Use of dopamine in prevention of contrast induced acute renal failure — A randomised study

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  Use of dopamine in prevention of contrast induced acute renal failure — A randomised study
  ELSEVIER International Journal of Cardiology 53 (1996) 233-236 Use of dopamine in prevention of contrast induced acute renal failure - A randomised study’ Aditya Kapoof’, Nakul Sinha”-*, R.K. Sharmab, S. Shrivastava”, S. Radhakrishnan”, P.K. Gael”, Rajiv Bajaja “Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Rae Bareli Road, Lucknow 226014, India bDepartment of Nephrology., Sanjay Gandhi Postgraduate Institute of Medical Sciences, Rae Bareli Road, Lucknow 226014, India Received 18 October 1995; accepted 2 December 995 Abstract We report the use of dopamine in renal doses (5 pg/kg/min) to prevent contrast induced nephropathy (GIN). Forty patients with diabetes mellitus who were undergoing coronary angiography were randomly divided into two groups. Gr I (20 patients) was infused with dopamine starting 30 min before cardiac catheterization and continued for 6 h thereafter. Gr II (20 patients) did not receive dopamine. Baseline blood chemistry was performed before catheteriza- tion and then repeated 24 h after the procedure. The mean age and sex distribution were similar in both the groups. Urograffin (76%; 120-150 ml) was used in all the cases. The mean serum creatinine and blood urea nitrogen (BUN) levels in Gr I patients before catheterization were 1.5 f 0.32 mg % and 16.3 _+ 8.05 mg %, respectively. The corresponding values for Gr II were 1.52 + 0.68 mg % and 19.6 f 13.4 mg %, respectively. After angiography, Gr I patients did not show significant changes in renal parameters (serum creatinine, 1.37 f 0.25 mg % and BUN, 14.7 ~fr 5.5 mg %) while Gr II patients showed a significant rise (serum creatinine, 1.96 f 1.2 mg % and BUN, 23.25 Ifr 12.7 mg %; P = 0.01 and P = 0.05, respectively). Ten patients in Gr II (50%) developed a 25% rise in serum creatinine levels within 24 h of injection of the contrast. None of the patients developed renal failure severe enough to warrant dialysis. Hence alterations of renal function are common after cardiac catheterization. Dopamine in renal doses appears to be an effective means to prevent deterioration in renal function induced by contrast. Keywords: Contrast; Dopamine; Nephropathy 1. Introduction Use of radiographic contrast media is consid- ered to be an important cause of hospital acquired 1 The abstract of this manuscript has been presented t the annual Cardiological Society of India (CSI) meeting n Nov. 1994 at Jaipur, India. * Corresponding uthor. acute renal failure. Even with prompt and optimal nephrology support services, the substantial mor- bidity and mortality associated with renal failure make it desirable to attempt to prevent this con- trast induced nephropathy (CIN). The aim of this prospective randomised controlled trial was to study the effect of dopamine, in renal doses (5 pgg/kg/min) as a means to prevent CIN. 0167-5273/96/ 15.00 1996 Elsevier Science reland Ltd. All rights reserved SSDI 0167-5273(95)02547-2  234 A. Kapoor et al. / International Journal of Cardiology 53 (1996) 233-236 2. Methods Forty patients of diabetes mellitus (irrespective of baseline renal function) who were undergoing coronary angiography were the subjects of the present study. Informed written consent was ob- tained from each patient and the study protocol conformed to the ethical guidelines as approved by the Institute’s Human Research Committee. All patients underwent biochemical investigations (besides the routine workup required for angiog- raphy) in the preceding week prior to angiogra- phy. These included assessment of baseline renal parameters and urine analysis before the contrast study. The patients were randomised by a prefixed random number generated coding protocol to ei- ther undergo the angiographic procedure in a routine manner or with use of dopamine. Gr I (20 patients) were started on dopamine infusion in renal doses (5 pg/kg/min) from 30 min before angiography to 6-8 h after the procedure. Gr II (20 patients) were not given dopamine. Urograffin (76%; 120-150 ml) was used for cardiac catheteri- zation. After the procedure, the investigations were repeated at 24 h and if necessary, after 72 h. 2.1. Statistical analysis Clinically important renal impairment was di- agnosed as a rise in serum creatinine of 25% or more, above baseline. Students t-test was used to calculate the significance of the results. A P-value < 0.05 was accepted as significant. All data are expressed as mean + S.D. 3. Results The patients were divided into two groups of 20 Table 2 Effect of dopamine infusion on renal parameters Table 1 