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| | | Year : 2011 | Volume : 22 | Issue : 1 | Page : 54-60 | | | Can continuous venovenous hemofiltration prevent contrast-agent induced nephropathy in patients with advanced chronic kidney disease after coronary angiography? | | | Amal Abdel Ghani, Naser Hussain, Bassam Al Helal
Department of Nephrology, Mubarak Al Kabeer Hospital, Ministry of Health, Kuwait
Click here for correspondence address and email | Date of Web Publication | 30-Dec-2010 | | |      | |  Abstract | | | To determine whether contrast induced nephropathy (CIN) post coronary angiography procedure can be prevented in chronic kidney disease (CKD) patients by continuous venovenous hemofiltration (CVVH), we evaluated 98 CKD patients [52 (53.1%) were males, the mean age was 60.7 ± 11.0 years] who underwent coronary angiography from January 2004 to December 2006. Serum creatinine (Cr) before the procedure was 411 ± 79.9 μmol/L and creatinine clearance (Cr Cl) was 18.04 ± 4.26 mL/min. All patients underwent post procedure CVVH for 21.34 ± 2.12 hours. The mean time interval between the procedure and the start of CVVH was 44.3 ± 18.8 min. The mean serum Cr at discharge was 403 ± 88.4 μmol/L (Cr Cl 18.5 ± 4.61 mL/min) and was 423 ± 88.9 μmol/L (Cr Cl17.6 ± 4.27 mL/min) 15 days after the procedure. One patient (1.02%) developed worsening of renal functions that required repeated CVVH during hospitalization and ended up on regular hemodialysis. There was no in-hospital mortality. We conclude that CVVH is effective in preventing CIN after coronary angiography in CKD patients. How to cite this article:
Ghani AA, Hussain N, Al Helal B. Can continuous venovenous hemofiltration prevent contrast-agent induced nephropathy in patients with advanced chronic kidney disease after coronary angiography?. Saudi J Kidney Dis Transpl 2011;22:54-60 |
How to cite this URL:
Ghani AA, Hussain N, Al Helal B. Can continuous venovenous hemofiltration prevent contrast-agent induced nephropathy in patients with advanced chronic kidney disease after coronary angiography?. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2014 Mar 3];22:54-60. Available from: http://www.sjkdt.org/text.asp?2011/22/1/54/74345 |
| Introduction | |  |
The incidence of contrast induced nephropathy (CIN) is now increasing owing to the increasing use of radiocontrast media (CM) in diagnostic imaging as well as interventional procedures. [1] The most widely accepted definition of CIN is an increase of 25% or more, or an absolute increase of 0.5 mg/dL (44 μmol/L) or more in serum creatinine (Cr) from baseline values, at 24-72 hours following exposure to CM. [2] CIN is one of the leading causes of hospital acquired acute renal failure (ARF) and is associated with increased morbidity and mortality. [3]
Among all procedures utilizing CM for diagnosis or therapeutic purposes, coronary angiography and percutaneous coronary intervention (PCI) are associated with the highest incidence of CIN. [1] The overall incidence of CIN in the general population is reported to be 0.6-2.3%. [4] However, in several patient subsets, the prevalence of CIN is significantly higher. [5],[6] The incidence of CIN in patients with underlying chronic kidney disease (CKD) is extremely high, ranging from 14.8 to 55%. [6],[7],[8] The higher the baseline Cr value, the greater is the risk of CIN. [9] Nevertheless, an increasing number of patients with CKD are being referred for PCI, owing to the greater prevalence of cardiovascular diseases among this group of patients. [10]
CIN is a potentially reversible condition, and currently available strategies such as hydration and use of N-acetylcysteine, mannitol, furosemide, dopamine, fenoldopam, or other renoprotective drugs have been proven effective in patients with normal or mildly impaired renal function. [11],[12]
Methods for prevention of CIN in patients with advanced renal failure remain unknown. Additionally, prophylactic hemodialysis (HD), started immediately after the administration of CM to this group of patients did not show any benefit in CIN prevention. [13] In contrast to HD, continuous venovenous hemofiltration (CVVH) is another alternative strategy for prevention of CIN in high-risk patients. [14],[15] The purpose of this study is to determine the efficacy of prophylactic CVVH in the prevention of CIN in patients with advanced CKD.
