Prediction of Acute Glomerular Filtration Rate Reductions Following Renin-angiotensin System Blockade in Chronic Kidney Disease: A Possible Application of Ultrasonography in Clinical Practice.
Intern Med
; 58(9): 1233-1241, 2019 May 01.
Article
em En
| MEDLINE
| ID: mdl-30626816
ABSTRACT
Objective Renal arteriolosclerosis is a risk factor for acute reductions in the glomerular filtration rate (GFR) when renin-angiotensin system (RAS) inhibitors are administered. Renal arteriolosclerosis can be detected by an increase in the resistive index (RI) on Doppler ultrasonography. The purpose of the present study is to determine whether or not the RI can predict acute GFR reductions following RAS blockade in chronic kidney disease (CKD). Methods We surveyed all CKD patients who were hospitalized in Otemae Hospital from January 2008 to December 2017. One hundred and eight patients who had been newly treated with RAS inhibitors were able to be followed for 14 weeks. The end point was an acute reduction in the GFR, defined as a decrease of ≥30%. Results Twenty-three of the 108 patients presented with acute GFR reductions. The cumulative probability of acute GFR reductions was 3.3% and 53% in patients with RI ≤0.70 and RI >0.70, respectively (p<0.001). A univariate Cox proportional-hazards analysis showed that the RI, age, GFR, systolic blood pressure, urinary protein excretion, diabetic kidney disease, coronary artery disease, and use of diuretics were significant variables. Multivariate hazard ratios were calculated from the RI and three established variables (age, GFR, diuretics), and the RI and use of diuretics were shown to be significant risk factors for acute GFR reductions. Conclusion These results suggest that an increase in the RI, as well as the use of diuretics, may be risk factors for acute GFR reductions following RAS blockade.
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Assunto principal:
Arteriosclerose
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Artéria Renal
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Sistema Renina-Angiotensina
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Bloqueadores do Receptor Tipo 1 de Angiotensina II
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Insuficiência Renal Crônica
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article