NSAIDS-impair PG-mediated dilation of afferent arterioles

ACEI/ARBS-inhinit angiotensin II-mediated efferent arteriole vasoconstriction

Immunosuppressants (Cyclosporine, Tacrolimus)-cause generalized vasoconstriction within the kidney

-equation will be given on test

*Cr-creatinine; nl product of muscle metabolism, used to estimate CrCl (helps for drug dosing in renal dysfunction pts); in mL/min

-serum creatinine in mg/dL

-weight in kg

-ALWAYS multiply by 0.85 for females, after plugging into formula

-GFR-measures overall kidney function; can be used to dose renal impairment pts

-fractional excretion of Na (FeNa)-dist. b/w prerenal ARF from nephrotoxic intrinsic renal ARF

-FeNa less than 1% = Pre-Renal

-FeNa  greater than 2%= intrinsic ATN

-intravascular volume expansion for hypovolemia, CV support for adequate CO

-Post-Renal-removal/reduction of obstruction

-Use diuretic for fluid overload

-Loop: Furosemide (Lasix) IV loading dose, then continuous infusions

-can use ethacrynic in pt's with sulfa allergies, but high ototoxic potential

-other Loops: Turosemide, Bumetanide

-use diuretics that work on different parts of the nephron so avoid R

-Metazolone (thiazide-like diuretics, produces diuresis at GFR of less than 20 mL/min

-diuretics help prevent hyperkalemia that is often associated with renal dysfunction

-possible tx of ARF; inconclusive

-low dose

-stimulate DA-1 receptors

-renal vasodilation; increase renal blood flow

AE: tachycardia, arrthythmias, myocardial ischemia, decreased respiratory drive, GI ischemia

-DA-1 receptor agonist for ST mgmt of severe HTN

-cause vasodilation of renal vasculature with potentially fewer AE's than Dopamine 

Dialysis (renal replacement therapy)

-refractory hypervolemia, hyperkalemia, or acidosis

-BUN greater than 100

-Intermittent hemodialysis (IHD)-several times weekly

-Continuous renal replacement therapy (CRRT)-provides slow fluid/solute removal on a 24 h baisis; better volume control (better in pts who can't tolerate rapid fluid removal)

-Supportive therapy: adequate nutrition, correction of acid-base abnl, fluid mgmt, dosage adjustments based on current kidney function 

-avoidance of nephrotoxins if possible, such as:

-radiocontrast dye-if it must be used do IV NS for max. renal perfusion; PO acetylcysteine, glycemic control in DM

-Amphotericin B-decreases nephrotoxicity by slowing influsion rate or substituting with liposomal amphotericin B 

GFR is less than 15 mL/min

-req. dialysis or transplant to remove uremic toxins and maintain hemodynamic stability 

-ID at risk pts and initiate interventions to slow progression to ESRD

1: GFR greater than 90 mL/min and albuminuria

2: GFR 60-89 mL/min

3: GFR 30-59 mL/min

4: GFR 15-29 mL/min

5: GFR less than 15 mL/min

-follow low-protein diet;can delay progression to ESRD; avoid malnutrition though; and consider this if GFR is less than 25 mL/min

-intensive BG control in DM pt's-use insulin pump and check BG frequently

-control bp-get to less than 130/80; usually req. at least 3 anti-HTN drugs; ACEI/ARBS decrease proteinuria and slow CKD to ESKD; d/c if SCr is greater than 30% of baseline; use diuretics and CCBs, and/or BB

-get pt to stop smoking

-decrease glomerular pressure and volume due to effects of angiotensin II

-decreased pressure and volume cause a decrease in the amt of protein filtered through the kidney, so decrease in proteinuria

-diuretics req. to control edema and bp

-use Loop diuretics-MOST effective and provide greater decrease in K

-thiazide diuretics aren't as helpful when the CrCL is less then 30 mL/min; but can be added to Loop to enhance Na/water excretion to overcome Loop R (common in kidney dz pts)

-1st line tx is HEMODIALYSIS

-also Ca Gluconate, insulin, glucose, albuterol, Na Polysytrene Sulfonate (Kayexalate)

Metabolic Acidosis assoc with CKD

Tx

-Na Bicarbonate in pts with Stage 3 and greater CKD

-det. by approx. the base deficit (using CO2)

-lipid-lowering therapies help to slow decline of GFR and decrease proteinuria

-Statins can help slow progession of CKD too

-renal activation of vit D is impaired, so decreased Ca absorption which stimulates PTH secretion

-Serum Ca balance is maintained at the expense of bone, could lead to bone dz

-Cinacalcet (Sensipar)-calcimimetic; increased sensitivity of Ca receptors in the parathyroid causes decreased secretion of PTH

-can also give Vit D to directly decrease PTH secretion; most active form available is D3, make sure not to overly suppress PTH levels, though

-in CKD Stage 3, restrict dietary phosphorous to 800-1000 mg/d

-dialysis to control phosphate

-Phosphate binding agents-bind phosphate in GI tract; form insopluble complex that's excreted in the feces; igiven with meals; dosed on phosphorous approx in the meal

-Drugs: Ca Carbonate, Calcium Acetate, Sevelamer (renagel), Others (don't use b/c can cause accumulation of Al or Mg): Aluminum or Mg hydroxide, Al or Mg Carbonate 

-eval for anemia is GFR is less than 60 mL/min

-goal of HgB is greater than 11 g/dL

-if EPO deficient use: Erythropoietin Alpha (Epogen): inject 1-3 times/wk; or Darbepoeitin (Aranesp) injection ever 1-2 wk

-AE: HTN, trombosis

-monitor HgB

-Fe supplementation parenterally-can decrease dosage of EPO

-AE: allergic rxn, HoTN, dizzy/syncope, dyspnea, HA, arthralgias/low back pain, staining of the skin (from Z-track injection)

-newer formulations (safer)-Iron Sucrose (Venofer), Na ferric gluconate (Ferrlecit)

-monitor for Fe and AEs