New Onset Diabetes After Transplant (NODAT)


Article Author:
Mahdis Solhjoo


Article Editor:
Salini Kumar


Editors In Chief:
Stephen Leslie
Karim Hamawy


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
7/5/2019 11:35:04 PM

Introduction

New-onset diabetes mellitus after transplantation (NODAT) is the occurrence of diabetes mellitus (DM) in a previously nondiabetic person after solid organ transplantation. NODAT frequently occurs after organ transplantation and increases the risk of infection and mortality rates.[1][2]

Etiology

Patients who have pre-existing risk factors for type 2 DM are more prone to develop NODAT. NODAT risk factors subclassify into two groups of nonmodifiable and modifiable risk factors.

Nonmodifiable risk factors:

Age:

Age is among the greatest risk factors in the development of NODAT. Studies demonstrated that the incidence of NODAT is 2.2 times higher in transplant recipients who are more than 45 years of age compared to younger adults.

Ethnicity:

NODAT is more common in the Black and Hispanic population compared to the White population. This difference in the incidence of NODAT can be due to the genetic diversity and variable effects of immunosuppressive agents on various ethnicities. As an example, tacrolimus has been reported to be a more potent cause of NODAT in the Black population. 

Family history of DM and genetic:

Genetic factors are known to be important in NODAT. Based on the evidence, NODAT is more common in people with a history of diabetes in their first-degree relatives. Development of NODAT has genetic links to the alleles human leukocyte antigen (HLA) A28, A30, B27, and Bw42. The association between single nucleotide polymorphisms (SNPs) and risk for NODAT has documentation in multiple studies. Also, studies show that the association of the R325W polymorphism in the SLC30A8 zinc transporter gene, with the R/r inheritance, relates to a higher risk of NODAT. Other specific gene variants which are associations with NODAT are KCNQ1, TCF7L2, KCNJ11-Kir6.2, and NFATc4. TCF7L2. These variants relate to impaired insulin secretion and an accelerated rate of gluconeogenesis. Pathogenesis of NODAT in kidney transplant recipients demonstrates a relationship to significant variations of IL-7R, IL-17E, IL-17R, and IL-17RB.

Pre-diabetes status:

Abnormal glucose tolerance is another risk factor for NODAT. Patients with pre-diabetic conditions such as fasting blood sugar levels between 90 and 100 mg/dL need to be monitored closely post-transplant and advised on lifestyle modifications to avoid weight gain which on its own can tip the patient to develop diabetes mellitus. 

Modifiable risk factors:

Obesity:

Obesity confers a significant modifiable risk factor for the development of NODAT. It acts by upregulating of inflammatory markers and C-reactive protein levels. Adipose tissue increases the production of tumor necrosis factor-alpha (TNF-alpha), which causes defects in the phosphorylation of the glucose receptor and decreases the expression of insulin-sensitive glucose transporters. This mechanism leads to insulin resistance and DM. Furthermore, adipose tissue induces IL-6 synthesis, which is associated with glucose intolerance. Increasing in adipose tissue results in the reduction of adiponectin, a hormone which reduces the risk of DM. In transplant recipients, the level of adiponectin is low before transplant, which in turn is a risk factor to develop NODAT. 

Post-transplant medications:

Corticosteroids are traditionally associated with hyperglycemia and DM by decreasing the peripheral insulin sensitivity, inhibiting pancreatic insulin production and secretion, increasing hepatic gluconeogenesis, and promoting protein degradation to free amino acids in muscles. The diabetogenic effect of corticosteroids in developing NODAT has been suggested to be related to both the dosage and the duration of therapy. In general, post-transplant steroid therapy increases the risk of NODAT by 42%. While a steroid-free regimen reduces the NODAT risk, glucose tolerance can significantly improve by reducing the daily dose of prednisone to 5 mg or lower post-transplantation. Using a higher dosage of prednisolone, such as 0.01 mg/kg/day will increase the risk of NODAT by 5%. Calcineurin inhibitors (CNI) are given to most transplant recipients and is associated with hyperglycemia. CNI reduces the number of glucose transporter type 4 (GLUT-4) receptor molecules on the adipocytes. GLUT-4 is an insulin-regulated protein, and its task is to transport the glucose into adipocytes and striated muscle cells. A decrease in the number of GLUT-4 receptors leads to a reduction of glucose uptake by these cells, which resultant hyperglycemia. Also, CNIs decreases the pancreatic beta-cell density by interfering with the activated T-cell signaling in pancreatic beta-cells. As a result, this pathway activates the mutated genes responsible for DM and leads to reduced insulin synthesis. Studies report that the incidence of NODAT is significantly higher in patients who got treatment with tacrolimus when compared to those who have had therapy with cyclosporine. Tacrolimus acts by inhibiting T-cell activity, which results in inhibition of interleukin-2 synthesis, and leads to a failure of T-cell production. Beyond the mechanism mentioned above, tacrolimus also causes hyperglycemia by reducing glucokinase activity in pancreatic islets leading to suppression of glucose-induced insulin release. The effect of tacrolimus in the development of glucose intolerance is reversible with drug discontinuation. Sirolimus is another immunosuppressant which has been associated with NODAT, especially when used in combination with CNI. There is no known recognized association between mycophenolate mofetil and azathioprine use and the development of NODAT.

Hypomagnesemia :

Hypomagnesemia after transplant is another risk factor for NODAT. CNIs can induce hypomagnesemia by inhibition of the renal magnesium transporter, resulting in renal magnesium wasting.

Viral infections:

 Infection and inflammation are two other factors which contribute to glucose intolerance and the development of DM. HCV infection has a diabetogenic effect by causing insulin resistance and decreasing hepatic glucose uptake and glycogenesis. Also, HCV has a cytopathic effect on pancreatic beta cells. Studies show that the incidence of NODAT is 25.6% in those who are HCV-positive while it is 14.4% in those with no HCV infection.[3][4][5][6][7][8] Antiviral therapy has been a recommended approach before transplant, but it is still unclear whether the response to therapy can improve glycemic control. Using tacrolimus in patients with HCV aggravates the risk of NODAT. Active cytomegalovirus (CMV) infection decreases the insulin secretion by impairing the pancreatic beta cells. CMV can induce cytokines release, which leads to apoptosis and mal-functioning of pancreatic beta-cells. As a result, CMV can predispose the patients to NODAT.[9][10][11][12]

Epidemiology

NODAT is more common in Black and Hispanic patients compared to Whites, which might be because of genetic polymorphisms among Black and Hispanic transplant recipients. NODAT incidence in the United States has been reported to be about 9.1% of patients at 3 months, 16% at 12 months, and 24% at 36 months post-transplantation. Also, NODAT has been estimated to occur in about 4 to 25% of renal transplants, 2.5 to 25% of liver transplants, 4 to 40% of heart transplants, and 30 to 35% of lung transplant recipients. The risk of NODAT increases in liver transplant if the patient has an HCV infection and can range between 40% and 60%. Some studies report the range of NODAT to be from 7% to 30% in the first year after the kidney transplantation. Also, the majority of organ recipients (about 76.5%) develop NODAT in the first 3 months. After 6 months, the incidence of DM is almost the same as the patients with no transplant. Using higher doses of immunosuppressive medications after transplant correlates with a higher incidence of NODAT.[13][14][15]

Pathophysiology

The pathophysiology of NODAT is almost as same as type 2 DM: increase in insulin resistance and decrease in insulin secretion. In NODAT, insulin hyposecretion seems to have a more important role in glucose intolerance. NODAT more likely occurs in patients who have other risk factors in developing DM type 2. Immunosuppression regimen is one of the leading causes of NODAT; this acts by affecting the insulin secretion and action.[16]

History and Physical

As with DM, most patients with NODAT are asymptomatic. The detection of many patients will be due to inpatient glucose monitoring and hyperglycemia on laboratory tests after transplant surgery. Hence, glucose testing is in the recommendations for post-transplant screening in all transplant patients; this can result in early detection of NODAT. Symptoms are the same as in non-transplant DM patients and include polyuria, polydipsia, polyphagia, weight loss, blurry vision, neuropathy, numbness of extremities, and symptoms of infection.  The physical exam includes vital signs, the extent of hydration, funduscopic eye exam, vascular and neurologic examinations, and a foot assessment. The physical examination findings might be unrevealing, although observable end-organ damage may occur.

