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Year : 2017  |  Volume : 11  |  Issue : 4  |  Page : 198-200

Renal transplantation in a patient with alport syndrome and cardiac dysfunction: Role of levosimendan

Department of Anaesthesia, Kerala Institute of Medical Sciences, Trivandrum, Kerala, India

Date of Web Publication28-Dec-2017

Correspondence Address:
Kusuma Ramachandra Halemani
A3 “SAYANA”, “SUHA” Residency, Poonthi Road, Kumarapura, Trivandrum - 695 011, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_50_17

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Anesthetic management in patients with end-stage renal disease and cardiac dysfunction coming for renal transplant is very challenging since the maintenance of adequate cardiac output is essential for good graft function. Levosimendan is an inodilator that increases cardiac output without increasing cardiac workload. Hence, it is the drug of choice in patients with ischemic heart disease and congestive cardiac failure. We present successful perioperative management of a renal transplant recipient with left ventricular dysfunction using levosimendan for maintenance of stable hemodynamics. Levosimendan, an inodilator, can be safely used in patients with cardiac dysfunction coming for renal transplantation.

Keywords: Anesthesia for renal transplant, cardiac failure, levosimendan for renal transplant recipient, renal transplant

How to cite this article:
Sajan S, Halemani KR. Renal transplantation in a patient with alport syndrome and cardiac dysfunction: Role of levosimendan. Indian J Transplant 2017;11:198-200

How to cite this URL:
Sajan S, Halemani KR. Renal transplantation in a patient with alport syndrome and cardiac dysfunction: Role of levosimendan. Indian J Transplant [serial online] 2017 [cited 2023 Feb 3];11:198-200. Available from: https://www.ijtonline.in/text.asp?2017/11/4/198/221853

  Introduction Top

Cardiac comorbidities associated with end-stage renal disease (ESRD) include [1] coronary artery disease (CAD) cardiomyopathy (uremic, dilated, or hypertrophic), congestive cardiac failure (CCF), pericardial effusion, pulmonary artery hypertension (PAH), and right heart failure. While majority of the problems are due to fluid overload, rapid progression of atherosclerosis and common risk factors makes them at risk for CAD.[2],[3] Renal transplant in patients with left ventricular (LV) dysfunction is risky as good cardiac output is essential for good graft function. At the same time, renal transplantation improves the quality of life and cardiac function also might improve due to reduction in fluid and uremic load, pulmonary pressures, and progression of atherosclerosis. Perioperative optimization of cardiac output might benefit the patient in the long term.

We present successful perioperative management of a case of ESRD with CAD-induced LV dysfunction posted for renal transplantation. We also like to draw attention to the benefits of levosimendan in such cases.

  Case Report Top

A 47-year-old male patient, a known case of Alport syndrome, hypothyroidism, and ESRD, was posted for living-related renal transplantation (LDRT). He was a known case of CAD for which he had undergone percutaneous coronary angioplasty twice. He had undergone LDRT 8 years back, and due to graft rejection, he was on hemodialysis (HD) thrice weekly for the past 4 years. He also had bilateral sensorineural hearing loss, right eye cataract, lenticonus, hypertension, and type 2 diabetes mellitus.

His LDRT was postponed twice, once because of cardiac arrest he suffered during HD (due to hypokalemia) and another time due to chest infection. At this time, the patient was readmitted for the LDRT from his sister. He was anuric and anemic and had class 4 dyspnea and orthopnea. As he had been on and off HD for the past 16 years (since 2000 after the LDRT failed), his both internal jugular veins (IJVs) and femoral veins were accessed several times. His present arteriovenous fistula was not working, and he was being dialyzed through right IJV-HD catheter.

He had Q-wave in inferior leads, negative “T-” waves in lateral leads, and LV hypertrophy on electrocardiogram. His echocardiogram showed akinesia of anterior wall, hypokinesia of inferior and lateral walls, ejection fraction of 37%, and moderate PAH. Chest X-ray (CXR) was clear.

The patient and relatives were counseled well and risk informed consent was taken. He underwent heparin-free HD on the preoperative day, and around 1.2 L of fluid was removed. Postdialysis electrolytes were normal. He was premedicated with pantoprazole 40 mg oral tablet on the night before surgery.

