Nephrology Flashcards
Labs to assess kidney function
SCr, BUN, CrCl, GFR, MDRD, Urinalysis, salt/H2O balance, acid/base balance
Problems with MDRD
although it is very accurate, very little research, all dosing is based on CrCl
Problems with CrCl
serum creatinine is just a “snapshot”, weight discrepancies , diet can effect, athletically fit
Problems with GFR
less reliable, varies w/ age, ethnicity, and body comp
Problems w/ 24 hr urine
cumbersome, prone to error
What do you not use to assess AKI
CrCl, too rapid of a change to be accurate, instead use I&Os
AKI definition
acute decrease in kidney function over hrs, days or weeks, associated w/ accumulation of waste products and volumes, increase of SCr of .5mg/dL in 24 hrs
AKI risk factors
pre-existing CKD, volume depletion/ decrease perfusion, using nephrotoxic agents, obstruction of urinary tract
Causes of AKI
Pre-renal (affecting blood flow before kidneys), Postrenal (problem with moving urine out of kidneys), Intrinsic (problem w/ kidney, preventing filtration or urine production)
When you hear pre-renal what should you think
Hypoperfusion, it’s the most common type of AKI, too
Pre-renal AKI can be caused by
dehydration, disruption of bllod flow, dec in BP, emboli, MI, CHF, liver failure
Treatment for Pre-renal
usually reversible (hydration, fixing other disease), but can cause CKD,
Postrenal is caused by
kidney stone, enlarged prostate, CA
Intrinsic is caused by
blood vessel disease, injury to tissue or cells, glomerulonephritis, acute interstitial nephritis, acute tubular necrosis, medications
Medications known to cause AKI
Aminoglycosides, NSAIDs, ACE-Is (usually only makes preexisting worse), contrast dye, amphotericin-B
Acute interstitial nephritis
sudden decline in kidney function from inflammation of interstitial kidney tissue, usually reversible if treated early (steroids)
Acute interstitial nephritis is caused by
Medications, infections, lupus, lymphoma, leukemia, sarcoidosis
Acute tubular necrosis
kidney tubule damaged and do not function normally, usually end result of acute renal failure
Nephrotoxic ATN caused by
aminoglycosides, amphotericin B, Cisplatin, contrast media, vancomycin
Treatment AKI
volume control with RRT and diuretics
start RRT if
Renal replacement therapy, Acid/base problem, electrolyte abnormality (usually K), Intoxication, fluid overload, uremia
Chronic kidney disease definition
kidney damage lasting more than 3 months, including structural or functional abnormality of the kidney w/ or w/out decreased GFR, with pathologic abnormalities or markers of damage; also GFR
Stage 1 CKD
kidney damage with normal or inc GFR
Stage 2 CKD
kidney damage w/ mild decrease GFR, 60-80 ml/min
Stage 3 CKD
moderate dec GFR, 30-50 ml/min
Stage 4 CKD
severe dec GFR, 15-29 ml/min
Stage 5 CKD
kidney failure,
CKD risk factors
diabetes, HTN, CVD, obesity, age, race, acute kidney injury, malignancy, family hx, hep C, HIV, Lupus, NSAIDS, polycystic kidney disease
Why do you not want to use CrCl for CKD
will overestimate renal function if it is moderate to severe, so use MDRD instead
CKD manifestations
abnormal sodium-water handling (edema, HTN, CVD), metabolic acidosis, anemia, uremia, abnormal Ca-P metabolism due to lack of Vit D
Management of CKD
treat fluid retention/overload, hyperphophatemia/hyperkalemia, hyperparathyroidism, dyslipidemia, anemia, proper drug dosing, prep for RRT
Treating fluid overload
restrict Na, avoid excessive amts of H2O at one time, keep all fluids in mind (diet, drugs etc)
Diuretics for Fluid overload
not for stage 5, do not use thiazides if CrCl
Treating hyperkalemia
restrict intake of Potassium to 3 gm/day, dialysis, calcium gluconate, albuterol, insulin+glucose, sodium polystyrene, sodium bicarbonate
Hyperphosphatemia causes
inhibition of Vit D activation, dec in ionized Ca conc, direct stimulation of parathyroid hormone secretion
Treating hyperphosphatemia
Diet of 800-1200 mg/day phos, phosphate binders- Calcium carbonate, calcium acetate (phoslo), aluminum hydroxide (amphogel), sevelamer (Renagel), lanthanum (Fosrenol)
MOA of phosphate binders
binds to phosphate found in diet and thus it is not absorbed and eliminated in feces, must take with a meal, be wary of hypercalcemia with calcium containing pho binders
Dosage of Phosphate binders
calcium acetate (phosplo)- 667 mg PO TID, sevelamer (renagel)- 800 PO TID
ADRs of phosphate binders
constipation, GI upset
hyperparathroidism treatment
Clacitriol (Rocaltrol), Paricalcitol (Zemplar), Doxercalciferol (Hectoral), Cinacalcet (Sensipar)
Calcitriol (rocaltrol)
active vit D, IV or PO, decreased PTH secretion by increasing [Ca] via increased gut absorption, monitor for hypercalcemia
Paricalcitol (Zemplar)
IV/PO, IV for ESRD pts, favorable due to decrease risk of hypercalcemia, dose based on PTH levels
Docercalciferol (Hectoral)
similar to paricalcitol, must avoid in pt w/ liver failure
Dyslipidemia in CKD
elevated LDL, be aggressive w/ treatment to decrease morbidity, frequently in glomerular disease w/ proteinuria
