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{{Chronic renal failure}} | {{Chronic renal failure}} | ||
{{CMG}} {{AE}} {{AN}} | {{CMG}};{{AE}}:{{AN}},{{SSW}} | ||
== Overview == | == Overview == |
Revision as of 19:18, 6 August 2018
Chronic renal failure Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: :Aarti Narayan, M.B.B.S [2],Sargun Singh Walia M.B.B.S.[3]
Overview
Effective measures for the primary prevention of chronic renal failure include treatment of reversible exacerbants such as volume depletion, nephrotoxins, urinary tract obstruction and other causes.
Primary Prevention
Effective measures for the primary prevention of chronic renal failure include:
- 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
- Volume Depletion