1.Scintigraphic evaluation of renovascular hypertension.
Hee Myung PARK ; Heun Young YUNE
Yonsei Medical Journal 1993;34(4):301-310
ACE inhibitor challenged renal scintigraphic studies offer noninvasive means of evaluating patients for renovascular hypertension, and provide help in selecting patients who will benefit most from interventional procedures designed for alleviation of renal artery stenosis. These studies provide functional assessment of each kidney which also helps the vascular surgeons to plan which renal artery to repair first, when bilateral renal arteries are stenotic, prior to an abdominal aortic aneurysm repair. Vasotec challenged Tc99mMAG3 renal scintigraphy is one of such tests with several advantages over other similar methods, and appears to have a great potential of being a preferred scintigraphic study for evaluation of renovascular hypertension.
Angiotensin-Converting Enzyme Inhibitors/diagnostic use
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Diagnosis, Differential
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Human
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Hypertension, Renovascular/physiopathology/*radionuclide imaging
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Radioisotope Renography
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Renal Artery Obstruction/radionuclide imaging
2.An experimental study on renal microvascular perfusion in dogs with acute cardiac insufficiency.
Jin-guo XIE ; Yi-li LIU ; Dao-gang ZHA ; Jian-ping BIN ; Jian LIU ; Ping-sheng WU
Chinese Journal of Cardiology 2005;33(7):643-647
OBJECTIVETo investigate the changes and the effects of captopril on the renal blood flow and microvascular perfusion in dogs with acute cardiac insufficiency.
METHODSAcute cardial insufficiency was induced by combining occlusion of the left anterior descending artery with right ventricular pacing in 12 mongrel dogs. The ascending aorta and left kidney were dissected and ultrasonic flow probes were placed on ascending aorta and renal artery to monitor cardiac output (CO) and renal blood flow (RBF). Contrast-enhanced ultrasound of the kidney was performed as CO was reduced to 25% (LCO25%) and 50% (LCO50%) from the basic measurement and microvascular flow velocity (beta), microvascular volume (A) and microvascular blood flow (renal cortex) were observed. After CO reduced to 50%, captopril 1 mg/kg and 2 mg/kg were injected successively and contrast-enhanced ultrasound of the kidney were performed again before and after injection.
RESULTSAt baseline, CO, RBF, CXbeta (beta of renal cortex), A and A x beta were (1.46 +/- 0.16) ml/min, (107.5 +/- 35.7) ml/min, 1.39 +/- 0.14, 120.3 +/- 14.8 and 167.4 +/- 25.0, respectively. After the LCO25% was reached, RAF, CXbeta, A and A x beta decreased to (72.50 +/- 32.4) ml/min, 0.87 +/- 0.082, 117.6 +/- 13.1, and 102.6 +/- 15.5, respectively. The corresponding values after the LCO50% was reached were (44.1 +/- 17.2) ml/min, 0.61 +/- 0.039, 106.9 +/- 12.0, and 64.7 +/- 8.83, respectively. It is suggested that the volume of the renal microvasculature remained stable until the LCO50% was reached. When captopril 1 mg/kg and 2 mg/kg were injected successively at LCO50%, MAP decreased from (85.4 +/- 7.8) mm Hg to (78.7 +/- 7.3) mm Hg and to (69.1 +/- 6.3) mm Hg (P < 0.05), respectively, while CO increased from 0.73 +/- 0.084 to 0.83 +/- 0.065 and to 0.9 +/- 0.054 (P < 0.05), respectively. RBF increased from (44.1 +/- 17.2) ml/min to 60.3 +/- 17.8 and to 79.4 +/- 17.8 (P < 0.05), respectively. After captopril 1 mg/kg and 2 mg/kg were injected, the increased flow ratios with CO were 0.15 +/- 0.084 and 0.31 +/- 0.011, respectively, and with RBF were 0.29 +/- 089 and 0.522 +/- 0.040, respectively. The increased renal blood flow ratio was higher than that of CO after captopril was used. The corresponding increases were from 0.61 +/- 0.039 to 0.75 +/- 0.020 and to 0.86 +/- 0.027 for CX beta, from 106.9 +/- 11.9 to 115.4 +/- 11.1 and to 116.6 +/- 8.9 for A, from 64.7 +/- 8.83 to 87.0 +/- 8.6 and to 100.6 +/- 8.9 for A x beta, respectively.
CONCLUSIONThe renal microvasculature plays a role by keeping its volume stable in the protection against renal ischemia when acute cardiac output decreases slightly. The role of captopril to improve renal microvascular perfusion is independent of increased total cardiac output or increased systemic blood pressure.
Angiotensin-Converting Enzyme Inhibitors ; pharmacology ; therapeutic use ; Animals ; Captopril ; pharmacology ; therapeutic use ; Cardiac Output, Low ; complications ; drug therapy ; physiopathology ; Dogs ; Female ; Kidney ; blood supply ; diagnostic imaging ; Male ; Perfusion ; Renal Circulation ; drug effects ; Ultrasonography
3.Effect of renin-angiotensin-system blockers on contrast-medium-induced acute kidney injury after coronary angiography.
Ja Jun GOO ; Jae Joon KIM ; Ji Hoon KANG ; Kyoung Nyoun KIM ; Ki Sup BYUN ; Mi kyung KIM ; Tae Ik KIM
The Korean Journal of Internal Medicine 2014;29(2):203-209
BACKGROUND/AIMS: With the increasing incidence of cardiovascular disease, angiocardiography using contrast-enhancing media has become an essential diagnostic and therapeutic tool, despite the risk of contrast-medium-induced acute kidney injury (CIAKI). CIAKI may be exacerbated by renin-angiotensin-system (RAS) blockers, which are also used in a variety of cardiovascular disorders. This study evaluated the effects of RAS blockade on CIAKI after coronary angiography. METHODS: Patients who underwent coronary angiography in our hospital between May 2009 and July 2011 were reviewed. Serum creatinine levels before and after coronary angiography were recorded. CIAKI was diagnosed according to an increase in serum creatinine > 0.5 mg/dL or 25% above baseline. RESULTS: A total of 1,472 subjects were included in this study. Patients taking RAS blockers were older, had a higher baseline creatinine level, lower estimated glomerular filtration rate (eGFR), and had received a greater volume of contrast medium. After propensity score matching, no difference was observed between the RAS (+) and RAS (.) groups. Multiple logistic regression identified RAS blockade, age, severe heart failure, contrast volume used, hemoglobin level, and eGFR as predictors of CIAKI. Multiple logistic regression after propensity matching showed that RAS blockade was associated with CIAKI (odds ratio, 1.552; p = 0.026). CONCLUSIONS: This study showed that the incidence of CIAKI was increased in patients treated with RAS blockers.
Acute Kidney Injury/*chemically induced/diagnosis/epidemiology/physiopathology
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Aged
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Angiotensin II Type 1 Receptor Blockers/*adverse effects
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Angiotensin-Converting Enzyme Inhibitors/*adverse effects
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Biological Markers/blood
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Chi-Square Distribution
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Contrast Media/*adverse effects/diagnostic use
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Coronary Angiography/*adverse effects
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Creatinine/blood
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Female
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Glomerular Filtration Rate/drug effects
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Humans
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Incidence
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Kidney/*drug effects/physiopathology
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Logistic Models
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Male
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Middle Aged
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Multivariate Analysis
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Odds Ratio
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Propensity Score
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Renin-Angiotensin System/*drug effects
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Republic of Korea/epidemiology
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Retrospective Studies
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Risk Assessment
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Risk Factors