Clinical features of Groups I and II Gr I Gr II Age 60.23 + 7.56 61.35 + 8.46 No. of patients (age 6 5 > 60) No. of males 16 17 Baseline EF % 58.2 & 3.5 59.5 f 3.9 Serum creatinine (mg 1.50 k 0.32 1.52 + 0.68 %) BUN (mg %) 16.3 + 8.05 19.6 k 13.4 Average dose of 122 f 16 125 f 15 contrast (ml) EF, ejection fraction on angiography. patients each - group I (those who received dopamine) and group II (those who did not). The age and sex distribution were similar in both the groups (Table 1). Urograffin (76%) was used for angiography in all patients. Pre-angiography, the mean serum creatinine and BUN levels in both the groups were comparable (Table 1). At 24 h post-angiography, Gr I patients did not show any rise in renal parameters while Gr II patients showed a significant increase in both renal parameters (Table 2). Ten patients in Gr II (50%) developed a > 25% increase in serum creatinine. Out of these, eight had an absolute increase of > 0.5 mg %. The patients with baseline pre-angio- graphic renal impairment (serum creatinine value of > 2 mg %) in Gr I did not show any signifi- cant rise in serum creatinine levels after angiogra- phy, rather all of them demonstrated a slight reduction in serum creatinine levels. On the other hand, both patients in Gr II with baseline renal impairment before procedure developed CIN (Table 3). Serum creatinine (mg %) Pre-angio. Post-angio. P-value BUN (mg %) Pre-angio. Post-angio. P-value Gr I 1.5 f 0.32 1.37 + 0.25 NS 16.3 k 8.05 14.7 f 5.5 NS Gr II 1.52 + 0.68 1.96 k 1.2 0.01 19.6 & 13.4 23.25 f 12.7 <0.05  A. Kapoor et al. 1 International Journal of Cardiology S3 (1996) 233-236 235 Table 3 Changes in serum creatinine in patients with baseline levels > 2 mg % n Serum creatinine (mg %) Pre-angiography Post-angiography Gr I 3 2.1 * 0.14 1.7 f 0.08 Gr II 2 3.2 + 1.1 5.05 + 1.75 In 30 patients (15 in each group), biochemical investigations could be repeated at 72 h post-an- giography (Table 4). Though none of the patients developed a further rise in serum creatinine levels at 72 h, Gr II patients still had significantly higher serum creatinine and BUN levels at 72 h com- pared to pre-angiographic levels. However, none of the patients in either group developed clinical features of azotemia, abnormal- ities of urine output or urine chemistry and none required dialysis support. 4. Discussion Currently, CIN is the third leading cause of acute renal failure among hospitalised patients. Various studies have reported the incidence of CIN in patients undergoing cardiac catheteriza- tion as O-23% [l-4]. Renal dysfunction in this setting is usually nonoliguric, though oliguric fail- ure can occur in up to 30% of cases. Numerous risk factors predisposing the patients to CIN have been implicated including pre-existing renal in- sufficiency, diabetes mellitus and severe congestive heart failure with reduced cardiac output [3-61. It Table 4 Serum creatinine and BUN levels at 72 h post-angiography 72 h post-angio. (n = 15) Gr 1 Gr 2 Serum creatinine (mg %) 1.4 f 0.23 1.9 _+ 1.26 BUN (mg %) 14.8 + 3.7 20.1 * 13.9 is debatable whether the incidence of CIN is altered by the use of nonionic or ionic contrast media [7,8]. Since the exact etiology is unclear, several potential mechanisms have been postu- lated in its genesis. These include possible im- mune-mediated injury, alterations of renal perfusion with ischaemic insult, altered glomeru- lar permeability, direct tubular toxicity and in- tratubular obstruction by crystal deposition [9-131. However, only rarely is dialysis needed in such cases, the reported incidence being about 1.4% [14]. But the risk of CIN is real and efforts must be made to prevent it. Judicious use of the amount of contrast is obviously desirable and important. Though intravenous ffuids, mannitol and nitrendipine have been used as preventive measures, no well controlled trial is available [15,16]. In our study, patients who received dopamine had an average fall of serum creatinine ( - 0.13 mg “A) and BUN levels ( - 1.6 mg %) within 24 h of angiography, though this was statistically in- significant. This is in agreement with the results of Hall et al. [17]. Gr II patients (who did not receive dopamine) showed a significant rise in both serum creatinine and BUN levels within the same period. Fifty percent of patients in this group had a > 25% increase in serum creatinine levels. Repeat estimations done in 15/20 (75%) patients in Gr II at 72 h revealed mean serum creatinine and BUN levels higher compared to pre-angiographic val- ues. Thus all patients who developed CIN showed a rise in serum creatinine and BUN values within 24 h of the use of contrast. Eight of 18 (44%) of the patients in Gr-II who had basal serum crea- tinine levels < 2 mg % developed CIN while