INTRODUCTION:Renal artery stenosis can lead to renovascular hypertension; however, the detection of stenosis alone does not guarantee the presence of renovascular hypertension. Renovascular hypertension depends on activation of the renin-angiotensin system, which can be detected by functional tests such as captopril renal scintigraphy. A method that allows direct measurement of the baseline and post-captopril glomerular filtration rate using chromium-51 labeled ethylenediamine tetraacetic acid (51Cr-EDTA) could add valuable information to the investigation of hypertensive patients with renal artery stenosis. The purposes of this study were to create a protocol to measure the baseline and post-captopril glomerular filtration rate using 51Cr-EDTA, and to verify whether changes in the glomerular filtration rate permit differentiation between hypertensive patients with and without renal artery stenosis.METHODS:This prospective study included 41 consecutive patients with poorly controlled severe hypertension. All patients had undergone a radiological investigation of renal artery stenosis within the month prior to their inclusion. The patients were divided into two groups: patients with (n=21) and without renal artery stenosis, (n=20). In vitro glomerular filtration rate analysis (51Cr-EDTA) and 99mTc-DMSA scintigraphy were performed before and after captopril administration in all patients.RESULTS:The mean baseline glomerular filtration rate was 48.6±21.8 ml/kg/1.73 m2 in the group wuth renal artery stenosis, which was significantly lower than the GFR of 65.1±28.7 ml/kg/1.73m2 in the group without renal artery stenosis (p=0.04). Captopril induced a significant reduction of the glomerular filtration rate in the group with renal artery stenosis (to 32.6±14.8 ml/ kg/1.73m2, p=0.001) and an insignificant change in the group without RAS (to 62.2±23.6 ml/kg/1.73m2, p=0.68). Scintigraphy with technetium-99m dimercapto-succinic acid (DMSA) did not show significant differences in differential renal function from baseline to post-captopril images in either group.CONCLUSIONS:Captopril induced a decrease in the GFR that could be quantitatively measured with 51Cr-EDTA. The reduction is more pronounced in hypertensive patients with RAS.

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A minha querida família: Otávio, Magali, Edinir, Carol e Tavinho, por sempre acreditarem em mim. A meu marido, amigo e companheiro, Luiz, pela paciência e amor. À minha amiga Marcela, por estar sempre a meu lado. A meu amigo Juliano, por me ouvir sempre. Agradecimentos Ao Dr. Marcelo Tatit Sapienza, meu orientador e amigo, por seus ensinamentos científicos e de vida. Ao Dr. Luiz Bortolotto, por sua disponibilidade e estímulo para realização deste trabalho. Ao Dr. José Nery Praxedes, por sua receptividade e incentivo. Ao Dr. Thiago Macedo, por seu apoio e dedicação aos pacientes. Às Doutoras Carla Ono e Tomoco Watanabe, pelos conselhos. Às amigas Cristina e Miriam, pelo apoio. A Rosana, por tanto me ajudar na marcação dos exames. Aos Físicos: Silvana e Alexandre, pelos ensinamentos, disponibilidade e amizade. A Edslaine, pela colaboração constante na execução desta pesquisa. À equipe de enfermagem do Centro de Medicina Nuclear, especialmente, ao Edyr, pela grande ajuda na concretização deste trabalho. Aos biomédicos: Douglas, Leandro, João, Ana, Sayuri e Ivani, pelo apoio e incentivo durante todos esses anos. E, especialmente, aos pacientes deste estudo, pela confiança, serei eternamente grata. Normatização AdotadaEsta tese está de acordo com as seguintes normas, em vigor no momento da confecção desta tese: Referências: adaptado de International Committee of Medical Journals Editors (Vancouver)