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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2015  |  Volume : 26  |  Issue : 3  |  Page : 589-591
Anesthetic management of renal transplantation in glucose-6-phosphate dehydrogenase-deficient patient

Department of Anaesthesiology and Critical Care, Institute of Kidney Diseases and Research Centre, Civil Hospital Campus, Ahmedabad, Gujarat, India

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Date of Web Publication20-May-2015

How to cite this article:
Shah RB, Shah VR, Butala BP, Parikh GP. Anesthetic management of renal transplantation in glucose-6-phosphate dehydrogenase-deficient patient. Saudi J Kidney Dis Transpl 2015;26:589-91

How to cite this URL:
Shah RB, Shah VR, Butala BP, Parikh GP. Anesthetic management of renal transplantation in glucose-6-phosphate dehydrogenase-deficient patient. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2021 Jun 23];26:589-91. Available from: https://www.sjkdt.org/text.asp?2015/26/3/589/157403
To the Editor ,

Glucose-6-phosphate dehydrogenase (G-6PD) deficiency is the most common enzymatic disorder of red blood cells (RBCs) in humans, affecting nearly 400 million people all over the world. [1] The G-6-PD enzyme catalyzes the first step in the pentose phosphate pathway, which leads to the production of antioxidants. [2] A G6-PD-deficient patient lacks the ability to protect RBC against oxidative stresses from certain drugs, metabolic conditions, infections and ingestion of fava beans.

Patients with end-stage renal disease possess several risk characteristics like cardiovascular diseases, hypertension, diabetes mellitus, problems of dialysis and disturbance in acid-base, electrolytes and fluid balance related to a marked decline in the glomerular filtration rate (GFR). Ischemia reperfusion injury is an inevitable event accompanying renal transplantation. [3] During this period, biochemical and inflammatory events occur within the tissue, leading to reactive oxygen species generation. These free oxygen radicals can precipitate hemolytic crisis in G-6-PD-deficient patients in the presence of other risk factors. Here, we present a 44-year-old male patient with G-6PD deficiency who underwent living related renal transplantation with normal functioning renal graft post-operatively. Our search of literature did not reveal any G-6-PD-deficient patient being anesthetized for renal transplantation.

A 44-year-old male patient weighing 60 kg having chronic kidney disease stage-5 was posted for living related renal transplantation with his wife as the donor. He was diagnosed to have G-6-PD deficiency Class III variant (WHO Classification), i.e. moderate enzyme deficiency (10-60% of normal) with intermittent hemolysis. He was taking tablet nifedipine 5 mg TDS and was on maintenance hemodialysis for seven months. Cardiorespiratory assessment was normal on clinical examination. Normal sinus rhythm was observed on electrocardiography (ECG) and 2-D echocardiography showed 60% ejection fraction with normal left ventricular size and function. Oral tacrolimus and mycophenolate was started the day before surgery and Inj. Methylprednisolone 500 mg intravenous (IV) was given on the day of surgery as part of the immunosuppressant drug protocol. He was dialyzed 24 h before surgery through arteriovenous fistula and his pre-operative laboratory investigation on the day of surgery was as follows: Hb = 11.8 gm%, S. creatinine = 5.5 mg%, RBS = 120 mg%, S. Na = 144 mmol/L, S. K = 4.5 mmol/L. Ceftriaxone 1 g and fluconazole 100 mg were given intravenously as prophylactic antimicrobials.

After pre-medication with fentanyl 200 μg IV, the patient was given balanced general anesthesia. Induction was performed with propofol 150 mg and atracurium 35 mg was given to facilitate endotracheal intubation and was maintained with halothane 0.2-0.8% in an oxygen-nitrous oxide mixture at a 1:1 ratio; additional doses of fentanyl and atracurium were administered as appropriate. Right-sided internal jugular vein was cannulated by Seldinger's technique. Intra-operative monitoring included electrocardiogram (ECG), oxygen saturation (SpO 2 ), non-invasive blood pressure (NIBP), central venous pressure (CVP), end tidal carbon dioxide (EtCO 2 ), airway pressures and temperature. 0.9% normal saline was used as intravenous fluid to maintain CVP at 12-15 mmHg. Twenty percent mannitol 60 g was given during vascular anastamosis. Cold ischemia time and anastamosis time were 60 min and 29 min, respectively. Urine output was established immediately on vascular clamp release and was 350 mL at the end of surgery. The blood loss was 150 mL and 2500 mL of 0.9% normal saline was infused. Surgery lasted for 3.5 h. At the end of surgery, residual neuromuscular blockade was reversed with neostigmine 3 mg and glycopyrrolate 0.4 mg and the trachea was extubated. Tramadol was used for control of post-operative pain. On the first post-operative day, 24-h urine output was 6050 mL and serum creatinine decreased from 8.30 mg/dL to 4.21 mg/dL, indicating normal functioning renal graft.

