Diabetes is a major etiologic factor towards chronic kidney disease leading to end stage renal disease causing a major health care burden globally. Prevalence of diabetic kidney disease is almost 25-30% at present, with a progressive rise due to the complex nature of this disease and poor understanding of the patients. Diabetes has been detected in almost half of the USA end stage kidney disease population with higher incidence of Type 1 as compared to Type 2 diabetes [1,2]. Uncontrolled insulin dependent diabetes complicated with chronic kidney disease and an Estimated Glomerular Filtration Rate (GFR) of less than 20ml/min have the following options to undergo:

·   Simultaneous Pancreas Kidney Transplant (SPK)

·    Pancreas Transplant Alone (PTA)

·    Segmental Pancreas And Kidney Transplant (SPKT)

·    Review Of Anti-Diabetic Treatment (RADT)

·     Islet Cell Transplantation (ICT)

·     Pancreas Transplant After Kidney Transplant (PAKT)

The definitive approach to support this particular population is a combined kidney pancreas transplant. Based on this approach this article will outline the basic principles of these transplants, and recipient and donor evaluation in order to assist a renal physician to deal with such a population holistically. Amongst these options, the preferred management is to proceed to SPK transplantation. An ideal candidate for this procedure is the one who has treatment refractory IDDM, along with progressively advancing CKD. A major limitation is the availability of these allografts. As kidney and pancreas transplants are obtained from the deceased donor, there is a longer waiting time compared to those requiring kidney transplantation alone. In some cases, kidneys are obtained from live donors and pancreas from the deceased. Another approach is to take both the allografts from a living donor where a segment of the pancreas is taken along with the kidney. Pancreas transplantation alone is also an option, but it is usually considered in those whose kidney function is substantial either through the functioning renal allograft or from the native kidneys. PTA is not a preferred option with advanced CKD, because the use of immunosuppression to protect pancreatic allograft will expedite deterioration of existing CKD, hastening the need for renal replacement therapy. The recipient will be at risk of needing dialysis or renal allograft soon after pancreas transplantation alone. This will subject him or her to another surgery, putting the existing pancreatic allograft at risk due to procedure related complications. Despite knowing this fact, some centers encourage pancreatic transplantation alone, and put the patient on the list for interval kidney transplant. For SPK transplantation, methods include segmental pancreatic graft from the deceased donor, or a live donor, usually placed on the right side, whereas a donor kidney can be placed on either side. The right side remains favored due to the right ward location of the inferior vena cava, and easier anastomosis with iliac vessels. Pancreatic drainage can be done through the anastomosing duct with the duodenum, stomach, or bladder. Enteric route drainage has resulted into lesser complication rates in terms of leaks and acidosis. Bladder route drainage has an advantage of detecting pancreatic allograft rejection. Islet cell transplantation is a highly specialized technique being practiced in very few centers around the globe. It requires a large number of islet cells procured from a cadaveric donor pool. After processing, these are injected into the portal vein by percutaneous ultrasound guided catheter, without any surgery. All the options mentioned above are possible and are being practiced successfully around the world. SPK is the best option but availability of allografts; local expertise and center capability for performing this procedure are the main deciding factors to adopt the modality. Immunosuppression use is not much different as compared to other solid organ transplant. Anti Thymocyte globulin is used as an induction agent of choice as compared to basiliximab, along with methylprednisolone. Maintenance immunosuppression is preferred to be of tacrolimus based triple therapy with mycophenolate and prednisolone, targeting tacrolimus trough levels of 8 to 10 ng/ml during first three months and then 6 to 8 ng/ml afterwards [3]. 

Complications

Complications are related to surgery, immunosuppression, infection, and rejection. SPK is a complex surgical procedure compared to PAK, PTA, and KTA and carries the highest rate of complications. The most vulnerable period is the first year after these procedures. The following are some of the most the well-known complications [10-13].

·     Post-operative related issues such as wound infection, dehiscence, anastomotic leak which could result in peritonitis, ileus, and intra-abdominal compartment syndrome.

·     Consequences of infection may lead to perpetuation of inflammatory cytokines, resulting in deterioration of the condition further developing Systemic Inflammatory Response Syndrome (SIRS), sepsis and shock leading to grave morbidity and mortality outcomes.