On the morning of surgery, he developed dyspnea and orthopnea while being transferred to the operation theater (OT). He had bilateral basal crepitations; CXR showed features of pulmonary edema, and arterial blood gases (ABGs) showed hypoxemia. After discussing with our nephrologist and cardiologist, we decided to do one more heparin-free HD. Around 1.5 L fluid was removed over a period of 2 h. He became symptomatically better and repeat CXR and ABG also improved. Considering the fact that he had been postponed twice and HD was beneficial for improving the symptoms, we decided to go ahead with the procedure in consensus with surgeons, nephrologist, and cardiologist.

The patient was transferred to OT, and preinduction monitors were attached. Left radial artery and an 18G intravenous (IV) cannula were put under local anesthesia. Left IJV showed a thrombus on ultrasound, so we decided to use HD catheter instead of central line. The left external jugular vein was accessed with 18G cannula.

Preinduction blood pressure (BP) was 170/90, heart rate was 90/min, and central venous pressure (CVP) was 12 mmHg. After preoxygenation for 5 min, injection (inj) midazolam 2 mg, inj fentanyl 150 ug, inj etomidate 10 mg, and succinylcholine 100 mg were given intravenously, and rapid sequence intubation was done. Anesthesia was maintained with air–oxygen mixture with sevoflurane and atracurium blouses. Vitals were stable throughout the induction. During the surgery, the patient developed hypotension, which was not responding to dopamine and noradrenaline. Considering his poor LV function, levosimendan at a dose of 0.05 ug/kg/min as infusion without initial bolus dose was started. The patient responded to therapy, and BP began to pick up and was maintained around a mean arterial pressure (MAP) of 80 mmHg.

Normal saline (0.9%) was used as IV fluid before the reperfusion, and ringer lactate was used once graft started functioning. Fluid therapy was targeted to maintain CVP of around 10 mmHg.

Inj hydrocortisone 200 mg, inj furosemide 80 mgm, and inj mannitol 100 ml were administered before reperfusion. Vitals were stable during the reperfusion. Urine output started within 5 min of reperfusion. Toward the end of procedure, his vitals were stable with minimal noradrenaline and levosimendan support. His airway pressures and ABG were normal. He was reversed with inj neostigmine 0.05 mg/kg and inj glycopyrrolate 0.02 mg/kg and was extubated once fully awake.

The patient was transferred to posttransplant care unit. Postoperative ABG and CXR were within normal limits, and urine output was good. His vitals remained stable, and we could taper off levosimendan on the postoperative day (POD) 1 and noradrenaline on POD2.

Postoperative pain was managed with inj paracetamol 1 g 8th hourly and inj tramadol 100 mg 12th hourly. He was discharged on PODS 15 with normal graft function on oral immunosuppressant. ABGs are given in [Table 1] and serum creatinine levels are shown in [Graph 1].
Table 1: Arterial blood gas values

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  Discussion Top

Renal function is a strong risk factor for CAD. Patients even with mild renal dysfunction [4] and on dialysis [5] show rapid progression of atherosclerosis and hence progression of CAD.

Patients with ESRD usually develop dilated cardiomyopathy or hypertrophic cardiomyopathy due to chronically increased intravascular volume and increased after load.[1] CAD and CCF are present in about 50% of patients beginning dialysis, and case fatality rate of each of these disease in a patient with ESRD is 10-fold high.[4],[5] Increase in serum creatinine level is one of the strongest predictors of mortality in these patients.[6]

Our patient was known to have ESRD since 23 years of age. The etiology of kidney disease was Alport syndrome, which is a disease with multimodal inheritance pattern,[7] X-linked dominant being the most common. It affects type 4 collagen and damages renal tubules, ear, and eyes.

Our patient had severe dyspnea and orthopnea on the day of surgery which got resolved with removal of another 1.5 L of fluid by HD. General anesthesia is the choice even though few case reports have been published on successful transplantation, using combined spinal-epidural anesthesia in patients with severe LV dysfunction.[8],[9] However, this was not chosen as platelet dysfunction associated with ESRD [1] was our concern.

Intraoperatively, his initial CVP was high. In patients with LV dysfunction, CVP is not the ideal choice for fluid status assessment.[8] Pulmonary capillary wedge pressure (PCWP) obtained by PA catheter, stroke volume variation (SVV) obtained by FloTrac, or transesophageal echocardiogram (TEE) are the better guides, TEE being the best.[1] Case reports published so far have used PA catheter as their monitor of choice.[8],[9] Complications associated with PA catheter have reduced its use in noncardiac surgeries.[10] We did not put PA catheter as there was HD catheter in the right IJV. We retrospectively acknowledge that we could have used either FloTrac or TEE.