Evaluation

NODAT is predictable by evaluation of the risk factors such as pre-diabetic status and obesity. Some studies suggest that assessment of pre-operative insulin resistance, insulin sensitivity, and beta cell function (c-peptide levels) may be helpful to predict NODAT, but remains unconfirmed by other studies.

Guidelines that define the criteria for the diagnosis of NODAT are identical to the diagnostic criteria in DM:

  • Symptoms of diabetes and random plasma glucose greater than or equal to 200 mg/dL (11.1 mmol/L)
  • Fasting plasma glucose greater than or equal to 126 mg/dL (7.0 mmol/L) which requires repetition on another day
  • Two-hour plasma glucose greater than or equal to 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test (OGTT)

OGTT is the gold standard for NODAT diagnosis, especially in the early stages of transplantation. Because of the reduction of red blood cell survival after transplant, the diagnosis of NODAT based on HbA1c is not accurate in the first 3 months after the transplantation and is therefore not recommended. Beyond 3 months, the new hemoglobin would be synthesized and glycated for the appropriate period, and HbA1c greater than or equal to 6.5 percent can be utilized to diagnose NODAT. Even many studies don't recommend HbA1c alone as a screening tool for NODAT in the first year after transplant.[3][17][18][12][19]

Early detection of NODAT is helpful as it reduces risk and complications of DM. The recommendation is for post-transplantation screening for NODAT in all patients undergoing solid organ transplants. Transplantation centers perform the screening tests weekly in the first month and continue screening at months 3, 6, and 12 post-transplantation. After the first year, the risk of NODAT is lower, and the recommendation is for yearly screening.[8]

Treatment / Management

Some of the factors that induce post-transplant hyperglycemia are postoperative surgical stress, pain, and high doses of immunosuppressants. Early detection of hyperglycemia is crucial because early optimization of inpatient plasma glucose has a beneficial effect on the long-term patient and graft survival. The goals for management is adequate glycemic control to minimize the hyperglycemia complications. The first steps for glycemic control should focus on non-pharmacological factors that elevate blood glucose. These steps include switching from more diabetogenic immunosuppressants to the less diabetogenic ones or alter the dose of the immunosuppressants with the view of optimizing glycemic control, e.g., reducing corticosteroid dose. Sometimes by simply tapering the corticosteroids soon after transplant can control without medical therapy.

However, the clinicians should be thoughtful about the possibility of acute rejection. If lifestyle modification and immunosuppressants adjustment are insufficient to control the hyperglycemia, then pharmacotherapy should be initiated. Significant numbers of the patients require insulin therapy to manage postoperative hyperglycemia while in the hospital. In hospitalized patients, as a result of frequent changes in immunosuppressants doses and varying nutritional intake, fluctuations of blood glucose level is common. Intravenous (IV) insulin is a good initial choice since it is easily titratable, which results in tight plasma glucose control and is safe, particularly post-transplant when graft function is still unstable. Choosing between insulin and oral hypoglycemic agents depends on the severity of hyperglycemia. Based on the IV insulin infusion requirement, subcutaneous insulin doses can be calculated after proper glycemic control or upon discharge. Oral hypoglycemic therapy at the time of discharge is an option in patients who required low-dose insulin therapy in the inpatient setting. There are no drug-drug interactions between immunosuppressants and oral antidiabetic agents. 

Metformin is one of the more popular agents which improves insulin sensitivity. Often the glomerular filtration rate increases adequately with well-functioning grafts so it can be used safely for most patients and is the first-line oral agent in NODAT management. Sulfonylureas enhance insulin secretion and are used in NODAT extensively. Their side effects can be post-transplant weight gain and hypoglycemia. Thiazolidinediones are selective agonists of the peroxisomal proliferator-activated receptor gamma and improve glucose tolerance and insulin sensitivity in NODAT. Thiazolidinediones are contraindicated in congestive heart failure and should be used with caution if there is graft malfunction. Repaglinide is a safe drug among the meglitinides and acts by inducing insulin secretion. Dipeptidyl peptidase-4 (DPP-4) antagonists act by inhibition of the degradation of glucagon-like peptide 1, which results in pancreatic insulin secretion. Among the DPP-4 antagonists, sitagliptin is a good choice in NODAT. Using incretin-based therapy such as vildagliptin and sitagliptin needs to be avoided in liver impairment, and renal insufficiency; their safety in NODAT is still under study.

