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Ovlivňuje 24hodinová exkrece kyseliny močové vznik močových konkrementů?
[Development of proteinuria after switch to sirolimus-based immunosuppression in long-term cardiac transplant patients]
Aliabadi AZ, Pohanka E, Seebacher G, Dunkler D, Kammerstätter D, Wolner E, Grimm M, Zuckermann AO.
Jazyk čeština Země Česko
- MeSH
- analýza přežití MeSH
- antihypertenziva terapeutické užití MeSH
- hormony kůry nadledvin terapeutické užití MeSH
- imunosupresiva škodlivé účinky terapeutické užití MeSH
- klinické zkoušky jako téma MeSH
- kombinovaná farmakoterapie MeSH
- kyselina mykofenolová analogy a deriváty terapeutické užití MeSH
- lidé MeSH
- monitorování životního prostředí MeSH
- prospektivní studie MeSH
- proteinurie chemicky indukované MeSH
- sirolimus farmakokinetika škodlivé účinky terapeutické užití MeSH
- statiny terapeutické užití MeSH
- transplantace srdce imunologie mortalita MeSH
- výběr pacientů MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
Calcineurin-inhibitor therapy can lead to renal dysfunction in heart transplantation patients. The novel immunosuppressive (IS) drug sirolmus (Srl) lacks nephrotoxic effects; however, proteinuria associated with Srl has been reported following renal transplantation. In cardiac transplantation, the incidence of proteinuria associated with Srl is unknown. In this study, long-term cardiac transplant patients were switched from cyclosporine to Srl-based IS. Concomitant IS consisted of mycophenolate mofetil +/- steroids. Proteinuria increased significantly from a median of 0.13 g/day (range 0-5.7) preswitch to 0.23 g/day (0-9.88) at 24 months postswitch (p = 0.0024). Before the switch, 11.5% of patients had high-grade proteinuria (>1.0 g/day); this increased to 22.9% postswitch (p = 0.006). ACE inhibitor and angiotensin-releasing blocker (ARB) therapy reduced proteinuria development. Patients without proteinuria had increased renal function (median 42.5 vs. 64.1, p = 0.25), whereas patients who developed high-grade proteinuria showed decreased renal function at the end of follow-up (median 39.6 vs. 29.2, p = 0.125). Thus, proteinuria may develop in cardiac transplant patients after switch to Srl, which may have an adverse effect on renal function in these patients. Srl should be used with ACEi/ARB therapy and patients monitored for proteinuria and increased renal dysfunction.
Development of proteinuria after switch to sirolimus-based immunosuppression in long-term cardiac transplant patients
Komentář [k článku Ovlivňuje 24hodinová exkrece kyseliny močové vznik močových konkrementů?].
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- $a Development of proteinuria after switch to sirolimus-based immunosuppression in long-term cardiac transplant patients
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- $a Calcineurin-inhibitor therapy can lead to renal dysfunction in heart transplantation patients. The novel immunosuppressive (IS) drug sirolmus (Srl) lacks nephrotoxic effects; however, proteinuria associated with Srl has been reported following renal transplantation. In cardiac transplantation, the incidence of proteinuria associated with Srl is unknown. In this study, long-term cardiac transplant patients were switched from cyclosporine to Srl-based IS. Concomitant IS consisted of mycophenolate mofetil +/- steroids. Proteinuria increased significantly from a median of 0.13 g/day (range 0-5.7) preswitch to 0.23 g/day (0-9.88) at 24 months postswitch (p = 0.0024). Before the switch, 11.5% of patients had high-grade proteinuria (>1.0 g/day); this increased to 22.9% postswitch (p = 0.006). ACE inhibitor and angiotensin-releasing blocker (ARB) therapy reduced proteinuria development. Patients without proteinuria had increased renal function (median 42.5 vs. 64.1, p = 0.25), whereas patients who developed high-grade proteinuria showed decreased renal function at the end of follow-up (median 39.6 vs. 29.2, p = 0.125). Thus, proteinuria may develop in cardiac transplant patients after switch to Srl, which may have an adverse effect on renal function in these patients. Srl should be used with ACEi/ARB therapy and patients monitored for proteinuria and increased renal dysfunction.
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