scholarly journals Metabolic Disorders with Kidney Transplant

2020 ◽  
Vol 15 (5) ◽  
pp. 732-742
Author(s):  
Elizabeth Cohen ◽  
Maria Korah ◽  
Glenda Callender ◽  
Renata Belfort de Aguiar ◽  
Danielle Haakinson

Metabolic disorders are highly prevalent in kidney transplant candidates and recipients and can adversely affect post-transplant graft outcomes. Management of diabetes, hyperparathyroidism, and obesity presents distinct opportunities to optimize patients both before and after transplant as well as the ability to track objective data over time to assess a patient’s ability to partner effectively with the health care team and adhere to complex treatment regimens. Optimization of these particular disorders can most dramatically decrease the risk of surgical and cardiovascular complications post-transplant. Approximately 60% of nondiabetic patients experience hyperglycemia in the immediate post-transplant phase. Multiple risk factors have been identified related to development of new onset diabetes after transplant, and it is estimated that upward of 7%–30% of patients will develop new onset diabetes within the first year post-transplant. There are a number of medications studied in the kidney transplant population for diabetes management, and recent data and the risks and benefits of each regimen should be optimized. Secondary hyperparathyroidism occurs in most patients with CKD and can persist after kidney transplant in up to 66% of patients, despite an initial decrease in parathyroid hormone levels. Parathyroidectomy and medical management are the options for treatment of secondary hyperparathyroidism, but there is no randomized, controlled trial providing clear recommendations for optimal management, and patient-specific factors should be considered. Obesity is the most common metabolic disorder affecting the transplant population in both the pre- and post-transplant phases of care. Not only does obesity have associations and interactions with comorbid illnesses, such as diabetes, dyslipidemia, and cardiovascular disease, all of which increase morbidity and mortality post-transplant, but it also is intimately inter-related with access to transplantation for patients with kidney failure. We review these metabolic disorders and their management, including data in patients with kidney transplants.

2020 ◽  
Vol 14 (2) ◽  
pp. 147-152
Author(s):  
Sulaiman MM ◽  
◽  
Shettima J ◽  
Ummate I ◽  
Loskorima U ◽  
...  

Background: Renal allograft recipients develop several complications such as infections and neoplasms. New onset diabetes mellitus is a common transplant complication but rarely coexist with Kaposi sarcoma. Case report: We report the case of a 42-year-old banker who presented with polyuria, polydipsia, polyphagia, weight loss and dark spots in the lower limbs 8 months after he had received a live-related kidney transplant in India. He is not a known diabetic and had no family history of diabetes mellitus. His post-transplant immunosuppressive drugs included Myfortic® (mycophenolate), tacrolimus and prednisolone. At presentation he was wasted, dehydrated and afebrile, with multiple hyperpigmented nodules and plaques in both his lower limbs. Random blood glucose was 38mmol/l, had 2+ glucosuria and no ketones. Biopsy of skin lesions showed features of Kaposi sarcoma. A diagnosis of post-transplant diabetes mellitus and Kaposi sarcoma was made. His treatment included soluble insulin and antibiotics. Tacrolimus was changed to sirolimus and mycophenolate was reduced to 360mg twice daily. Conclusion: Coexistence of diabetes mellitus and karposi sarcoma occurs rarely among kidney transplant recipients. Evaluation of transplant recipient who developed diabetes for malignancies such as karposi sarcoma will improve patient and graft survival.


Author(s):  
Ana M Lopes ◽  
Sofia Teixeira

Summary Molecular alterations of the transcription factor hepatocyte nuclear factor 1B (HNF1B) are associated with systemic disease, with kidney disease and maturity-onset diabetes of the young (MODY) as the most characteristic manifestations. Other features comprise pancreatic exocrine insufficiency, liver and biliary anomalies, and genital tract malformations. HNF1B-associated disease is clinically heterogeneous, and therefore the diagnosis is challenging. The authors describe the case of a 19-year-old man with new-onset diabetes after kidney transplantation (NODAT). The kidney disease presented during fetal life as bilateral hyperechogenic kidneys. Renal function progressively deteriorated during childhood, and at the age of 19, the patient was submitted to a living-kidney transplant. Two weeks after transplant, NODAT developed. Given the young age and normal body weight, NODAT was unexpected, and the possibility of HNF1B-associated disease was considered. Screening for mutations in HNF1B was undertaken, and a known mutation was found. As this case highlights, HNF1B-associated disease should be considered when NODAT unexpectedly develops in young kidney transplant recipients with a suggestive renal disease. Learning points HNF1B anomalies are associated with systemic disease, including kidney disease, diabetes mellitus, pancreatic exocrine insufficiency, liver test abnormalities and genital tract malformations. Phenotype is variable and there are no pathognomonic manifestations, but kidney disease appears to be the most common feature and diabetes the most frequent extra-renal phenotype. Spontaneous gene alterations are common, and the lack of family history should not exclude the diagnosis. HNF1B defects should be considered when NODAT develops in a young adult kidney transplant recipient with a suggestive kidney disease and without extensive risk factors for diabetes. The most appropriate treatment for HNF1B-associated diabetes is not established, but immunosuppressive therapy superimposed on a beta-cell dysfunction seems to determine the need for insulin therapy after a variable period. Immunosupressive regimens free of calcineurin inhibitors should be considered in patients with HNF1B-associated disease to minimize the risk of developing NODAT.


2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii348-iii348
Author(s):  
Claudio Musetti ◽  
Salvatore Terrazzino ◽  
Sarah Cargnin ◽  
Marco Quaglia ◽  
Guido Merlotti ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document