Because the transplant patients are at increased risk of hypoglycemia and frequently have a concurrent history of heart disease, guidelines recommend an HbA1c goal of 7 to 7.5% in these patients. Studies demonstrated that in patients with hypertension and congestive heart failure, using ACEIs or ARBs has a significant role in reducing the incidence of NODAT. Treatment of infections such as HCV should be a consideration before transplant.[20][18][8][7][12]

Differential Diagnosis

  • Diabetes mellitus
  • Stress hyperglycemia

Prognosis

NODAT outcome is affected by different factors, including the type of organ transplant, age, obesity, other cardiovascular risk factors, and immunosuppressants. Studies show a higher mortality rate in patients with NODAT compared to those with type 2 DM. NODAT decreases patient survival by increasing both cardiovascular events and the risk of infections. NODAT is associated with a higher prevalence of rejection and post-transplant renal failure. Studies showed that graft survival in patients with NODAT was 48% while it was 70% in a patient without NODAT. Also, studies demonstrate that in kidney transplant recipients, cardiovascular events are 2 to 3 fold more in NODAT in compare with other patients. Additionally, diabetic microvascular complications develop rapidly in patients with NODAT than traditional DM.[21][22][18]

Complications

NODAT can cause similar complications to traditional DM, including neuropathy, ophthalmopathy, nephropathy, ketoacidosis, and episodes of hypoglycemia. Even though these manifestations are similar to DM, the rate at which they occur is remarkably accelerated. Other than the increased risk of transplant rejection, there is a higher incidence of infection and late cardiovascular events, which leads to a higher mortality rate.[16][2][13]

Consultations

  • Endocrinologists
  • Ophthalmologists
  • Podiatrists
  • Cardiologists
  • Nephrologists
  • Dietitians
  • Diabetic nurse educator

Deterrence and Patient Education

NODAT management should ideally start before the organ transplant. Pre-transplant patients should receive counseling regarding the risk factors of developing NODAT and the ways to prevent it. Attention to avoid weight gain is an established step to prevent NODAT. Weight loss can prevent NODAT in overweight patients with prediabetic status. In high-risk groups such as obese patients, the goal should include weight loss with diet and increasing physical activity with target weight loss of 5% to 10% of total body weight and following up with the dietitian before and after transplant. Patients should be recommended to have healthy low-calorie and a low-fat diet. Although, weight loss immediately after transplant is not a recommended approach, as it will delay wound healing.

After being diagnosed with NODAT, as with DM, self-glucose monitoring, and compliance with treatment are essential. Also, patients should be aware of the importance of an annual eye exam, which is even more important than in traditional diabetes patients. NODAT patients are prone to have an acceleration of cataracts due to the universal use of both corticosteroid and immunosuppressants. Foot exams should be part of every clinical visit. Immunosuppressants place NODAT patients at increased risk of different infections, so compliance with annual influenza and pneumococcal vaccines are critical in this population. Those patients who desire to get pregnant should be encouraged to wait at least for 1 year after the transplantation to decrease the risk of rejection. The transplant team should be involved in all stages before, during, and after pregnancy to reduce the comorbidities on both mother and baby.[3][18]

Enhancing Healthcare Team Outcomes

Coordination of care among all team members including nurses, internists, nutritionists, surgeons, endocrinologists, nephrologists and, infectious disease specialists is an essential factor in the management of pre-existing diabetes or NODAT in transplant patients. Adequate blood glucose control, as well as treatment of comorbidities, is the backbone in the management of NODAT as it increases patient survival and decreases the risk of graft rejection. Selecting the right immunosuppressants with the appropriate dose is one of the steps to prevent NODAT, but the risk of developing diabetes after transplantation should be weighed against the risk of transplant rejection. At the time of discharge, its the responsibility of each caring team to explain the above to the patient. Also, education coordination by the nurses and clinicians of the patient and the family about the medical therapies and their side effects is critical as it can impact the patient survival.[3][7] [Level I]

