NDT Advance Access originally published online on March 22, 2006
Nephrology Dialysis Transplantation 2006 21(7):1833-1837; doi:10.1093/ndt/gfl096
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Original Articles: Clinical Nephrology
Increased systolic blood pressure with rofecoxib in congenital furosemide-like salt loss
Department of Pediatrics, Philipps University Marburg, D-35033 Marburg, Germany and 1 Setchenov Moscow Medical Academy, 11988 Moscow, Russian Federation
Correspondence and offprint requests to: Martin Kömhoff, MD, Department of Pediatrics, Philipps-University, Deutschhausstr. 12, D-35033 Marburg, Germany. Email: koemhoff{at}med.uni-marburg.de
Background. To analyse whether congenital furosemide- or thiazide-like renal salt loss protects against the potential prohypertensive effects of two cyclooxygenase (COX) inhibitors: rofecoxib, a COX-2 selective inhibitor, and indomethacin, an unselective COX-inhibitor.
Methods. In a retrospective analysis, the effects of rofecoxib and indomethacin on blood pressure (bp: transformed into age-independent standard deviation scores (SDS) values), creatinine clearance (CRC), fractional excretion of sodium (FeNa), and renal excretion of systemic prostaglandins were studied in 28 patients with a genetically proven congenital hypokalaemic salt-losing tubulopathy (SLT) (11 female and 17 male, age: 2–25 years), 19 with a furosemide-like SLT, and nine with a thiazide-like SLT.
Results. In furosemide-like SLT patients, systolic SDS bp values were significantly higher with rofecoxib (1.03±0.16 SDS, n = 107) compared with indomethacin (0.56±0.09 SDS, n = 282; P = 0.007, 95% CI: 0.12–0.8). Without the drugs, systolic SDS bp values were elevated by 0.63±0.11 SDS, n = 164. Both drugs reduced renin and aldosterone-plasma levels to a similar extent. SDS values were significantly correlated with the excretion of the vasoconstrictor thromboxane (T x B2) (R2: 0.038, P = 0.021, n: 159), but not with CRC or FeNa. Blood pressure was not increased in thiazide-like SLT patients treated with rofecoxib.
Conclusion. Congenital furosemide-like renal salt loss does not protect against the prohypertensive effects of rofecoxib. The positive correlation between bp SDS values with T x B2 but not with FeNa or CRC point towards an altered vascular homeostasis as one mechanism increasing blood pressure.
Keywords: Bartter syndrome; coxib; hypertension; NSAID; thromboxane
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