-
patient related risk factors
>60, intravasc vol dep, dec EABV, GFR <60 ml/min
-
co-morbidities causing risk factors
DM, HF, sepsis
-
ACE and ARB increasing SCr is ok until
increase by >30% beyond baseline
-
tubular cell toxicity
impairment of mitochondrial fxn, interference w tubular transport, increased oxidative stress, free radical formation, most common is acute tubular necrosis
-
inflammation-pathogenic mechanism of drug-induced nephrotoxicity
glomerulonephritis, acute interstitial nephritis, chronic interstitial nephritis
-
crystal nephropathy
crystal production precipitates and obstructs causing interstitial rxn
-
rhabdomyolysis
myoglobin causes direct toxicity, tubular obstruction, alterations in GFR, statins and illegal drugs of abuse
-
NSAIDs, ACE, ARBs cause nephrotoxicity by:
altering intra-glomuler hemodynamics
-
pts at risk, NSAIDs, ACEs and ARBs causing nephrotoxicity
DRUGS ALTERING INTRA-GLOMERULAR HEMODYNAMICS-underlying renal insufficiency, intravascular vol depl, elderly, concomittant use of NSAIDs, ACE, ARBs, cyclosporine, and/or tacrolimus
-
prevention for DIN w NSAIDs, ACE and ARBs
DRUGS ALTERING INTRA-GLOMERULAR HEMODYNAMICSuse analgesics with less PG effect, correct vol depl prior, esp if chronic dep, monitor renal fxn and vital signs following init or dose inc esp if w pts at risk, e.g. SCr q 2 weeks
-
pts at risk for DIN w cyclosporine, tacrolimus
DRUGS ALTERING INTRA-GLOMERULAR HEMODYNAMICSunderlying renal insuff, intravasc vol dep, elderly, concomitt NSAIDs, ACE, ARB cyclosporine, and tacrolimus AND excessive dose, concomitant with other nephro drugs or drugs that inhibit cyclosporin or tacrolimus metabolism
-
prev for DIN with cyclosporine, tacrolimus
DRUGS ALTERING INTRA-GLOMERULAR HEMODYNAMICSmonitor serum drug concentrations and renal fxn, use lowest effective dose, calc channel blockers to dilate afferent arteriole
-
pts at risk for DIN w AGs
DRUGS ASSOCIATED WITH TUBULAR CELL TOXICITY-5-15% of pts, underlying renal insuffic, dur >10d, trough conc >2mcg/ml, concom liver disease, hypoalbuminemia
-
-
DRUGS ASSOCIATED WITH TUBULAR CELL TOXICITY--use extended interval
- - admin during active period of day
- -Limit duration of therapy
- -Monitor serum drug levels and renal function 2-3
- times a week
- -Maintain trough levels < 1 mcg/ml
-
pts at risk for DIN w Amp B
-
DRUGS ASSOCIATED WITH TUBULAR CELL TOXICITY-underlying renal insuff, rapid inf, lg daily doses >3gm,
deoxycholate>lipid formulations, prolonged duration
-
prevention for DIN for Amp B
-
DRUGS ASSOCIATED WITH TUBULAR CELL TOXICITY-saline hydration before and after dose admin, consider administering as a continuous inf over 24 hours, use liposomal formulation, limit duration of therapy and cumulative dose
-
pts at risk for DIN for contrast dye
-
DRUGS ASSOCIATED WITH TUBULAR CELL TOXICITY-underlying renal insuff, age >70, diabetics, heart failure, vol depl, repeated exposures
-
prevent for DIN in contrast dye
-
DRUGS ASSOCIATED WITH TUBULAR CELL TOXICITY-use low osmolar contrast in the lowest possible dose and avoid multiple procedures in 24-48 hrs, 0.9% saline or sod bicarb (154mEq/L) inf pre and post procedure, withold NSAIDs and diuretics at least 24 hours pre and post procedrure(preventative), monitor renal fxn 24-48 hrs post procedure, consider N-acetylcystein peri-proc
-
Pts at risk for DIN-APAP, ASA, NSAIDs
CAUSING CHRONIC INTERSTITIAL NEPHROPATHY-HISTORY OF CHRONIC PAIN, OLDER AGE WOMEN, CUMULATIVE CONSUMPTION OF ANALG >1GM/DAY FOR >2 YRS
-
prevention for DIN caused by APAP, ASA and NSAIDs, causing chronic insterstitial nephropathy
avoid long term use, particularly more than 1 analgesic simulataneously, use alt agents in pts with chronic pain
-
pts at risk for DIN caused by lithium
causing chronic interstitial nephropathy, elevated drug levels
-
prevention for DIN caused by lithium
causing chronic interstitial nephropathy, maintain drug levels within the therapeutic range, avoid vol depletion
-
pts at risk for DIN caused by acyclovir, sulfa abx, mtx, triamterene, cipro
causing crystal nephropathy, vol depl, underlying renal insufficiency, excessive dose, IV route
-
prevention of DIN caused by acyclovir, sulfa abx, mtx, triamterene, cipro
causing chronic interstitial nephropathy, d/c or reduce dose, ensure hydration, establish high urine flow, use the oral route
-
Aristolochia fangchi
interstitial renal fibrosis, urothelial carcinoma
-
Djenkol bean (pithecellobium labatum)
tubular and glomerular cell necrosis
-
Impila (Callilepis laureola)
necrosis of proximal tubule and loop of Henle
-
Wild mushrooms
tubular interstitial nephritis and fibrosis
-
Cat's clow (uncaria tomentosa)
Acute renal failure
-
Licorice (Glycyrrhiza glabra)
hypernatremia, hypokalemia
-
Senna, cascara sagrada, rhubarb
hypokalemia
-
-
Juniper berry, parsley, dandelion, horsetail, asparagus root, lovage root, goldenrod, Uva ursi, stinging nettle leaf; alfalfa
increase diuresis of water without electrolytes
-
some asian, chinese, and ayurvedic herbal products may contain heavy metals and unlisted drugs(NSAIDs)
nephrotoxicity
-
Echinacea
increased probablity of transplant rejection
-
St. John's Wort
increased probability of transplant rejection
|
|