Diagnosis and management of NODAT require an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results. Clinicians (MDs, DOs, NPs, PAs) will typically be the ones to diagnose the condition and order the lab tests. They will also place the initial orders for therapeutic management, which nursing will administer. Nursing will also be responsible for monitoring patient response and serum glucose, documenting and reporting back to the prescribing clinician. Pharmacists can make medication recommendations based on the patient's current drug profile, comorbid conditions, and also verify dosing, and report recommendations to the nurses or prescribers. [Level V]


Interested in Participating?

We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE activities, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 500 specialties.

Improve Content - Become an Author or Editor

This is an academic project designed to provide inexpensive peer-reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team.

New Onset Diabetes After Transplant (NODAT) - Questions

Take a quiz of the questions on this article.

Take Quiz
A 32-year-old female with a history of end-stage renal disease and systemic lupus erythematosus is undergoing a kidney transplant. Her only medication is hydroxychloroquine. Her vital signs are within normal limits while her BMI is 32. After the transplant, her blood glucose level ranges between 240-324 mg/dL. New-onset diabetes mellitus after transplantation (NODAT) has diagnosed in the patient. Which of the following is most accurate about the patient's condition?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 55-year-old white female with a history of hypertension, dyslipidemia, and, end-stage renal disease is being evaluated for a kidney transplant. Her medications are aspirin, metoprolol, atorvastatin, and vitamin D. After the surgery, her blood glucose increases to 324 mg/dL and intravenous insulin therapy is started for the glucose control. Which of the following medications is known to increase blood glucose after transplant?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up

