperglycemia
more common ain in the young
tinu and sle
more common ain in elderly
drug induced
gold standard ain dx
biopsy
distal rta with atin
sjogren syndrome
most common dx test in ain
urine eosinophil test
key finding of atin
interstitial inflammation and tubulits
hyperca, hypercalciuria urinary concn defects nephrocalcinosis nephrolithiasis and aki/ckd
focal lymphocytic infiltrate and interstitial noncaseating granulomas of giant cells histiocytes and lymphocytes
sarcoidosis
dry eyes dry mouth, lymphoplasmacytic interstitial infiltrate, ati
sjogren syndrome
multi system do with elev serum igg4 salivary glands, pancreas retroperitoneum and kidneys
igg4 possible plasma positive in a stori form pattern
iig4 related
uveitis painful red eyes photophobia
mixedwith noncaseating granuloma formation
tinu
number of eosinophil per 20x
> 10
4 leading anticancer agents
ifosfamide (atn)
bcg
tki (tma)
pemetrexed
dx criteria for aristocholic acid induced interstitial nephrotis
egfr < 60 2 of the 3 - hypocellular interstitial fibrosis - ingestion of aa containing products - dna adducts in the renal tissue or urinary tract
chronic tubulointerstitial disease in families, ingestion of bread contaminated with aa
balkan endemic nephropathy
progressive ckd, gout and hypertension, fanconi
lead nephropathy
zn smelter workers
ca phos stones
fanconi
cadmium
most commonly isolated organisms from abscesses
p. mirabilis
e. colo
Kleb pneumo
s. aureus
cut off for medically managed cysts
5 cm
txfor infected renal cyst
cotri, chloramphenicol, fqx 4 weeks
Adpkd criteria
at least 3 15-39 yo
2 cysts in each 40-59
> 60: 4 or more cysts in the kidnet