both patients with basal serum creatinine > 2 mg % showed a further rise in serum creatinine value and developed CIN. This is in agreement with other studies which show that diabetics with basal impairment of renal function are more prone to develop CIN compared to those with normal renal function [18]. Use of dopamine in these patients with baseline renal impairment (three pa- tients in Gr I) not only prevented the rise in serum creatinine values following use of contrast but resulted in improvement in renal function (Table 3) as is evidenced by a fall in serum creatinine in  236 A. Kapoor et al. /International Journal of Cardiology 53 (1996) 233-236 these patients. Thus dopamine in the present study was also able to prevent CIN in the high risk patients with pre-existing renal impairment. Dopamine, acting via dopaminergic receptors (DA) causes an increase in renal blood flow, inhibits Na+ /H + transport in proximal tubules and counteracts the effects of mineralo-corticoids in the collecting tubules. The increase in glomeru- lar filtration rate is mediated via DA receptors [191* Our study suggests hat low dose dopamine, in renal doses, is an effective means to prevent con- trast induced nephropathy in patients undergoing contrast angiography. Dopamine is also useful in preventing further renal function deterioration in patients with pre-existing renal impairment. Do- pamine infusion should be started half an hour before contrast study and continued for 6-8 h following the procedure. Acknowledgements This study was supported by an intramural grant from Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow. References [2] Kumar S, Hull JD, Lathi S, Cohen AJ, Pletka PG. Low incidence of renal failure after angiography. Arch Intern Med 1981;141:1268-1270. [3] Taliercio CP, Vlietstra RE, Fisher LD, Burnett JC. Risks for renal dysfunction with cardiac angiography. Ann In- tern Med 1986;104:501-504. [4] Davidson CJ, Hlatky M, Morris KG, Fleper K et al. Cardiovascular and renal toxicity of a non ionic radio- graphic contrast agent after cardiac catheterization: a prospective trial. Ann Intern Med 1989;110:119-124. [5] Moore RD, Stainberg EP, Powe NR, White RI Jr et al. Frequency and determinants of adverse reactions induced by high osmolality contrast media. Radiology 1989;170:727-732. [6] Barrett BJ, Parfrey PS, Yavasour HM, McDonald J et al. Contrast nephropathy in patients with impaired renal function: high versus low osmolar media. Kidney Int 1992;41:1274-1279. [7] Hill JA, Winniford M, Fossen B, Goldfarb S, Miurphy M, Halpem E. For the Iohexol Cooperative study; nephrotoxicity following cardiac angiography: a ran- domised double blind multicenter trial to ionic and non- ionic contrast media in 1194 patients. Circulation 1991;84-II:333 (Abstr). [8] Schwab SJ, Hlatky MA, Pieper KS, Davidson CJ et al. Contrast nephrotoxicity: a randomised control trial of nonionic and an ionic radiographic contrast agent. New Engl J Med 1989;320:149-153. [9] Porter GA. Contrast associated nephropathy. Am J Car- diol 1989;64:22E-26E. [lo] Porter GA, Kloster FE, Bristow JD. Sequential effects of angiography contrast agents on renal and systemic hemo- dynamics. Am Heart J 1971;81:80-89. [ll] Workman RJ, Shalt MI, Jackson RV, Diggs J, Frazer MG, Briscoe C. Relationship of renal hemodynamics and functional changes following intravascular contrast to the renin angiotensin system and renal prostacyclin in the dog. Invest Radio1 1983;18:160-166. [12] Haltas S, Billstorm A, Tejler L. Proteinuria following nephroangiography IX. Chemical and morphological analysis in dogs. Acta Radio1 1981;22:427-433. [13] Gelman LM, Rowe JW, Coggins CH. Effects of an angiographic contrast agent on renal function. Cardio- vast Med 1979;4:313. [14] Gomes AS, Baker JD, Martin Paredero V, Dixon SM, et al. Acute renal dysfunction after major arteriography. Am J Roentgen01 1985;145:1249-1253. [15] Tommaso CL. Contrast induced nephrotoxicity in pa- tients undergoing cardiac catheterization Catheter Car- diovasc Diagn 1994;31:316-321. [16] Neumayer HH, Junge W, Kutner A, Wenning A. Preven- tion of radiocontrast-media-induced nephrotoxicity by the calcium channel blocker nitrendipine. A prospective ran- domized clinical trial. Nephrol Dial Transplant 1989;4:1030-1036. [17] Hall KA, Wong RW, Hunter GC, Camazime BM et al. Contrast induced nephrotoxicity: the effects of vasodilator therapy. J Surg Res 1992;53:317-320. [18] Parfrey PS, Griffiths SM, Barrett BJ, et al. Contrast material induced renal failure in patients with diabetes mellitus, renal insufficiency or both. New Engl J Med 1989;320:143-149. [19] Schwartz LB, Gewertz BL. The renal response to low dose dopamine. J Surg Res 1988;45:574.
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