nephrology Flashcards
normal calcium with high pth
secondary due to CKD with normal phos
cannot be primary, has to be secondary
start activated vitamin D
hyponatremia+ normal plasma osmolarity in the presence of lipids/proteins (panc/ multiple myeloma) with no ingested osmoles
pseudohyponatremia
minimal change disease (podocyte foot processes) treatment
steroids, if contraindicated->cyclosporine
if refractory->cyclophosphamide
Thyrotoxic periodic paralysis
2/2 hypokalemia
precipitated by strenous exercise/high carb meal
treat hyperhyroidism
Metabolic alkalosis+ hypokalemia+ normal-low BP
Bartter syndrome
autosomal recessive
Preggo htn
No ACEI/ARB/direct renin inhibitor
labetalol if >160/105
lithium kidney
diagnosis
nephrogenic diabetes insipidus
water restriction test, then desmopressin administration
> 60 yo BP goal
150/90. Adding a second agent is more effective than increasing existing dose.
Acute acid-base compensation
chronic
for every 10 drop in co2, 2 drop in bicarb
for every 10, 4-5
for every 10 increase, 3-4
CKD with normal anion gap metabolic acidosis
oral bicarb, maintain bicarb 23-29
interstitial nephritis urinalysis
cause
membranous glomerulopathy
rapidly progressive glomerulonephritis
sterile pyuria and leukocyte casts
drugs (mesalamine)
heavy proteinuria and nephrotic syndrome (primary: anti pla2r, sec: cancer, autoimmune disease, hepatitis b, syphilis, meds). most associated with clots
hematuria, erythrocyte casts, hypertension
Preeclampsia
HELLP
hypertension+ proteinuria OR htn+end organ damage
hemolysis+ elevated LFTs+ low platelets
hyperphosphatemia in CKD treatment
sevelamer/ lanthum
hyporesponsiveness to EPO
give iron especially if
iron deficiency
transferrin <30% / ferritin <500
Lines in CKD5/ESRD patient
central venous access
preggo na
mild hyponatremia and hypo osmolality
IgA vasculitis (henoch-schonlein purpura)
URI->then fatigue, jt pain, abd pain, glumeronephritis, palpable purpura
NORMAL COMPLEMENT LEVELS
Vomiting urine labs
bartter
sjogren’s
increased sodium, low chloride, elevated urine potassium
increased everythang
hyperchloremic metabolic acidosis
Shiga-toxin associatd hemolytic uremic syndrome
diagnosis
bloody diarrhea, then microangiopathic hemolytic anemia, thrombocytopenia, kidney failure, shiga toxin e. coli
peripheral blood smear (even in TTP, smear before ADAMST13)
**can also be caused by chemo(bevacizumab, sunitinib)
Suspected kidney stone when CT is contraindicated (preggo)
kidney ultrasound
calcium oxalate stones with elevated urine oxalate (from too much oxalate or low calcium/fatty acids binding calcium)
deceased citrate in urine
idiopathic hypercalciuria
increase calcium intake/ cholestyramine (esp in patients who have undergone small bowel resection)/ UOP of at least 2L
give citrate to bind calcium in urine and prevent stones
thiazide
Medication induced tubulointerstitial disease (AIN/CIN) (tenofovir, PPI)
slowly progressive, no clear trigger, subnephrotic proteinuria, bland sediment, atrophic kidneys on u/s
glucosuria, hypophosphatemia
membranoprolif glomerulonephritis
chronic hep b, hematuria, dysmorphic casts, proteinuria, reduced GFR
Beware of refeeding syndrome in alcoholics and malnourished. can occur even with dextrose containing fluids, due to
hypophosphatemia
Hypertension diagnosis
Rule out meds such as
140/90 3 different times over 1 week or longer
NSAIDs (also cause hyperkalemia) and herbs
Anion gap metabolic acidosis in patients with short bowel
ethylene glycol/methanol/propylene glycol
D-lactic acidosis
confusion, slurred speech, ataxia
osmolal gap >10
dialysis catheter related infection
abx, then remove catheter if blood cultures are positive
Metabolic alkalosis with uncertain volume status
measure urine chloride
low: hypovolemia, give saline
high: saline resistant
Bilateral abdominal masses with kidney symptoms
ADPKD, hematuria and acute pain occur with rupture of cysts
MRA to screen for cerebral aneurysm only if family history of aneurysm/hemorrhage or personal history or occupation where sudden rupture would affect others
TLS
Rasburicase
Dialysis if
hyperphosphatemia, hyperuricemia, hyperkalemia, hypocalcemia
rapidly decreases uric acid
oliguric/anuric/persistent hyperkalemia/syptomatic hypocalcemia/
Rasburicase vs allopurinol
reduces circulating uric acid vs prevents formation