·     Thrombosis of the pancreatic graft, especially pancreatic artery thrombosis. Risk factors include a state of hypotension peri or post operatively and prolonged ischemic time leading to ischemia reperfusion injury and technical issues. It is the most feared complication, and usually happens within the first week post transplantation, while deep venous thrombosis risk is highest in the first month of transplant.

·     Failure of the graft which is usually manifested within the first three months post transplantation, with higher incidence in PTA than with SPK transplant. US reported incidence is 7% and 5% respectively. There is no unanimously agreed definition of this condition. Pancreatic allograft function failure is suspected when the recipient needs insulin for their diabetic control, persistent hyperglycemia and rise of glycosylated hemoglobin with suppressed C peptide level. Rejection is variable, can involve either of the two or both the allografts. Recipient urinary amylase is indicative of pancreatic allograft rejection. Rise in serum creatinine could point towards SPK allograft dysfunction provided both the organs have come from the same donor.

·     Graft failure is dependent on donor and recipient factors. Donor associated risk has been calculated from the scoring system, termed Pancreas Donor Risk Index (PDRI). It is calculated based on the variables which include ethnicity, age, sex, BMI, cause of death, organ preservation time and serum Creatinine. PDRI has an inverse relationship the higher the score, the lower the predicted graft survival [14].

·     Recipient factors which has worse allograft outcome include age more than 45 years, BMI >30 and Afro American descent [15-17].

·    Infection remains an area of concern, especially recurrent urinary tract infections in the case of bladder drained pancreas transplant. Cytomegalovirus (CMV) is a greater risk when the donor is seropositive and the recipient negative, particularly in the setting of multiple immunosuppressive agents and the use of T cell depleting agents such as anti-thymocyte globulin (rATG) which is a commonly used induction agent. Another opportunistic infection based on the degree of immunosuppression is BK Virus, which needs periodic surveillance. Failure to detect this virus in a timely manner may result in loss of both the allografts [18].

·  Hyperglycemia can be of multi factorial etiology and needs to be anticipated pre transplant and monitored closely post transplantation. Detection of the cause is important to rectify and could be a result of graft dysfunction, graft failure, immunosuppressive drugs such as tacrolimus, cyclosporine, steroids, and recurrence of autoimmunity. Calcineurin Inhibitors (CNI) damage beta cells resulting in reduced insulin synthesis and secretion. Steroids cause insulin resistance. Persistence of hyperglycemia at 1-year post transplant is known as New Onset Diabetes after Transplant (NODAT). Tacrolimus is considered more diabetogenic with incidence of 8.4% as compared to cyclosporine having 6% and sirolimus with incidence risk of 6.6%. Not all studies support higher diabetes risk with tacrolimus use [19-23].

·    Metabolic acidosis is a particular concern with pancreatic drainage to the bladder. It is caused by sodium bicarbonate loss resulting in non-anion gap acidosis, hyponatremia, and dehydration. This condition can be managed with high dose supplemental sodium bicarbonate indefinitely, for as long as the pancreatic graft is bladder drained. To avoid this issue most pancreatic transplants are drained enterically. Enteric drainage has the advantage of almost no issues of acidosis and dehydration as were seen in bladder drainage. The advantage of enteric drainage has been supported over bladder drainage from a study published from a single center [21,24,25].

·   Post-transplant Erythrocytosis (PTE) is a condition which is associated with solid organ transplants particularly SPK with bladder drainage. Enteric drainage SPK has solved this issue and it is negligible with this procedure. The most plausible explanation is the euvolemic state of the recipient with enteric drainage, thus no dehydration. The incidence of PTE is 8 to 15% and is suspected with persistent rise of hemoglobin >17g/dl and hematocrit >51% for six months or more, provided there is no element of chronic lung disease or malignancy. This condition is associated with malaise, headache, and thromboembolic events and may result in allograft loss. Angiotensin converting enzyme or receptor inhitor are the main stay of treatment provided all other causes have been ruled out. Venesection is advised if Hb remains more than 18.5g/dl [26-33].

