Chronic renal failure primary prevention
|
Chronic renal failure Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Chronic renal failure primary prevention On the Web |
|
American Roentgen Ray Society Images of Chronic renal failure primary prevention |
|
Risk calculators and risk factors for Chronic renal failure primary prevention |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Treatment of Reversible Exacerbants
- Volume Depletion
- May be subtle
- Autoregulation impaired with DM, hypertension, CRI--decreases GFR with mild volume depletion
- Careful trial of volume repletion may--return of baseline renal function
- (Increase dietary Na, reduce diuretic dosing)
- Nephrotoxins
- NSAIDS
- Most toxic in setting of volume depletion, CHF, diuretic use
- Reduce prostaglandin (PG) synthesis--unopposed vasoconstriction with decreased GFR
- Can also cause ATN (acute tubular necrosis)
- Aminoglycosides
- Nonoliguric ARF typically occurs at 7-10 days
- Increased risk with older patients, prolonged therapy and greater total dose
- IV contrast
- ARF usually occurs within 24-48 hours of dye administration
- Peak Cr after 5-7 days with return to baseline at 10-14 days
- Risk ARF increased with DM and higher volume of dye
- Note: certain meds increase serum Cr (via inhibiting Cr secretion or interfering with assay) without changing GFR, e.g. cimetidine, trimethoprim (TMP), cefoxitin, flucytosine; BUN will not rise because GFR is preserved
- NSAIDS
- Urinary Tract Obstruction
- Most commonly due to prostatic hypertrophy in men
- Other causes:
- Nephrolithiasis
- Tumor
- Neurogenic bladder
- Results in reduced GFR and impaired tubular function
- Consider ultrasound, urologic evaluation