Effect of Trimethoprim-Sulfamethoxazole on the Renal Excretion of Creatinine in Man

Berglund, Fredrik; Killander, Johan; Pompeius, R

doi:10.1016/s0022-5347(17)67149-0

Cited by 206 publications

(85 citation statements)

References 12 publications

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“…In 1975, Berglund et al [29] found that therapy with 160 mg trimethoprim and 800 mg sulphamethoxazole b.i.d. in 21 patients reversibly increased plasma creatinine by an average of 2 mg L 21 (18 mmol L 21 ) without influencing GFR, measured by the clearance of I-iothalamate.…”

Section: Trimethoprimmentioning

confidence: 99%

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Andreev

Koopman

Arisz

1999

Journal of Internal Medicine

163

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Abstract. Andreev E, Koopman M, Arisz L (Medical University-Sofia, Sofia, Bulgaria and University of Amsterdam, Amsterdam, The Netherlands). A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible? (Review.) J Intern Med 1999; 246: 247±252. This is a review of the available information about drugs which cause an increase in plasma creatinine concentration without decreasing glomerular filtration rate (GFR). The GFR is the main, but not the single, determinant of the plasma creatinine levels. Several drugs, such as cimetidine, trimethoprim, corticosteroids, pyrimethamine, phenacemide, salicylates and active vitamin D metabolites, have been reported to increase plasma creatinine without influencing its glomerular filtration. Cimetidine, trimethoprim, pyrimethamine and salicylates can inhibit secretion of creatinine by the proximal tubule. Corticosteroids and vitamin D metabolites probably modify the production rate and the release of creatinine. The exact mechanism of phenacemide±creatinine interaction is not fully explained. These drug-induced alterations in plasma creatinine concentration have clinical significance when GFR is estimated by using plasma creatinine.

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Section: Trimethoprimmentioning

confidence: 99%

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Andreev

Koopman

Arisz

1999

Journal of Internal Medicine

163

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“…In kidney transplant patients, many other factors may affect creatinine metabolism. For example, corticosteroids may alter the muscle massto-total body weight ratio (3), and the use of drugs, such as trimethoprim, may affect creatinine secretion in the proximal tubule (3,4).…”

Section: Introductionmentioning

confidence: 99%

Accuracy of Different Equations in Estimating GFR in Pediatric Kidney Transplant Recipients

Souza¹,

Cochat²,

Rabilloud³

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objective The knowledge of renal function is crucial for the management of pediatric kidney transplant recipients. In this population, the most commonly used plasma creatinine (PCr)-based or cystatin C (CystC)-based GFR-predicting formulas may underperform (e.g., corticosteroids and trimethoprim may affect PCr concentration, whereas prednisone and calcineurin inhibitors may affect CystC concentration). This study evaluated the performance of six formulas in pediatric kidney transplant recipients.Design, setting, participants, & measurements The study used PCr-based formulas (bedside Schwartz, SchwartzLyon), CystC-based formulas (Hoek, Filler), and combined PCr-CystC-based formulas (CKD in Children [CKiD] 2012 and Zappitelli). The performance of these formulas was compared using inulin clearance as reference and assessed according to CKD stages in a historical cohort that included 73 pediatric kidney transplant recipients (199 measurements). The ability of the formulas to identify GFRs,60, ,75, and ,90 ml/min per 1.73 m 2 was assessed.Results At measured GFR (mGFR) $90 ml/min per 1.73 m 2 (nine patients; 23 measurements), the Zappitelli formula had the highest 30% accuracy (P30) (95% [95% confidence interval (95% CI), 87% to 100%]) and the bedside Schwartz had the highest 10% accuracy (P10) (56% [95% CI, 32% to 72%]). At mGFR$60 and ,90 ml/min per 1.73 m 2 (22 patients; 91 measurements), all formulas had P30 values .80%. However, only the CKiD 2012 formula had a P10 value .50%. At mGFR,60 ml/min per 1.73 m 2 (42 patients; 85 measurements), the CKiD 2012 and Schwartz-Lyon formulas had the highest P10 (45% [95% CI, 34% to 55%] and 43% [95% CI, 33% to 54%]) and P30 (90% [95% CI, 84% to 97%] and 91% [95% CI, 86% to 98%]). All studied equations except Hoek and Filler had areas under the receiver-operating characteristic curves significantly .90% in discriminating patients with renal dysfunction at various CKD stages (GFR,60, ,75, and ,90 ml/min per 1.73 m 2 ).Conclusions In pediatric kidney transplant recipients, the CKiD 2012 formula had the best performance at mGFRs,90 ml/min per 1.73 m 2 . CystC-based formulas were not superior to PCr-based formulas.

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“…All equations will misinterpret a patient with ketoacidosis 41 or IgM myeloma 42 as su¡ering a loss in GFR and another with hyperbilirubinaemia 43 as demonstrating an improvement in function where there is in reality no such loss or improvement, but rather re£ects an analytical error in the measurement of serum creatinine. Administration of medications such as trimethoprim, 44 cimetidine 45 or feno¢brate 46 will similarly be interpreted by those equations as a loss in GFR rather than the changes in tubular secretion or creatinine production that they really are. Furthermore, published clinical studies of dopamine or dobutamine in heart failure have used creatininebased equations to demonstrate a bene¢cial e¡ect on renal function with a gain in GFR when it is really only interference with the Ja¡e reaction.…”

mentioning

confidence: 99%

Creatinine and glomerular filtration rate: evolution of an accommodation

Diskin

2007

Ann Clin Biochem

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This brief review examines the history of the use of creatinine as a measure of renal function. While there are more accurate markers of glomerular filtration, creatinine was chosen for convenience. Since the relationship of creatinine to glomerular filtration depends upon a tenuous balance of counterbalancing factors, practitioners should be alert to situations that alter that balance. While the averaging of variations over time helps to avoid some of the problems with diurnal variations in the past, the present-day reliance upon equations based upon a solitary serum value is likely to amplify those problems in clinical situations when the effect of disease, medications, diet and time of day upon that balance are not considered.

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Effect of Trimethoprim-Sulfamethoxazole on the Renal Excretion of Creatinine in Man

Cited by 206 publications

References 12 publications

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Accuracy of Different Equations in Estimating GFR in Pediatric Kidney Transplant Recipients

Creatinine and glomerular filtration rate: evolution of an accommodation

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