G-6-PD deficiency is an X-linked, hereditary genetic defect caused by mutations in the G-6PD gene, resulting in protein variants with different levels of enzyme activity. More than 140 mutations of the G-6-PD gene have been identified. The highest frequencies are detected in Africa, Asia, the Mediterranean region and in the Middle East. Usually, most G-6-PDdeficient individuals are asymptomatic throughout their life and are unaware of their status. Four major clinical manifestations in G-6-PDdeficient patients are drug-induced hemolytic anemia, infection-induced hemolytic anemia, congenital non-spherocytic hemolytic anemia and neonatal jaundice.

Apart from optimizing intravascular fluid volume status to maximize kidney perfusion, the anesthetic management in such patients should focus on avoiding the drugs implicated in hemolysis, [2] reducing the surgical stress with adequate analgesia and monitoring for and treating the hemolysis, should it occur. Altikat et al [4] found in their study that, although isoflurane, sevoflurane, diazepam and midazolam had an inhibitory effect on G-6-PD activity in vitro, halothane, ketamine and prilocaine had none. Co-trimoxazole, routinely used for Pneumocystis carinii prophylaxis in renal transplant recipients, was specifically avoided in this patient as it has a definite association with hemolytic crisis in G-6-PD-deficient patients. [2] Nevertheless, it is often difficult to establish which specific drug directly causes hemolytic crisis in vivo in G-6-PD-deficient patients. First, an agent deemed to be safe for some G-6-PD-deficient individuals is not necessarily safe for all patients because pharmacokinetics can vary between individuals. Second, multiple drugs including those for general anesthesia are being administered perioperatively. Third, hemolysis in G-6-PD deficiency is a self-limiting process.

Infection is probably the most typical cause of hemolysis in people with G-6-PD deficiency. Additionally, our patient was on three immunosuppressants peri-operatively to prevent graft rejection. We applied strict aseptic and antiseptic precautions to prevent crossinfection, especially during invasive procedures like endotracheal intubation and central venous catheterization. Opportunistic infections affecting immunosuppressed patients like hepatitis viruses A and B, cytomegalovirus and pneumonia are all notable causes of precipitating hemolytic crisis in G-6-PDdeficient patients.

Hemolysis prevention is paramount for the anesthetic management of such patients, because the clinical consequences after an insult resulting in hemolysis may be extremely variable: From hemolytic anemia to acute renal failure to death in case of massive hemolysis. Three mechanisms have been described to account for hemolytic anemia in transplant recipients: Immunosuppressant drug induced, autoimmune hemolysis and alloimmune hemolysis resulting from donor lymphocytes derived from the allograft (passenger lymphocyte syndrome). Achkar et al [5] found in their prospective analysis that hemolytic anemia after transplantation occurs more frequently in ABO-compatible non-identical renal transplant due to passenger lymphocyte syndrome. Thus, the above factors causing hemolysis should be ruled out before diagnosing hemolysis due to G-6-PD deficiency. No clinical and laboratory evidence of hemolytic crisis were observed on post-operative follow-up for one week in this patient.

In conclusion, although essentially a benign condition, complications of G-6-PD deficiency and its consequences can be serious, which may lead to poor renal prognosis. Early diagnosis of G-6-PD deficiency and essentially preventive treatment by expulsion of oxidizing products, such as drugs and infections, can ensure safe administration of anesthesia and problem-free peri-operative period.

Conflict of interest: None declared.

   References Top

Cappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet 2008;371: 64-74.  Back to cited text no. 1
Luzzatto L, Metha A, Vulliany T. Glucose-6-phosphate dehydrogenase deficiency. In: Scriver CR, Beaudet AL, Sly WS, et al, eds. The metabolic and molecular basis of inherited disease. 8th ed. Columbus: McGraw-Hill; 2001. p. 4517-53.  Back to cited text no. 2
Sprung J, Kapural L, Bourke DL, O'Hara JF Jr. Anesthesia for kidney transplant surgery. Anesthesiol Clin North America 2000;18:919-51.  Back to cited text no. 3
Altikat S, Ciftci M, Buyukokuroglu ME. In vitro effects of some anesthetic drugs on enzymatic activity of human red blood cell glucose-6-phosphate dehydrogenase. Polish J Pharmacol 2002;54:67-71.  Back to cited text no. 4
Achkar R, Chiba AK, Zampieri-Filho JP, Pestana JO, Bordin JO. Hemolytic anemia after kidney transplantation: A prospective analysis. Transfusion 2011;51:2495-9.  Back to cited text no. 5

Correspondence Address:
Dr. Rajkiran B Shah
Department of Anaesthesiology and Critical Care, Institute of Kidney Diseases and Research Centre, Civil Hospital Campus, Ahmedabad, Gujarat
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DOI: 10.4103/1319-2442.157403

PMID: 26022034

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