| Subjects and Methods | | |
A prospective, single-center study was conducted in chest disease hospital of Kuwait from January 2004 to December 2006. All patients with CKD who were scheduled for PCI were included in the study. Inclusion criteria included age above 25 years, stable serum Cr concentration above 300 μmol/L and creatinine clearance (Cr Cl) of <35 mL/min within one month prior to the procedure. Exclusion criteria included presentation with cardiogenic shock, pregnancy, lactation, contraindications to heparinization, intravascular administration of contrast or exposure to nephrotoxic drugs during the previous two weeks, use of non-steroidal anti-inflammatory drugs during the previous 48 hours, renal transplantation, and patients with end-stage renal disease requiring regular dialysis. Angiotensin converting enzyme inhibitors were held on the day of the procedure. Intravenous hydration protocols, mannitol, Acetylcysteine, dopamine, were not used during the procedure. All patients signed a written informed consent.
The study patients were started on CVVH as soon as possible after the procedure, and the time interval from contrast exposure to initiation of dialysis was recorded. CVVH was performed through a double lumen intravenous femoral catheter (Quinton, Bothell, WA, USA) placed by the attending nephrologists before the procedure. CVVH for 18-24 hours was started using Prisma continuous fluid management system (by Gambro Lakewood Co. Sweden) using M100 dialyzer sets (AN69 membrane), with surface area of 0.90 m 2 , with bicarbonate buffered solution for continuous renal replacement therapy (CRRT) from Hospal having the following solute composition in mmol/L: calcium Ca 2+ : 1.75, magnesium mg 2+ : 0.5, sodium Na + : 140, chloride Cl - : 109.5, lactate - : 3, bicarbonate HCO3 ~: 32. Blood flow rate was set at 100 mL/min and the substitution fluid rate was 2 L/hour without any fluid removal. Anticoagulation was achieved by giving heparin bolus of 500 IU at the start of CVVH and then constant heparin infusion to maintain activated partial thromboplastin time between 130 and 150 seconds.
Blood urea nitrogen (BUN) and serum Cr were measured before the procedure, at the end of the CVVH session, then daily for the following three days, at hospital discharge, and 15 days after the day of the procedure. Cr Cl was calculated at the same time using Cockcroft and Gault equation. [16] The incidence of contrast nephropathy defined as >25% increase from baseline serum Cr values was calculated. Emergency CRRT was performed if there was oliguria for more than 48 hours despite administration of more than 1 g of furosemide over 24 hours, or if there was evidence of congestive heart failure, or if serum potassium was above 6 mmol/L. CRRT was discontinued when there was evidence of recovery of renal function with the restoration of urine output of >500 mL/day. The need for permanent HD was persistent with Cr Cl < 5 mL/min. The incidence of CIN, in-hospital mortality, and the need for long-term dialysis were calculated.
| Statistical Analysis | | |
Data were analyzed using SPSS for windows version 13 (SPSS, Inc., Chicago, IL, USA). Numerical variables were expressed as mean ± SD, whereas categorical variables were expressed as frequencies and percentages.
| Results | | |
Ninety-eight patients were enrolled in the study [52 (53.1%) were males, and 46 (46.9%) were females]. Patients' clinical data are shown in [Table 1]. Pre procedure serum Cr ranged from 302 - 631 μmol/L, with a mean of 411 ± 79.9 μmol/L; pre procedure Cr Cl ranged from 12.2 - 31.1 mL/min, with a mean of 18.0 ± 4.26 mL/min. All patients were subjected to post procedure CVVH. The mean time interval between the procedure and the start of CVVH was 44.3 ± 18.8 min. The mean duration of the session was 21.3 ± 2.12 hours. None of the studied subjects had femoral catheter related complications, but three patients (3.06%) required catheter replacement for clotting. The dialysis course was smooth without intra dialytic complications. The mean serum Cr after CVVH was 143 ± 40.4 μmol/L, and was 310 ± 46.4 μmol/L at 48 hours after the procedure, 398 ± 63.2 μmol/L at 72 hours after the procedure, 403 ± 88.4 μmol/L at the time of discharge and 422 ± 88.9 μmol/L 15 days after the procedure [Figure 1]. The mean Cr Cl was 18.5 ± 4.61 mL/min and 17.6 ± 4.27 mL/min at the time of discharge and 15 days after the procedure, respectively [Figure 2]. One patient (1.02%) developed CIN that required repeated CVVH sessions during hospitalization and ended up on regular long-term hemodialysis treatment. There was no in-hospital mortality in the study patients.