Recipient Workup

Age: The database of United Network for Organ Sharing (UNOS) USA of pancreatic transplant recipients from 1996 to 2012 has shown better graft survival in recipients younger than 50 years and worse in 6o years or older. Patients aged 45-65 years are considered for pancreas transplantation provided there are no significant co-morbidities [36].

eGFR: For patients with type 1 diabetes and eGFR <20ml/min, SPK transplant is a preferred consideration. Otherwise, dialysis dependent candidates are accepted at any point of time, provided they meet the criteria.

Insulin requirement: Insulin dose is calculated, and C peptide levels are measured in order to assess the need and benefit of pancreatic transplant. Pancreas transplantation is considered beneficial in those who are insulin dependent with C peptide <2ng/ml. Generally, it is believed that those who require higher insulin >1 unit/kg/day may not achieve insulin independence post pancreas transplant. The reason being the possibility of insulin resistance or presence of antibodies against insulin producing islet cells. Recurrent episodes of Hypoglycemia, or hypoglycemia unawareness, merit urgent transplantation.

BMI: For SPK transplantation, the acceptable BMI limit is 30. This is less than KTA, which allows transplantation up to BMI 36-40, based on the center. The reason for a lower BMI limit in pancreas recipients is to have a lower risk of complication, better wound healing, less insulin resistance and lower post-transplant diabetes risk [37-39].

The optimum procedure for a particular recipient is planned based on the availability of the organ. Pancreatic drainage whether bladder or enteric is based on the local expertise. There is no difference in survival advantage but in terms of complication enteric drainage is superior to bladder drainage SPK [45-49].

HLA matching

All recipients are screened for Human Leukocyte Antigen (HLA) and antibodies are detected by various sophisticated tests, sensitivity, and specificity of which has been transformed over a period of time. Antigens are defined molecularly through DNA analysis, providing description of antigens at allelic-level. Anti-HLA antibodies are being detected by flow cytometry, solid-phase immunoassays, and single-antigen bead assays such as Luminex. Non-HLA antibodies can also be detected by these assays. Long term graft survival is better with better matched HLA but this advantage vanishes with cold ischemic time of more than 36 hours [50-54].

Donor evaluation

Organ Procurement and Transplant Network (OPTN) suggest that live donors should be interviewed by a social worker and transplant coordinator, followed by psychology and psychiatry team. Clinical assessment must be performed by a physician, transplant surgeon and initiation of laboratory workup based on the details available from the past medical, surgical, family, drug, and social history. A donor must be provided with an independent donor advocate, whose job it is to make sure that the donor has been provided with adequate information including pros and cons of the donation and transparency of the transplant process. After obtaining consent for donation blood grouping, HLA typing, and PRA analysis is commenced. A donor may need to be educated about the paired exchange program [55].

The summary points of Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline on the evaluation and care of living kidney donors (Transplantation 2017) are as follows:

·    There should be a comprehensive screening for active or latent infections including hepatitis viruses, cytomegalovirus and Epstein Barr virus, tuberculosis, and syphilis.

·    Diabetes status must be evaluated meticulously with oral glucose tolerance test and suitability should be assessed on a case-by-case basis, along with other risk factors. Age less than 18 years is a contraindication for donation but there is no upper age limit, provided there are no other risks.

·      Albuminuria >150mg/day is an exclusion criteria for donation [56].

·      Hematuria >10 RBC/ HPF are not accepted but few centers may accept following detailed urological evaluation with cystoscopy and kidney biopsy.

·      Hypertensive donors can be accepted whose blood pressure is controlled with one or two antihypertensive agents without evidence of target organ damage [57].

·      Based on a 2005 survey, the majority of US transplant centers accept a donor with history of nephrolithiasis provided the absence of stones and normal metabolic studies. Metabolic abnormalities associated with stone risk include very low citrate and very high calcium or oxalate [52].

·      Donor BMI criteria is variable among centers [58].

·       Organ donation is contraindicated from individuals with a history of hematologic malignancies, melanoma, choriocarcinoma, monoclonal gammopathy, and testicular, lung, and breast cancers [59].

Follow up of the recipient

Once the allograft recipient is discharged from the hospital, they need close follow up. The frequency of this is guided by local resources and center policy and capabilities. It is usually initially twice a week for three months, then every two weeks for three months, followed by monthly for four to six months. The purpose is to monitor immunosuppressant drug levels and toxicity, inter current illness or opportunistic infection, diabetes monitoring with other electrolytes and early detection of rejection. During this time period the recipient is also assessed for general wellbeing, psychosocial improvement, quality of life and compliance. Meanwhile the recipient can be educated in the importance of compliance and self-care. The concerns of the patient can be addressed, and they are encouraged to report any unusual signs or symptoms immediately.

