NDT Advance Access published online on March 22, 2006
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfl096
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1 Department of Pediatrics, Philipps University Marburg, D-35033 Marburg, Germany
* To whom correspondence should be addressed. 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.
Received July 28, 2005
Accepted February 17, 2006
Original Article
Increased systolic blood pressure with rofecoxib in congenital furosemide-like salt loss
Martin Kömhoff 1 *,
Günter Klaus 1,
Sofia Nazarowa 2,
Stephan C. Reinalter 1,
and
Hannsjörg W. Seyberth 1
2 Setchenov Moscow Medical Academy, 11988 Moscow, Russian Federation
Martin Kömhoff, E-mail: koemhoff{at}med.uni-marburg.de
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