Dopamine was our first choice of drug. Noradrenaline is known to reduce renal blood flow and hence is not the first line of drug.[1] Dobutamine can be used, but the MAP has to be more than 70 mmHg.[1] As dopamine was not effective, we started noradrenaline. Later, we added levosimendan, an inodilator that is beneficial for patients with poor LV function. Combination of noradrenaline and levosimendan prevents excessive drop in systemic vascular resistance caused by levosimendan.[11] Hence, we continued using both of them and tapered off dopamine.

Levosimendan is a new calcium channel sensitizer developed for the treatment of CCF. Experimental studies indicate that levosimendan increases the myocardial contractility by sensitizing troponin C to calcium ions. During diastole, sensitization is diminished due to a change in calcium ion concentration level which does not cause a deterioration of diastolic relaxation but does cause an improvement.[11] Levosimendan is not nephrotoxic, but its dose should be reduced in patients with renal disease.[11]

Thus, levosimendan increases cardiac output with a decrease in PCWP without increasing cardiac workload.[11] In this, it differs from milrinone, an inodilator used in CCF. The dose of levosimendan is 6–12 mcg/kg as a loading dose followed by 0.05–0.2 mcg/kg/min as IV infusion. As loading dose can cause further drop in BP, we skipped it and an infusion of 0.05 mcg/kg/min was started.

The patient is stable at present (7 months since transplant), and his present echocardiogram shows good LV function with 61% ejection fraction and no regional wall motion abnormality.

  Conclusion Top

Hemodynamic management of patients with cardiac dysfunction coming for renal transplants is a challenge for anesthesiologist. While adequate fluid administration can be guided by the use of TEE or SVV, levosimendan can be the inotrope of choice.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Martinez BS, Gasanova I, Adesanya AO. Anesthesia for kidney transplantation a review. J Anesth Clin Res 2013;4:270-6.  Back to cited text no. 1
Ojo AO, Hanson JA, Wolfe RA, Leichtman AB, Agodoa LY, Port FK, et al. Long-term survival in renal transplant recipients with graft function. Kidney Int 2000;57:307-13.  Back to cited text no. 2
Muntner P, He J, Hamm L, Loria C, Whelton PK. Renal insufficiency and subsequent death resulting from cardiovascular disease in the United States. J Am Soc Nephrol 2002;13:745-53.  Back to cited text no. 3
Ritz E, McClellan WM. Overview: Increased cardiovascular risk in patients with minor renal dysfunction: An emerging issue with far-reaching consequences. J Am Soc Nephrol 2004;15:513-6.  Back to cited text no. 4
Lindner A, Charra B, Sherrard DJ, Scribner BH. Accelerated atherosclerosis in prolonged maintenance hemodialysis. N Engl J Med 1974;290:697-701.  Back to cited text no. 5
Shulman NB, Ford CE, Hall WD, Blaufox MD, Simon D, Langford HG, et al. Prognostic value of serum creatinine and effect of treatment of hypertension on renal function. Results from the hypertension detection and follow-up program. The Hypertension Detection and Follow-up Program Cooperative Group. Hypertension 1989;13:I80-93.  Back to cited text no. 6
McCarthy PA, Maino DM. Alport syndrome: A review. Clin Eye Vis Care 2000;12:139-50.  Back to cited text no. 7
Srivastava D, Tiwari T, Sahu S, Chandra A, Dhiraaj S. Anaesthetic management of renal transplant surgery in patients of dilated cardiomyopathy with ejection fraction less than 40%. Anesthesiol Res Pract 2014;2014:525969.  Back to cited text no. 8
Bhosale G, Shah V. Combined spinal-epidural anesthesia for renal transplantation. Transplant Proc 2008;40:1122-4.  Back to cited text no. 9
Busse L, Davison DL, Junker C, Chawla LS. Hemodynamic monitoring in the critical care environment. Adv Chronic Kidney Dis 2013;20:21-9.  Back to cited text no. 10
Cleland JG, Nikitin N, McGowan J. Levosimendan:First in a new class of inodilator for acute and chronic severe heart failure. Expert Rev Cardiovasc Ther 2004;2:9-19.  Back to cited text no. 11


  [Table 1]


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