Conclusion

SPK is currently the best surgical modality for IDDM with advanced CKD. All patients posted for SPK must be eligible, and therefore need thorough evaluation. This surgical modality carries a risk of multiple complications and they need to be fully explained to the patient. Graft failure is the most feared complication. The definition of graft failure varies from different centers, and its prognosis is highly dependent on various donor and recipient factors. However, there are no protocols developed to confirm rejection, and therefore, frequent follow-ups to screen for rejection and other complications are required, and it is a real challenge in terms of diagnosis and management.

Conflict of Interest

There is no conflict of interest to declare.

Funding

There is no funding to declare.

Ethical Approval

No ethical approval is required for review articles.

 References

1.      United States Renal Data System. USRDS 2018 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States. National Institutes of Health, editor, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 2017.

2.        Koye DN, Magliano DJ, Reid CM, Pavkov ME, Steven J, et al. Trends in Incidence of ESKD in People With Type 1 and Type 2 Diabetes in Australia, 2002-2013 (2019) Am J Kidney Dis 73: 300.     http://doi.org/10.1053/j.ajkd.2018.10.005

3.        Chiang JL, Kirkman MS, Laffel LM and Peters AL. Type 1 diabetes through the life span: a position statement of the American Diabetes Association. Diabetes Care (2014) 37: 2034-2054.      https://doi.org/10.2337/dc14-1140

4.        Dean PG, Kukla A, Stegall MD and Kudva YC. Pancreas transplantation (2017) BMJ 357: 1321.

https://doi.org/10.1136/bmj.j1321

5.           https://optn.transplant.hrsa.gov/media/1116/03_pa_graft_failure_definition.pdf

6.    Rickels MR, Stock PG, de Koning EJP, Piemonti L, Prastschke J, et al. Defining Outcomes for β-cell Replacement Therapy in the Treatment of Diabetes: A Consensus Report on the Igls Criteria From the IPITA/EPITA Opinion Leaders Workshop (2018) Transplantation 102: 1479-1486.

https://doi.org/10.1097/TP.0000000000002158

7.    Gruessner AC and Gruessner RW. Pancreas Transplantation of US and Non-US Cases from 2005 to 2014 as Reported to the United Network for Organ Sharing (UNOS) and the International Pancreas Transplant Registry (IPTR) (2016) Rev Diabet Stud 13: 35-58.        https://doi.org/10.1900/RDS.2016.13.35

8.   Axelrod DA, Sung RS, Meyer KH, Wolfe RA and Kufman DB. Systematic evaluation of pancreas allograft quality, outcomes and geographic variation in utilization (2010) Am J Transplant 10: 837-845. https://doi.org/10.1111/j.1600-6143.2009.02996.x

9.     Kandaswamy R, Stock PG, Gustafson SK and Skeans MA, Curry MA, et al. OPTN/SRTR 2016 Annual Data Report: Pancreas (2018) Am J Transplant 18: 114.

https://doi.org/10.1111/ajt.14558

10.   Gruessner AC and Sutherland DE. Pancreas transplants for United States (US) and non-US cases as reported to the International Pancreas Transplant Registry (IPTR) and to the United Network for Organ Sharing (UNOS). In: Clinical Transplants 1997, Cecka JM, Terasaki PI (Eds), UCLA Tissue Typing Laboratory, Los Angeles.

11.     Newell KA, Woodle ES, Millis JM, Piper JB, Huss E, et al. Pancreas transplantation with portal venous drainage and enteric exocrine drainage offers early advantages without compromising safety or allograft function (1995) Transplant Proc 27: 3002-3003.

12.     Monroy-Cuadros M, Salazar A, Yilmaz S and McLaughlin K. Bladder vs enteric drainage in simultaneous pancreas-kidney transplantation (2006) Nephrol Dial Transplant 21: 483.      https://doi.org/10.1093/ndt/gfi252

13.     Sibley RK, Sutherland DE, Goetz F and Michael AF. Recurrent diabetes mellitus in the pancreas iso and allograft. A light and electron microscopic and immunohistochemical analysis of four cases (1985) Lab Invest 53: 132-144.

