Treatments Quiz 2 Flashcards
Plasma Creatinine
Simple but innacurate esp. w/ mild renal impairment.
Reduced w/ low muscle mass
Raised w/ high protein meal.
Cystatin C
Low mol. wt protein produced by all nucleated cells
Not affected by diet, gender, age, muscle mass
Affected by steroids
Great test –> Mayo uses this
Creatinine Clearance
Urine collections unreliable
Overstimates GFR (tubular secretion of creatine)
Cockroft Gault Formula
Used to estimate creatinine clearance
140-age x wt / 72 x S cr
More accurate than plasma creatinine especially w/ mild renal impairment.
Overestimates in obesity and low protein diet.
Modification of Diet in Renal Disease (MDRD)
186 x (serum creatinine) ^-1.154 x (age)^-.203 x .742 (f) x 1.210 (AA)
More accurate than Cockroft Gault (not according to Muster)
CKD-EPI Equation
Most accurate
Variables for age, sex, race, and serum creatinine levels
Plasma clearance
Best approximation of true GFR
Invasive, may use radioisotopes.
Management of CKD
- ) Treat reversible causes of renal dysfunction (pre-renal - dehydration, hypotension; Renal - nephrotoxic drugs; Post-renal - stone, BPH)
- ) Preventing or slowing the progression of renal disease (ACEi or ARBs, HTN, Protein restriction), hyperlipidemia, glycemic control, weight control, and smoking)
- ) Treatment of complications of renal dysfunction (volume overload, hyperkalemia, metabolic acidosis, hyperphosphatemia, hyperparathyroidism - consequence of PO4 increase, anemia)
- ) Preparation and initiation of renal replacement therapy
ACEi and ARB
Indicated in diabetic and non-diabetic renal diseases
Up to 25% increase in creatinine can occur within 4 weeks –> not a reason to change unless large jump.
Must recheck levels –> most common cause of large jump = dehydration from diuretics.
Higher increases in heart failure, volume depleted state, and bilateral stenosis (contraindication)
Monitor creatinine and potassium
Start w/ small dose and gradually increase the dose
Phosphate Binders
Used to treat hyperphosphatemia in CKD
First line is limiting phosphorous restriction (big one is dairy)
First line binders: Calcium Carbonate (TUMS); Calcium Acetate (Acetate) –> cheap and effective, but only works at low levels–> hypercalcemia
Second line binders: Lanthanum carbonate, Sevalamer, and Sucroferric Oxyhydroxide –> expensive, effective, no calcium toxicity issus
Calcitrol
Vitamin D analog used to treat secondary hyperparathyrodism.
Decrease PTH, but increase PO4- –> must treat high PO4- first w/ binders.
Doxecalciferol
Vitamin D analog used to treat secondary hyperparathyrodism.
Decrease PTH, but increase PO4- –> must treat high PO4- first w/ binders.
Paricalcitol
Vitamin D analog used to treat secondary hyperparathyrodism.
Decrease PTH, but increase PO4- –> must treat high PO4- first w/ binders.
Cinacalcet
Calcimimetic - secondary treatment for hyperparathyroidism.
Used when PO4- is high
Very expensive
Erythropoetin (Procrit)
Short acting EPO used when Hg is below 10 in CKD
Darbepoetin
Long acting EPO used when Hg is below 10 in CKD
Acetazolamide
MOA: Carbonic Anhydrase inhibitor that acts in the proximal tubule. Not used for diuretics clinically for diuresis –> too many side effects.
Uses: glaucoma, urinary alkilinization, metabolic alkalosis, acute altitude sickness
Side effects: hyperchloremic metabolic acidosis, renal stones, renal potassium wasting
Furosemide
Lasix
Class: Loop diuretic
MOA: Inhibits NKCC in thick ascending limb (normally 25% of sodium reabsorption). Normally tubular fluid becomes hypo-osmolar here (no aquaporins), but loop diuretics block this resulting in increased retention of ions and water later in nephron.
Increase NaCl and K excretion.
Major uses: pulmonary edema, edema, hyperkalemia, acute renal failure, anion overdose (bromide, fluoride, iodide)
Active for 6 hours (laSIX)
Bumetanide
Class: Loop diuretic
MOA: Inhibits NKCC in thick ascending limb (normally 25% of sodium reabsorption). Normally tubular fluid becomes hypo-osmolar here (no aquaporins), but loop diuretics block this resulting in increased retention of ions and water later in nephron.
Increase NaCl and K excretion.
Major uses: pulmonary edema, edema, hyperkalemia, acute renal failure, anion overdose (bromide, fluoride, iodide)
Clorthalidone
Class: Thiazide diuretics
MOA: Block NaCl transporter in DCT (normally accounts for 8% of NaCl reabsorption. Block results in increased excretion of Na, Cl, and K (Na/K exchange in collecting tubule)
*thiazides are sulfonylureas –> bind to SUR( sulfonyl urea receptor) on potassium channel controlling inuslin release –> suppress insulin release.
Uses: HTN (decreased rate of stroke, DM, CHF, and CAD complications), HF, nephrolithiasis caused by hypercalcemia, nephrogenic diabetes insipidus.
Side effects: Hyperglycemia, hyperuricemia (gout), hypokalemia, hyperlipidemia, hyponatremia
Hydrochlorothiazide
Class: Thiazide diuretics
MOA: Block NaCl transporter in DCT (normally accounts for 8% of NaCl reabsorption. Block results in increased excretion of Na, Cl, and K (Na/K exchange in collecting tubule)
*thiazides are sulfonylureas –> bind to SUR( sulfonyl urea receptor) on potassium channel controlling inuslin release –> suppress insulin release.
Shown to vasodilate as well due to action on K+ channels –> dual mechanism.
Best evidence of drugs from this class.
Uses: HTN (decreased rate of stroke, DM, CHF, and CAD complications), HF, nephrolithiasis caused by hypercalcemia, nephrogenic diabetes insipidus.
Side effects: Hyperglycemia, hyperuricemia (gout), hypokalemia, hyperlipidemia, hyponatremia
Metalozone
Class: Thiazide diuretics
MOA: Block NaCl transporter in DCT (normally accounts for 8% of NaCl reabsorption. Block results in increased excretion of Na, Cl, and K (Na/K exchange in collecting tubule)
*thiazides are sulfonylureas –> bind to SUR( sulfonyl urea receptor) on potassium channel controlling inuslin release –> suppress insulin release.
Uses: HTN (decreased rate of stroke, DM, CHF, and CAD complications), HF, nephrolithiasis caused by hypercalcemia, nephrogenic diabetes insipidus.
Side effects: Hyperglycemia, hyperuricemia (gout), hypokalemia, hyperlipidemia, hyponatremia
Spironolactone
Class: Potassium Sparing Diuretic/ Aldosterone Antagonit
MOA: Inhibit aldosterone receptor –> blocks exhcange of intraluminal Na for extraluminal K, less potassium secreted.
Major use: hyperaldosteronism, CHF
Side effects: hyperkalemia, gynecomastia, hypercholemic metabolic acidosis, acute renal failure, kidney stones
Eplerone
Class: Potassium Sparing Diuretic/ Aldosterone Antagonit
MOA: Inhibit aldosterone receptor –> blocks exhcange of intraluminal Na for extraluminal K, less potassium secreted.
Prevents fribrotic changes in kidneys and heart caused by aldosterone.
Major use: hyperaldosteronism, CHF
Side effects: hyperkalemia, hypercholemic metabolic acidosis, acute renal failure, kidney stones
