Nephrotoxicity creatinine changes

Creatinine, an endogenous end product of muscle metabolism, is often measured in plasma and urine to determine creatinine clearance. Since, creatinine is freely filtered at the glomerulus and is not reabsorbed or secreted by the proximal tubule of most species, creatinine clearance provides a good measure of the GFR. Another endogenous compound, urea, is also cleared mainly by renal filtration and excretion. Increases in the blood or serum concentration of urea are indicative of decreased GFR. However, increases in BUN concentration occur only after substantial renal damage has been established. Thus, BUN concentration is not a sensitive indicator of nephrotoxicity and changes usually occur later than changes in other parameters (e.g., enzymuria). 

INEFFECTIVE TISSUE PERFUSION RENAL The patient taking an aminoglycoside is at risk for nephrotoxicity. The nurse measures and records the intake and output and notifies the primary health care provider if the output is less than 750 ml/day. It is important to keep a record of the fluid intake and output as well as a daily weight to assess hydration and renal function. The nurse encourages fluid intake to 2000 ml/day (if the patient s condition permits). Any changes in the intake and output ratio or in the appearance of the urine may indicate nephrotoxicity. The nurse reports these types of changes to the primary health care provider promptly. The primary health care provider may order daily laboratory tests (ie, serum creatinine and blood urea nitrogen [BUN]) to monitor renal function. The nurse reports any elevation in the creatinine or BUN level to tiie primary health care provider because an elevation may indicate renal dysfunction. 

Monitoring Closely monitor patients coinfected with HBV and HIV who discontinue tenofovir with both clinical and laboratory follow-up for at least several months. Monitor patients at risk for, or with a history of, renal dysfunction and patients receiving concomitant nephrotoxic agents for changes in serum creatinine and phosphorus. Consider bone monitoring for HIV infected patients who have a history of pathologic bone fracture or are at substantial risk for osteopenia. 

Nephrotoxicity (characterized by increased serum creatinine level and decreased urine output), neurotoxicity (including tremor, headache, and mental status changes), and pleural effusion are common adverse reactions. 

Male and female Swiss-Webster mice were exposed to 60 ppm [240 mg/m ] vinylidene chloride for 4 h (Speerschneider Dekant, 1995). Urine was collected over a 48-h period and animals were then killed. Male mice were more sensitive to vinylidene chloride-induced nephrotoxicity, as assessed by changes in urinary volume, creatinine, glucose and y-glutamyltranspeptidase levels. Increased necrosis was observed in exposed male mice and female mice pretreated with testosterone. Female mice had no observable kidney lesions or alteration in urinary parameters, suggesting the role of CYP2E1 in vinylidene chloride-induced nephrotoxicity. 

The safety and efficacy of ABCD have been stndied in 220 bone marrow transplant recipients enrolled in the same five phase I or phase II stndies (23). The median dose in this population was 4 (range 0.4—8.0) mg/kg, and the median duration of treatment was 16 (range 1-409) days. Overall, 37 (19%) of the patients had nephrotoxicity, defined as a doubling of serum creatinine from baseline, an increase of 88 pmol/l from baseline, or at least a 50% fall in calculated creatinine clearance. There were no significant changes in hepatic transaminases, alkaline phosphatase, or total bilirubin. Fever and chills were reported by 12 and 11% of patients respectively. Other acute, severe, infusion-related adverse events were hypoxia (4.1%), hypertension (2.7%), and hypotension (2.7%). 

There are numerous methods to determine the nephrotoxic potential of a chemical or to study the mechanism(s) by which a chemical induces nephrotoxicity. In humans, the concern is most often related to either drug-induced or occupationally associated nephrotoxicity. Evaluation of nephrotoxicity in humans is limited primarily to the measurement of urinary changes (e.g., volume, enzymes, protein, etc.), BUN or serum creatinine concentrations, creatinine clearance, or renal biopsy. The measurement of an increase in urinary N-acetyl-jS-D-glucosaminidase (NAG) or alanine aminopeptidase (AAP) levels,... 

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