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50 Cards in this Set

  • Front
  • Back
when is coronary artery calcium score indicated?
asymptomatic patients with intermediate risk of CAD (10%-20% 10-year risk) --> high score (>400) is an indication for more intensive preventive treatment
what is Fanconi syndrome?
disease of proximal renal tubules; where BAGUP (bicarbonate, amino acids, glucose, uric acid, phosphate) are passed into the urine, instead of being reabsorbed
findings in minimal change disease
normal light and immunofluorescence microscopies; effacement of podocyte foot processes on electron microscopy.
biopsy findings in primary membranous glomerulopathy
diffuse glomerular membrane thickening without cellular infiltration, and coarsely granular deposits of IgG and C3 along the capillary loops by immunofluorescence microscopy. Electron microscopy shows moderate podocyte foot process effacement
clinical clue to diagnosis of multiple myeloma
elevated total urine protein, (quantifies both albumin and non-albumin protein (paraprotein)) with small amounts of protein on urine dipstick (measures only albumin)
when to change HCTZ to furosemide
GFR <30, HCTZ becomes ineffective as a diuretic
kidney biopsy, what is an acceptable BP?
<160/95
contraindications to kidney biopsy (7)
uncontrolled HTN, coagulopathy, thrombocytopenia, hydronephrosis, atrophic kidney, numerous kidney cysts, and acute pyelonephritis
describe FENA in urinary obstruction
in early obstruction, urine sodium and FENa may be low; in late obstruction, urine sodium and FENa may be high (tubular damage)
lab findings in gentamicin toxicity
hypokalemic metabolic alkalosis
describe pathophysiology of gentamicin nephrotoxicity
Aminoglycosides are divalent cations that activate calcium-sensing receptor in TALOH; this inhibits Na-K-Cl cotransporter, mimicking effect of loop diuretics and leading to hypokalemic metabolic alkalosis
fibrosing skin disease caused by an inflammatory reaction to gadolinium that accumulates in the body due to kidney failure
nephrogenic systemic fibrosis
in DM, when to test for microalbuminuria?
annual testing to assess urine albumin excretion in patients with type 1 diabetes of 5 years' duration and in all patients with type 2 diabetes starting at the time of diagnosis by measuring the albumin–creatinine ratio
how is microalbuminuria diagnosed?
albumin–creatinine ratio of 30 to 300 mg/g; diagnosis requires an elevated albumin–creatinine ratio on two of three random samples obtained over 6 months
how do NSAIDs cause hyperkalemia?
inhibit renin synthesis, resulting in hyporeninemic hypoaldosteronism, decreased potassium excretion, and hyperkalemia
formula for TTKG
TTKG = [Urine Potassium ÷ (Urine Osmolality/Plasma Osmolality)] ÷ Serum Potassium OR Uffine K / serum K all div by Uosm/Posm
how to interpret TTKG?
TTKG in patient on normal diet is 8 to 9; >10 in hyperkalemic states, reflecting excretion of excess potassium; if not then prob hypoaldosterone state
fevers and leukopenia post kidney transplant
CMV infection
mechanism of kidney injury due to tenofovir
drug-related damage to mitochondrial DNA (most significantly in renal tubules causing tubular dysfunction)
mechanism of kidney injury due to Bactrim?
Trimethoprim, particularly in acid urine, blocks the epithelial sodium channel in the cortical collecting duct, leading to increased lumen positive potential, impaired potassium and proton secretion, hyperkalemia, and metabolic acidosis
X-linked disease affecting basement membranes due to a collagen protein synthesis defect. Clinical disease is characterized by sensorineural hearing loss, ocular abnormalities, and a family history of kidney disease and deafness
Alport syndrome
differential diagnosis of combined increased anion gap metabolic acidosis and respiratory alkalosis
salicylate toxicity, liver disease, and sepsis
ferritin levels that exclude or diagnose iron deficiency
>100ng/mL excludes and <15 diagnoses iron def
formula for urine potassium–creatinine ratio
Urine Potassium (meq/L) × 100 [(mg × L)/(dL × g)] ÷ Urine Creatinine (mg/dL)
interpretation of urine K-crea ratio
> 20 meq/g c/w kidney potassium wasting, << 15 meq/g suggests extrarenal potassium loss, cellular redistribution, or decreased intake
metabolic alkalosis, urine cl levels low, differentials?
vomiting or decreased effective arterial blood volume (prior diuretics)
metabolic alkalosis, urine Cl levels high, differentials?
on diuretics, Bartter or Gitelman syndrome
define hypercalciuria
urine calcium >300
treatment of calcium stones with hypercalciuria
thiazide diuretic, promotes distal reabsorption of calcium
kidney injury which results when a patient with vascular risk factors and hypertension attains a blood pressure lower than usual measurements
normotensive ischemic AKI
time frame for AIN to occur
1 week of exposure
JNC 7 definition of prehypertension
average blood pressure reading of 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic
blood pressure that is higher at home than in the office setting
Masked hypertension
White coat hypertension
3 office BP >140/90 mm Hg, 2 home BP <140/90 mm Hg and no target organ damage.
Resistant hypertension
BP above goal despitee 3 antihypertensives, including 1 diuretic
pathophysiology of Gitelman syndrome
defect is due to inactivating mutations in the gene for the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule, and the electrolyte profile is analogous to that induced by thiazide diuretics
electrolyte and acid base abnormality in diuretic abuse and surreptitious vomiting
hypokalemic metabolic alkalosis
define gestational hypertension
refers to hypertension that develops after 20 weeks' gestation in the absence of proteinuria or other maternal end-organ damage
what is preeclampsia?
new-onset hypertension accompanied by the development of proteinuria, develops any time after 20 weeks of pregnancy but usually occurs close to term.
classic presentation of AIN
fever, rash, and eosinophilia with elevated crea (only in 10%)
how to interpret fractional excretion of urea
<35% prerenal (less influenced by diuretics)
propofol-related infusion syndrome is characterized by
type B lactic acidosis, hypertriglyceridemia, rhabdomyolysis, and J-point elevation or a Brugada-like pattern on EKG
treatment of primary membranous glomerulopathy
control risk factors - ACEi for HTN and statin if HL
differentiate type A and type B lactic acidosis
Type A due to tissue hypoperfusion / hypoxia. Type B due to medication / toxin; or in advanced malignancy, liver disease, or G6PD def
drugs that cause type B lactic acidosis
linezolid, acetaminophen overdose, metformin, the NRTis stavudine and didanosine, propofol, and salicylates
kidney stones that will pass and will not pass?
5mm or less will pass, 10mm or more will not
at what levels of creatine kinase should one suspect rhabdo?
>5000
abnormal ARR
>25 considered abnormal
when to start bicarbonate therapy in CKD?
Stage 4-5 with bicarb 15-20 (delays progression of CKD)
treatment of hyperoxaluria
calcium carbonate supplements