New Onset Diabetes After Transplant (NODAT) - References

References

Lane JT,Dagogo-Jack S, Approach to the patient with new-onset diabetes after transplant (NODAT). The Journal of clinical endocrinology and metabolism. 2011 Nov;     [PubMed]
Nie H,Wang W,Zhao Y,Zhang X,Xiao Y,Zeng Q,Zhang C,Zhang L, New-Onset Diabetes After Renal Transplantation (NODAT): Is It a Risk Factor for Renal Cell Carcinoma or Renal Failure? Annals of transplantation. 2019 Feb 4;     [PubMed]
Lima C,Grden A,Skare T,Jaworski P,Nisihara R, Risk factors for new-onset diabetes mellitus after kidney transplantation (NODAT): a Brazilian single center study. Archives of endocrinology and metabolism. 2018;     [PubMed]
Gupta S,Pollack T,Fulkerson C,Schmidt K,Oakes DJ,Molitch ME,Wallia A, Hyperglycemia in the Posttransplant Period: NODAT vs Posttransplant Diabetes Mellitus. Journal of the Endocrine Society. 2018 Nov 1;     [PubMed]
Ye X,Kuo HT,Sampaio MS,Jiang Y,Bunnapradist S, Risk factors for development of new-onset diabetes mellitus after transplant in adult lung transplant recipients. Clinical transplantation. 2011 Nov-Dec;     [PubMed]
Davidson J,Wilkinson A,Dantal J,Dotta F,Haller H,Hernández D,Kasiske BL,Kiberd B,Krentz A,Legendre C,Marchetti P,Markell M,van der Woude FJ,Wheeler DC, New-onset diabetes after transplantation: 2003 International consensus guidelines. Proceedings of an international expert panel meeting. Barcelona, Spain, 19 February 2003. Transplantation. 2003 May 27;     [PubMed]
Peev V,Reiser J,Alachkar N, Diabetes mellitus in the transplanted kidney. Frontiers in endocrinology. 2014;     [PubMed]
Palepu S,Prasad GV, New-onset diabetes mellitus after kidney transplantation: Current status and future directions. World journal of diabetes. 2015 Apr 15;     [PubMed]
Shabir S,Jham S,Harper L,Ball S,Borrows R,Sharif A, Validity of glycated haemoglobin to diagnose new onset diabetes after transplantation. Transplant international : official journal of the European Society for Organ Transplantation. 2013 Mar;     [PubMed]
Shivaswamy V,Boerner B,Larsen J, Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes. Endocrine reviews. 2016 Feb;     [PubMed]
Ghisdal L,Baron C,Le Meur Y,Lionet A,Halimi JM,Rerolle JP,Glowacki F,Lebranchu Y,Drouet M,Noël C,El Housni H,Cochaux P,Wissing KM,Abramowicz D,Abramowicz M, TCF7L2 polymorphism associates with new-onset diabetes after transplantation. Journal of the American Society of Nephrology : JASN. 2009 Nov;     [PubMed]
Tavira B,Coto E,Díaz-Corte C,Ortega F,Arias M,Torres A,Díaz JM,Selgas R,López-Larrea C,Campistol JM,Ruiz-Ortega M,Alvarez V, KCNQ1 gene variants and risk of new-onset diabetes in tacrolimus-treated renal-transplanted patients. Clinical transplantation. 2011 May-Jun;     [PubMed]
Kim YG,Ihm CG,Lee TW,Lee SH,Jeong KH,Moon JY,Chung JH,Kim SK,Kim YH, Association of genetic polymorphisms of interleukins with new-onset diabetes after transplantation in renal transplantation. Transplantation. 2012 May 15;     [PubMed]
Bayés B,Lauzurica R,Granada ML,Serra A,Bonet J,Fontseré N,Salinas I,Romero R, Adiponectin and risk of new-onset diabetes mellitus after kidney transplantation. Transplantation. 2004 Jul 15;     [PubMed]
Spranger J,Kroke A,Möhlig M,Bergmann MM,Ristow M,Boeing H,Pfeiffer AF, Adiponectin and protection against type 2 diabetes mellitus. Lancet (London, England). 2003 Jan 18;     [PubMed]
Bayés B,Granada ML,Pastor MC,Lauzurica R,Salinas I,Sanmartí A,Espinal A,Serra A,Navarro M,Bonal J,Romero R, Obesity, adiponectin and inflammation as predictors of new-onset diabetes mellitus after kidney transplantation. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons. 2007 Feb;     [PubMed]
Boudreaux JP,McHugh L,Canafax DM,Ascher N,Sutherland DE,Payne W,Simmons RL,Najarian JS,Fryd DS, The impact of cyclosporine and combination immunosuppression on the incidence of posttransplant diabetes in renal allograft recipients. Transplantation. 1987 Sep;     [PubMed]
Revanur VK,Jardine AG,Kingsmore DB,Jaques BC,Hamilton DH,Jindal RM, Influence of diabetes mellitus on patient and graft survival in recipients of kidney transplantation. Clinical transplantation. 2001 Apr;     [PubMed]
Chakkera HA,Weil EJ,Castro J,Heilman RL,Reddy KS,Mazur MJ,Hamawi K,Mulligan DC,Moss AA,Mekeel KL,Cosio FG,Cook CB, Hyperglycemia during the immediate period after kidney transplantation. Clinical journal of the American Society of Nephrology : CJASN. 2009 Apr;     [PubMed]
Pham PT,Pham PM,Pham SV,Pham PA,Pham PC, New onset diabetes after transplantation (NODAT): an overview. Diabetes, metabolic syndrome and obesity : targets and therapy. 2011;     [PubMed]
Ghisdal L,Van Laecke S,Abramowicz MJ,Vanholder R,Abramowicz D, New-onset diabetes after renal transplantation: risk assessment and management. Diabetes care. 2012 Jan;     [PubMed]
Kumar S,Sanyal D,Das P,Bhattacharjee K,Rungta R, An observational Prospective Study to Evaluate the Preoperative Risk Factors of New-onset Diabetes Mellitus after Renal Transplantation in a Tertiary Care Centre in Eastern India. Indian journal of endocrinology and metabolism. 2018 Sep-Oct;     [PubMed]

Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of Surgery-Urologic. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for Surgery-Urologic, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in Surgery-Urologic, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of Surgery-Urologic. When it is time for the Surgery-Urologic board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study Surgery-Urologic.