Effects of Saline, Mannitol, and Furosemide on Acute Decreases in Renal Function Induced by Radiocontrast Agents

Solomon, Richard; Werner, Craig T.; Mann, Denise; D’Elia, John A.; Silva, Patricio

doi:10.1056/nejm199411243312104

Cited by 1,150 publications

(643 citation statements)

References 24 publications

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“…The most frequently used protocol for hydration with saline to prevent CI‐AKI in patients with chronic kidney disease in controlled trials involves fluid supplementation for 12 hours before and after the procedure, rather than 24 hours before and after the procedure, at a speed of 1 mL/kg per hour. In these patients, the CI‐AKI incidence has been reported to be ≈10%, which is similar to that observed in the present study using the same protocol 12, 19, 20, 21, 22. However, more than three quarters of the patients in our real‐world study received a lower hydration volume (<17 mL/kg) than that administered in the above‐mentioned studies.…”

Section: Discussionsupporting

confidence: 88%

Excessively High Hydration Volume May Not Be Associated With Decreased Risk of Contrast‐Induced Acute Kidney Injury After Percutaneous Coronary Intervention in Patients With Renal Insufficiency

Liu¹,

Li²,

Chen³

et al. 2016

JAHA

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BackgroundNo well‐defined protocols currently exist regarding the optimal rate and duration of normal saline administration to prevent contrast‐induced acute kidney injury (CI‐AKI) in patients with renal insufficiency.Methods and ResultsHydration volume ratios (hydration volume/weight; HV/W) were calculated in 1406 patients with renal insufficiency (estimated glomerular filtration rate [eGFR], <90 mL/min per 1.73 m2) undergoing percutaneous coronary intervention (PCI) with routine speed hydration (1 or 0.5 mL/kg per hour). We investigated the relationship between hydration volume, risk of CI‐AKI (increase in serum creatinine ≥0.5 mg/dL or 25% within 48–72 hours), and prognosis. Mean follow‐up duration was 2.85±0.88 years. Individuals with higher HV/W were more likely to develop CI‐AKI (quartiles: Q1, Q2, Q3, and Q4: 4.3%, 6.6%, 10.9%, and 15.0%, respectively; P<0.001). After adjusting 12 confounders, including age, sex, eGFR, anemia, emergent PCI, diabetes mellitus, chronic heart failure, diuretics, contrast volume, lesions, smoking status, and number of stents, multivariate analysis showed that a higher HV/W ratio was not associated with a decreased CI‐AKI risk (Q2 vs Q1: adjusted odds ratio [OR], 1.13; Q3 vs Q1: adjusted OR, 1.51; Q4 vs Q1: adjusted OR, 1.87; all P>0.05) and even increased CI‐AKI risk (HV/W >25 mL/kg: adjusted OR, 2.11; 95% CI, 1.24–3.59; P=0.006). Additionally, higher HV/W was significantly associated with an increased risk of death (Q4 vs Q1: adjusted hazard ratio, 3.44; 95% CI, 1.20–9.88; P=0.022).ConclusionsExcessively high hydration volume at routine speed might be associated with increased risk of CI‐AKI and death post‐PCI in patients with renal insufficiency.

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Section: Discussionsupporting

confidence: 88%

Excessively High Hydration Volume May Not Be Associated With Decreased Risk of Contrast‐Induced Acute Kidney Injury After Percutaneous Coronary Intervention in Patients With Renal Insufficiency

Liu¹,

Li²,

Chen³

et al. 2016

JAHA

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“…Moreover, although ␤-adrenergic blockers and ACE inhibitors improve survival in patients after AMI, 37 these agents are often underused in patients with RI compared with those with normal renal function. 4,38,39 All attempts must be made to prevent contrast nephropathy, including adequate hydration, 40 minimizing contrast use, 29 use of low-osmolar contrast, 41 and possibly administration of N-acetylcysteine. 42 Patients with baseline RI warrant close surveillance and intensive medical management, including tight control of diabetes, hypertension, and dyslipidemia 20 ; dietary modification; and potentially frequent stress testing for early recognition of disease progression.…”

