4 As an option, selective

inhibitors of Cox (Cox-2 inhibitors more than Cox-1, such as celecoxib) have been employed, seeking a renal effect, with reduction of undesirable GI effects.11 The majority of studies have observed that sNSAIDs are associated with a lower risk of ulcers and complications than nsNSAIDs.12 In the present study, celecoxib promoted a better compliance Selleckchem PD332991 to the treatment and a reduction in severe GI involvement (such as gastric ulcers), with metabolic and electrolyte stability and improvement in growth speed and weight gain.4 In addition, celecoxib was associated with a lower rate of hyperfiltration than indomethacin. Hyperfiltration is associated to focal glomerulosclerosis occurrence. Thus, the use of celecoxib can be a good option for BS patients, although larger studies are needed in order to prove its safety and efficacy. In the last decade, an increase in cardiovascular events has been observed during the use of COX-2 selective inhibitors. Those studies were made in patients with high cardiovascular risk, such as the elderly or those in use of acetylsalicylic acid. There are few long-term trials evaluating cardiovascular safety of celecoxib, but no conclusion can be drawn.13 and 14 The balance between the production of prostacyclin and thromboxane is thought to play a role in regulation of platelet aggregation LY294002 solubility dmso and in vascular

tone. BS is associated with overproduction of prostaglandins and thromboxane.15 It can thus be speculated that the side-effect on cardiovascular system is not a risk factor in BS patients. However, no such well-defined clinical trials have been conducted. Long-term follow-up of patients under the use of sNSAID has demonstrated that alongside its beneficial effect, patients for can develop proteinuria, which is an aggravating to the progression to end-stage renal disease.2 In this situatio,n

an RAAS inhibitor can be used as a replacement drug to NSAID. Few reports have been published on the use of these drugs.16 Seyberth & Schlingmann2 stated that “only in the case of persistent hypokalemia (plasma potassium <3.0 mEq/L) that occurs despite adequate and tolerated inhibition of prostaglandin synthesis and salt and potassium supplementation, one might consider the use of drugs that interfere with the RAAS”. However, close monitoring of renal function and blood pressure is mandatory. This supplemental therapy might have an additional beneficial effect on proteinuria.17 In the present study, in patients who developed proteinuria during treatment with celecoxib, the replacement by enalapril provided electrolyte and metabolic balance with significant reduction of proteinuria. In addition, good tolerance and compliance were observed with this treatment. It is noteworthy that the administration of an inhibitor of RAAS in these patients can determine severe hypotension.