| Discussion | | |
Patients with CKD have a predisposition to accelerated atherosclerosis; thus, they represent an increasing percentage of the patients undergoing PCI. [17] The clinical outcome of patients in whom CIN develops after PCI is particularly poor, with a reported in-hospital mortality rate of more than 20% and cumulative one year mortality rate of more than 35%. [3],[18],[19],[20],[21]
Mortality even increased to 45-62% if dialysis was required. [19],[21] Given the clinical and prognostic implications, strategies to reduce the incidence of CIN are needed particularly in high-risk patients. [22] Several strategies have been evaluated for the prevention of CIN. Among these strategies, only saline hydration, [23],[24] the use of low-osmolality contrast agents, [25] and treatment with N-acetylcysteine [26],[27],[28] or fenoldopam [29],[30] have been shown to provide some protection and to reduce the incidence of CIN. However, the efficacy of these measures is still controversial in patients with severe renal impairment. [27] The pharmacokinetic properties of water-soluble iodinated CM disclose only its extracellular fluid distribution, are minimally protein bound, are not metabolized and are excreted mainly by the glomerular filtration. [31] In normal subjects, elimination of CM occurs rapidly; approximately 50% of the CM is recovered in urine within two hours. In subjects with severe CKD, the same 50% will be eliminated in urine 16-84 hours after injection of the CM. [32] Considering the properties of the iodinated CM, it is hypothesized that it can be removed by dialysis.
Our study showed that doing CVVH as soon as possible after contrast injection in patients with CKD reduced the incidence of CIN to 1.02%, which is significantly less than that reported in studies in which other preventive strategies such as saline hydration or N-acetylcysteine were used. However, our results are in accordance with the previous studies in which CVVH or HD were used. [33],[34],[35],[36] To date, there have been few trials evaluating HD for prevention of CIN, [37],[38] and both HD and CVVH effectively removed iodinated CM from the blood. [39] Despite this a recent systemic review of studies comparing the periprocedural HD with conventional prophylactic measures found that HD does not decrease the risk or the need for acute dialysis associated with CIN. [36] CVVHF and continuous venovenous hemodiafiltration (CVVHDF) have also been studied for the prevention of CIN after PCI in patients with CKD .[36] In 2003, Marenzi et al, [34] reported the superiority of CVVH over saline hydration in prevention of CIN after PCI in patients with CKD, where CIN was reported in 5% of the CVVH group versus 50% in the control group. However, Gabutti et al, [40] studied the effect of CVVHDF performed during and after PCI in patients with CKD and concluded that CVVHDF was not effective in prevention of CIN. Marenzi et al, [35] compared the use of saline hydration with the use of pre and post procedure CVVH or the use of post procedure CVVH and concluded that pre and post CVVH was superior to the other two strategies. On the other hand, Vogt et al, [13] did not show any beneficial effect of prophylactic HD for three hours after the procedure. Moreover, patients who received HD were more likely to have a decline in renal function and required additional HD treatment. A possible explanation for these results is that HD can induce hypovolemia and consequently may worsen renal ischemic injury, delay recovery of renal functions, and result in a need for prolonged dialysis. [41] On the other hand, the beneficial effect of CVVH can be attributed to its association with hemodynamic stability, allowance of better hydration and regulation of volume status, infusion of large volume of bicarbonate containing solution, [42] and removal of CM from the circulation with a resultant reduction in the kidneys' exposure to CM. [14],[15],[43]
Lastly, heparin used during pre procedure CVVH may have a beneficial effect as it may inhibit acute inflammation, attenuate the ischemic reperfusion injury, and reduce the oxidative stress that may be involved in the pathogenesis of CIN. [44],[45] Therefore, considering the relatively high cost and the time consuming nature of CVVH, the limited availability of an intensive care unit (ICU) beds, and the lengthy immobilization of patients, this procedure should be restricted to high-risk patients.
This study was limited because it was a single center study and the results may be different in other centers and the effect of CVVH was not compared with the conventional hydration protocols; however, the results were compared with previous reports.
In conclusion, CVVH, despite being expen sive and time consuming, has a significantly beneficial effect in preventing CIN after PCI in CKD patients, and it should be considered as a preventive strategy in this group of patients.
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Correspondence Address:
Amal Abdel Ghani
Nephrology Department, Mubarak Al Kabeer Hospital, P.O. Box 43787
Kuwait
PMID: 21196613
[Figure 1], [Figure 2]
[Table 1] | |
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