Section: Discussionmentioning

confidence: 99%

Impact of Renal Insufficiency in Patients Undergoing Primary Angioplasty for Acute Myocardial Infarction

et al. 2003

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Background-The prognostic importance of renal insufficiency (RI) in patients undergoing primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) has not been well characterized. Methods and Results-PCI was performed in 2082 AMI patients without shock presenting within 12 hours of symptom onset in a prospective, multicenter randomized trial. RI was defined as a calculated (Cockroft-Gault) creatinine clearance (CrCl) Յ60 mL/min. RI at baseline was present in 18% of patients. Compared with patients without RI, patients with RI were older and were more likely to be female; to have hypertension, peripheral vascular disease, or cerebrovascular disease; and to present in heart failure. Mortality was markedly increased in patients with versus without baseline RI both at 30 days (7.5% versus 0.8%, PϽ0.0001) and at 1 year (12.7% versus 2.4%, PϽ0.0001). Mortality rates increased incrementally for every 10-mL/min decrease in baseline CrCl. By multivariate analysis, reduced baseline CrCl was a powerful independent predictor of 30-day mortality (hazard ratio, 5.77; PϽ0.0001) and remained associated with reduced survival at 1 year (hazard ratio, 1.98; Pϭ0.08). Hemorrhagic complications and transfusion requirements were also increased more than 2-fold in patients with RI, as were severe restenosis (diameter stenosis Ն70%; 20.6% versus 11.8%, Pϭ0.024) and infarct artery reocclusion (14.7% versus 7.3%, Pϭ0.02). Conclusions-Baseline RI in patients with AMI undergoing primary PCI is associated with a markedly increased risk of mortality, as well as bleeding and restenosis. Novel approaches are needed to improve the otherwise poor prognosis of patients with RI and AMI.

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“…The positive effect of adequate hydration in reducing rates of CIN was established in the randomized study of Solomon et al [49]. In 78 patients with chronic renal insufficiency undergoing cardiac angiography, hydration with 0.45% saline 12 hr before and 12 hr after angiography provided better protection against renal function deterioration than did hydration with 0.45% saline plus mannitol or saline plus furosemide (CIN 11% vs. 28% vs. 40%; P ¼ 0.05).…”

Section: Hydrationmentioning

confidence: 99%

Contrast‐induced nephropathy

Pučelíková

Dangas

Mehran

2007

Cathet Cardio Intervent

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Contrast induced nephropathy (CIN) is an iatrogenic disorder, resulting from exposure to contrast media. Contrast-induced hemodynamic and direct cytotoxic effects on renal structures are highly evident in its pathogenesis, whereas other mechanisms are still poorly understood. CIN is typically defined as an increase in serum creatinine by either 0.5 mg/dl or by 25% from baseline within the first 2-3 days after contrast administration. Although rare in the general population, CIN has a high incidence in patients with an underlying renal disorder, in diabetics, and the elderly. The risk factors are synergistic in their ability to produce CIN. The best way to prevent CIN is to identify the patients at risk and to provide adequate peri-procedural hydration. The role of various drugs in prevention of CIN is still controversial and warrants future studies. Despite remaining uncertainty regarding the degree of nephrotoxicity produced by various contrast agents, in current practice non-ionic low-osmolar contrast media are preferred over the high-osmolar contrast media in patients with renal impairment.

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Effects of Saline, Mannitol, and Furosemide on Acute Decreases in Renal Function Induced by Radiocontrast Agents

Cited by 1,150 publications

References 24 publications

Excessively High Hydration Volume May Not Be Associated With Decreased Risk of Contrast‐Induced Acute Kidney Injury After Percutaneous Coronary Intervention in Patients With Renal Insufficiency

Excessively High Hydration Volume May Not Be Associated With Decreased Risk of Contrast‐Induced Acute Kidney Injury After Percutaneous Coronary Intervention in Patients With Renal Insufficiency

Impact of Renal Insufficiency in Patients Undergoing Primary Angioplasty for Acute Myocardial Infarction

Contrast‐induced nephropathy

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