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临床试验/NCT04225013
NCT04225013已完成不适用

Early Diagnosis as a Strategy in Reducing the Incidence of Acute Renal Failure and Mortality Associated With Contrast Media Administration in Cardiovascular Procedures

R. Laura Vicente Vicente1 个研究点 分布在 1 个国家目标入组 150 人开始时间: 2015年6月1日最近更新:
适应症

试验速览

阶段
不适用
状态
已完成
发起方
入组人数
150
试验地点
1
主要终点
Urinary N-acetyl-beta-D-glucosaminidase

研究概览

简要总结

Renal damage due to contrast media (CM) administration is one of the main complications of cardiac intervention and is called contrast-induced nephropathy (CIN). Patients suffering from CIN have a high probability of developing acute renal failure. Today there is no treatment capable of reversing kidney damage, so the best strategy is prevention, by early diagnosis. In this regard, a line of research is currently being carried out focused on the identification of new markers capable of detecting susceptibility/predisposition to renal damage before the administration of a potentially nephrotoxic drug, even at doses that alone should not produce Kidney damage. This concept has been called predisposition to kidney damage.

Taking into account all of the above, the objective of this work is to evaluate the ability of the new markers (previously identified in preclinical models) to detect the predisposition to the CIN before administering the CM.

详细描述

Kidney damage is one of the most frequent complications of cardiac intervention. This pathology is called contrast-induced nephropathy (CIN) and is defined as an increase in plasma creatinine greater than or equal to 0.5 mg/dL, or greater than or equal to 25% with respect to baseline, during the 5 days after contrast medium (CM) administration.

The appearance of acute renal damage significantly increases the health costs associated with interventional procedures. This is derived from the increase in the length of hospital stay, in care units, and from the application of dialysis as the only existing treatment. In the United States, it has been estimated that the development of acute in-hospital renal damage increases health expenditure by $ 7933 per patient per day, mainly due to the increase in hospitalization time. Thus, not only the very early detection, but especially the prevention of acute renal damage are key aspects for the prognosis of the patients, and for the control of the health expenditure associated with them.

Iodized CMs are the leading cause of acute renal damage of toxic origin in humans. CMs produce renal ischemia derived from a vasoconstriction that has two effects: on the one hand reduction of glomerular filtration, and on the other, tubular ischemic damage that amplifies the reduction of filtrate and, with it, renal dysfunction.

Different scales have been proposed to determine the risk of developing CIN, which include different variables such as the presence of arterial hypotension, the use of counterpulsation balloon, the age over 75 years, the presence of anaemia, diabetes, the amount of CM used and renal function. Each item is assigned a certain score in the case of being present in the patient and depending on the final score, the possible risk of contrast nephropathy after the procedure and even the risk of dialysis is estimated. However, these scales are not widely used in clinical practice and their usefulness is doubtful.

Currently the detection of renal damage associated with CM is performed using the plasma creatinine marker. The main drawback of this detection mode is that creatinine levels increase when renal functionality is already altered. In other words, detection occurs when renal functionality has decreased by approximately 70%. This is why new markers capable of detecting damage in their earliest stages are currently being evaluated, when the damage is less widespread. Also in the last decade a new concept of biomarker called a marker of predisposition to kidney damage has emerged. This concept has been revealed after verifying that certain treatments significantly increase the risk of suffering an acute renal failure, and do so in a hidden and silent way.

研究设计

研究类型
Observational
观察模型
Case Control
时间视角
Retrospective

入排标准

年龄范围
18 Years 至 100 Years(Adult, Older Adult)
性别
All
接受健康志愿者

入选标准

  • Patients of legal age who agree to participate in the study an do not comply with any of the exclusion criteria

排除标准

  • Patients who are terminally ill
  • Patients who do not wish to sign the informed consent

结局指标

主要结局

Urinary N-acetyl-beta-D-glucosaminidase

时间窗: Time 0: before administration of the contrast media

It is an enzyme whose urinary excretion is elevated in case of kidney damage. It is capable of detecting damage before the classic plasma creatinine and urea markers. There are no reference values for humans, so the means of patients who do not develop contrast-induced nephropathy (Control group) should be compared with those who develop the damage (Case group)

Urinary Kidney Injury Molecule -1

时间窗: Time 0: before administration of the contrast media

It is a biomarker of early kidney damage. It is able to detect kidney damge in early stages, before the clinical markers creatinine and plasma urea. There are no reference values for humans, so the means of patients who do not develop contrast-induced nephropathy (Control group) should be compared with those who develop the damage (Case group)

Urinary albumin

时间窗: Time 0: before administration of the contrast media

It is a biomarker of early kidney damage. It is able to detect kidney damge in early stages, before the clinical markers creatinine and plasma urea. There are no reference values for humans, so the means of patients who do not develop contrast-induced nephropathy (Control group) should be compared with those who develop the damage (Case group)

Urinary biomarkers of predisposition to kidney injury

时间窗: Time 0: before administration of the contrast media

It is a group of markers thar are in patent phase so their names can not be mentioned. They are able to detect the susceptibility to kidney damage before administering a nephrotoxic agent. There are no reference values for humans, so the means of patients who do not develop contrast-induced nephropathy (Control group) should be compared with those who develop the damage (Case group)

Urinary Neutrophil gelatinase-associated lipocalin (NGAL)

时间窗: Time 0: before administration of the contrast media

It is a biomarker of early kidney damage. It is able to detect kidney damge in early stages, before the clinical markers creatinine and plasma urea. There are no reference values for humans, so the means of patients who do not develop contrast-induced nephropathy (Control group) should be compared with those who develop the damage (Case group)

次要结局

  • Contrast-induced nephropathy (CIN) development(Time 0 (baseline, before contrast media) and daily for 5 days after contrast media)
  • Percentage of patients with Risk factor's(These data will be collected once, at time 0 (moment of inclusion in the study))
  • Contrast media(These data will be collected once, at day 1 (after contrast media administration))
  • Body weight(These data will be collected once, at time 0 (moment of inclusion in the study))
  • Height(These data will be collected once, at time 0 (moment of inclusion in the study))
  • Age(These data will be collected once, at time 0 (moment of inclusion in the study))
  • Sex(These data will be collected once, at time 0 (moment of inclusion in the study))

研究者

发起方
R. Laura Vicente Vicente
申办方类型
Other
责任方
Sponsor Investigator
主要研究者

R. Laura Vicente Vicente

Principal Investigator

Fundación Instituto de Estudios de Ciencias de la Salud de Castilla y León

研究点 (1)

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