14.     Axelrod DA, Sung RS, Meyer KH, Wolfe RA and Kaufman. Systematic evaluation of pancreas allograft quality, outcomes and geographic variation in utilization (2010) Am J Transplant 10: 837-845. https://doi.org/10.1111/j.1600-6143.2009.02996.x

15.     Gruessner RW, Dunn DL, Gruessner AC, Matas AJ, Najarian JS, et al. Recipient risk factors have an impact on technical failure and patient and graft survival rates in bladder-drained pancreas transplants (1994) Transplantation 57: 1598-1605.

https://doi.org/10.1097/00007890-199406150-00011

16.     Sampaio MS, Reddy PN, Kuo HT, Poommipant N, Cho YW, et al. Obesity was associated with inferior outcomes in simultaneous pancreas kidney transplant (2010) Transplantation 89: 1117-1125. https://doi.org/10.1097/tp.0b013e3181d2bfb2

17.     Luan FL, Kommareddi M, Cibrik DM, Samaniego M, Ojo AO, et al. Influence of recipient race on the outcome of simultaneous pancreas and kidney transplantation (2010) Am J Transplant 10: 2074-2081.

https://doi.org/10.1111/j.1600-6143.2010.03211.xi

18.     Lipshutz GS, Mahanty H, Feng S, Hirose R, Stock PG, et al. BKV in simultaneous pancreas-kidney transplant recipients: a leading cause of renal graft loss in first 2 years post-transplant (2005) Am J Transplant 5: 366-373.

https://doi.org/10.1111/j.1600-6143.2004.00685.x

19.     Sibley RK, Sutherland DE, Goetz F and Michael AF. Recurrent diabetes mellitus in the pancreas iso- and allograft. A light and electron microscopic and immunohistochemical analysis of four cases (1985) Lab Invest 53: 132.

20.     Tydén G, Reinholt FP, Sundkvist G and Bolinder J. Recurrence of autoimmune diabetes mellitus in recipients of cadaveric pancreatic grafts (1996) N Engl J Med 335: 860-863.      https://doi.org/10.1056/nejm199609193351205

21.     Robertson RP. Islet transplantation as a treatment for diabetes a work in progress (2004) N Engl J Med 350: 694.

22.     Ekberg H, Tedesco-Silva H, Demirbas A, Vitko S, Nashan B, et al. Reduced exposure to calcineurin inhibitors in renal transplantation (2007) N Engl J Med 357: 2562.      https://doi.org/10.1056/nejmoa067411

23.    Johnson C, Ahsan N, Gonwa T, Halloran P, Stegall M, et al. Randomized trial of tacrolimus (Prograf) in combination with azathioprine or mycophenolate mofetil versus cyclosporine (Neoral) with mycophenolate mofetil after cadaveric kidney transplantation (2000) Transplantation 69: 834.     https://doi.org/10.1097/00007890-199805131-00659

24.    Newell KA, Woodle ES, Millis JM, Bruce DS, Cronin DC, et al. Pancreas transplantation with portal venous drainage and enteric exocrine drainage offers early advantages without compromising safety or allograft function (1995) Transplant Proc 27: 3002.

25.    Monroy-Cuadros M, Salazar A, Yilmaz S and McLaughlin K. Bladder vs enteric drainage in simultaneous pancreas-kidney transplantation (2006) Nephrol Dial Transplant 21: 483-487.     https://doi.org/10.1093/ndt/gfi252

26.    Guerra G, Indahyung R, Bucci CM, Magliocca JF, Meier-kriesche, et al. Elevated incidence of posttransplant erythrocytosis after simultaneous pancreas kidney transplantation (2010) Am J Transplant 10: 938-942. https://doi.org/10.1111/j.1600-6143.2010.03012.x

27.     Gaston RS, Julian BA and Curtis JJ. Posttransplant erythrocytosis: an enigma revisited (1994) Am J Kidney Dis 24: 1.

28.     Vlahakos DV, Marathias KP, Agroyannis B and Madias NE. Posttransplant erythrocytosis (2003) Kidney Int 63: 1187-1194.      https://doi.org/10.1046/j.1523-1755.2003.00850.x

29.     Augustine JJ, Knauss TC, Schulak JA, Bodziak KA, Siegel C, et al. Comparative effects of sirolimus and mycophenolate mofetil on erythropoiesis in kidney transplant patients (2004) Am J Transplant 4: 2001-2006.

30.     Kiberd BA. Post-transplant erythrocytosis: a disappearing phenomenon? (2009) Clin Transplant 23: 800-806.

31.     Einollahi B, Lessan-Pezeshki M, Nafar M, Pour-Reza-Gholi F, Firouzan A, et al. Erythrocytosis after renal transplantation: review of 101 cases (2005) Transplant Proc 2 37: 3101-3102. https://doi.org/10.1016/j.transproceed.2005.08.023

32.     Wickre CG, Norman DJ, Bennison A, Barry JM and Bennett. Postrenal transplant erythrocytosis: a review of 53 patients (1983) Kidney Int 23: 731-737.      https://doi.org/10.1038/ki.1983.86

33.     Barenbrock M, Spieker C, Rahn KH and Zidek W. Therapeutic efficiency of phlebotomy in posttransplant hypertension associated with erythrocytosis (1993) Clin Nephrol 40: 241.

34.     Shapiro R, Jordan ML, Scantlebury VP, Vivas CA, Jain A, et al. Renal allograft rejection with normal renal function in simultaneous kidney/pancreas recipients: does dissynchronous rejection really exist? (2000) Transplantation 69: 440-442.

35.  Troxell ML, Koslin DB, Norman D, Rayhill S and mittalhenkle A. Pancreas allograft rejection: analysis of concurrent renal allograft biopsies and posttherapy follow-up biopsies (2010) Transplantation 90: 75-84.   https://doi.org/10.1097/tp.0b013e3181dda17e

36.     Siskind E, Maloney C, Akerman M, Ashburn S, Barlow M, et al. An analysis of pancreas transplantation outcomes based on age groupings-an update of the UNOS database (2014) Clin Transplant 28: 990-994. https://doi.org/10.1111/ctr.12407

37.     Neidlinger N, Singh N, Klein C, Odorico J, Rio del AM, et al. Incidence of and risk factors for posttransplant diabetes mellitus after pancreas transplantation (2010) Am J Transplant 10:3 98-406.

38.     Sampaio MS, Reddy PN, Kuo HT, Poommipanit, Cho YW, et al. Obesity was associated with inferior outcomes in simultaneous pancreas kidney transplant (2010) Transplantation 89: 1117-1125. https://doi.org/10.1097/tp.0b013e3181d2bfb2

39.     Kahn BB and Flier JS. Obesity and insulin resistance (2000) J Clin Invest 106: 473-481.    https://doi.org/10.1172/JCI10842

40.     Gruessner RW, Dunn DL, Gruessner AC, Matas AJ, Najarian JS, et al. Recipient risk factors have an impact on technical failure and patient and graft survival rates in bladder-drained pancreas transplants (1994) Transplantation 57: 1598-1605.

41.     Becker BN, Odorico JS, Becker YT, Groshek M, Werwinski C, et al. Simultaneous pancreas-kidney and pancreas transplantation (2001) J Am Soc Nephrol 12: 2517-2527.

42.     Douzdjian V, Abecassis MM, Corry RJ and Hunsicker LG. Simultaneous pancreas-kidney versus kidney-alone transplants in diabetics: increased risk of early cardiac death and acute rejection following pancreas transplants (1994) Clin Transplant 8: 246.

43.    Manske CL, Thomas W, Wang Y and Wilson RF. Screening diabetic transplant candidates for coronary artery disease: identification of a low risk subgroup (1993) Kidney Int 44 :617-621.     https://doi.org/10.1038/ki.1993.289

44.    Ohtake T, Kobayashi S, Moriya H, Negishi K, Okomoto K, et al. High prevalence of occult coronary artery stenosis in patients with chronic kidney disease at the initiation of renal replacement therapy: an angiographic examination (2005) J Am Soc Nephrol 16: 1141-1148.      https://doi.org/10.1681/asn.2004090765

45.    Mai ML, Ahsan N and Gonwa T. The long-term management of pancreas transplantation (2006) Transplantation 82: 991-1003.     https://doi.org/10.1097/01.tp.0000238666.60361.3d

46.    Gaber AO, Shokouh-Amiri MH, Hathaway DK, Hammontree L, Kitabchi AE, et al. Results of pancreas transplantation with portal venous and enteric drainage (1995) Ann Surg 221: 613.      https://doi.org/10.1097/00000658-199506000-00001

47.    Kuo PC, Johnson LB, Schweitzer EJ and Bartlett ST. Simultaneous pancreas/kidney transplantation a comparison of enteric and bladder drainage of exocrine pancreatic secretions (1997) Transplantation 63: 238-243. https://doi.org/10.1097/00007890-199701270-00011

48.  Bloom RD, Olivares M, Rehman L, Raja RM, Yang S, et al. Long-term pancreas allograft outcome in simultaneous pancreas-kidney transplantation: a comparison of enteric and bladder drainage (1997) Transplantation 64: 1689-1965. https://doi.org/10.1097/00007890-199712270-00010

49.     Demartines N, Schiesser M and Clavien PA. An evidence-based analysis of simultaneous pancreas-kidney and pancreas transplantation alone (2005) Am J Transplant 5: 2688-2697.     https://doi.org/10.1111/j.1600-6143.2005.01069.x

50.     Fuggle SV and Martin S. Tools for human leukocyte antigen antibody detection and their application to transplanting sensitized patients (2008) Transplantation 86: 384-390.     https://doi.org/10.1097/tp.0b013e31817c90f5

51.     Gebel HM and Bray RA. HLA antibody detection with solid phase assays: great expectations or expectations too great? (2014) Am J Transplant 14: 1964-1975.      https://doi.org/10.1111/ajt.12807

52.     Tait BD, Süsal C, Gebel HM, Peter WN, Andrea AZ Zachary et al. Consensus guidelines on the testing and clinical management issues associated with HLA and non-HLA antibodies in transplantation (2013) Transplantation 95: 19-47. 

53.     Cecka JM and Terasaki PI. The UNOS Renal Transplant Registry. In: Clinical Transplants 1993, Terasaki PI, Cecka JM (Eds), UCLA Tissue Typing Laboratory, Los Angeles.

54.     Takemoto SK, Terasaki PI, Gjertson DW and Cecka JM. Twelve years' experience with national sharing of HLA-matched cadaveric kidneys for transplantation (2000) N Engl J Med 343: 1078-1084.  https://doi.org/10.1056/nejm200010123431504

55.     OPTN (Organ Procurement and Transplantation Network)/UNOS (United Network for Organ Sharing). OPTN Policies, Policy 14: Living Donation.

56.     Mandelbrot DA, Pavlakis M, Danovitch GM, Johnson HR, Krap SJ, et al. The medical evaluation of living kidney donors: a survey of US transplant centers (2007) Am J Transplant 7: 2333-2343. https://doi.org/10.1111/j.1600-6143.2007.01932.x

57.     Lentine KL, Kasiske BL, Levey AS, Adams PL, Alberú J, et al. KDIGO Clinical Practice Guideline on the Evaluation and Care of Living Kidney Donors (2017) Transplantation 101: S109.      https://doi.org/10.1097/TP.0000000000001769

58.      Naik A, Cibrik D, Sakhuja A and Lentine K. Temporal trends and variation in BMI thresholds for living donation across the US.

59.     Zhang S, Yuan J, Li W and Ye Q. Organ transplantation from donors (cadaveric or living) with a history of malignancy: review of the literature Transplant Rev (2014) Am J Transplant 3: 349.      https://doi.org/10.1016/j.trre.2014.06.002

 Corresponding author

Dr. Akbar Mahmood, MRCP, PG dip Renal Transplant, Liverpool University, Certificate in Medicine (KSA) Renal Consultant Bradford Royal Infirmary Hospital Bradford, UK, Tel: +447830630475, Email: drakbar696@hotmail.com

Citation

Mahmood A, Lawati HAA and Czajka R. Kidney pancreas transplant, a brief comprehension to care (2020) J Obesity and Diabetes 4: 15-20. 

Keywords

Insulin dependent diabetes mellitus, Chronic kidney disease, Kidney pancreas transplant.