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1.
Early Post-Renal Transplant Hyperglycemia.
Iqbal, A, Zhou, K, Kashyap, SR, Lansang, MC
The Journal of clinical endocrinology and metabolism. 2022;(2):549-562
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Abstract
CONTEXT Though posttransplant diabetes mellitus (PTDM, occurring > 45 days after transplantation) and its complications are well described, early post-renal transplant hyperglycemia (EPTH) (< 45 days) similarly puts kidney transplant recipients at risk of infections, rehospitalizations, and graft failure and is not emphasized much in the literature. Proactive screening and management of EPTH is required given these consequences. OBJECTIVE The aim of this article is to promote recognition of early post-renal transplant hyperglycemia, and to summarize available information on its pathophysiology, adverse effects, and management. METHODS A PubMed search was conducted for "early post-renal transplant hyperglycemia," "immediate posttransplant hyperglycemia," "post-renal transplant diabetes," "renal transplant," "diabetes," and combinations of these terms. EPTH is associated with significant complications including acute graft failure, rehospitalizations, cardiovascular events, PTDM, and infections. CONCLUSION Patients with diabetes experience better glycemic control in end-stage renal disease (ESRD), with resurgence of hyperglycemia after kidney transplant. Patients with and without known diabetes are at risk of EPTH. Risk factors include elevated pretransplant fasting glucose, diabetes, glucocorticoids, chronic infections, and posttransplant infections. We find that EPTH increases risk of re-hospitalizations from infections (cytomegalovirus, possibly COVID-19), acute graft rejections, cardiovascular events, and PTDM. It is essential, therefore, to provide diabetes education to patients before discharge. Insulin remains the standard of care while inpatient. Close follow-up after discharge is recommended for insulin adjustment. Some agents like dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 receptor agonists have shown promise. The tenuous kidney function in the early posttransplant period and lack of data limit the use of sodium-glucose cotransporter 2 inhibitors. There is a need for studies assessing noninsulin agents for EPTH to decrease risk of hypoglycemia associated with insulin and long-term complications of EPTH.
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Hypercalcemia associated with Pneumocystis jirovecii pneumonia in renal transplant recipients: case report and literature review.
Coche, S, Cornet, G, Morelle, J, Labriola, L, Kanaan, N, Demoulin, N
Acta clinica Belgica. 2021;(1):75-78
Abstract
Background: Pneumocystis jirovecii associated pneumonia is a potentially life-threatening opportunistic infection, occurring most frequently in the first year after renal transplantation, and may be associated with hypercalcemia. Clinical presentation:We report the case of a renal transplant recipient presenting with Pneumocystis jirovecii associated pneumonia and hypercalcemia due to ectopic production of 1,25-dihydroxyvitamin D, 6 years after renal transplantation. Calcemia and 1-25 hydroxyvitamin D levels normalized after our patient was treated by trimethoprim-sulfamethoxazole. Discussion: We review similar cases to delineate the clinical and biological profile of patients with Pneumocystis jirovecii pneumonia associated hypercalcemia. Conclusion:Physicians should evoke this diagnosis in renal transplant recipients presenting with pulmonary infection associated with hypercalcemia.
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3.
Effectiveness and Safety of Bariatric Surgery in Patients with End-Stage Chronic Kidney Disease or Kidney Transplant.
Guggino, J, Coumes, S, Wion, N, Reche, F, Arvieux, C, Borel, AL
Obesity (Silver Spring, Md.). 2020;(12):2290-2304
Abstract
OBJECTIVE This study aimed to evaluate (1) the effectiveness, complications, and postoperative access to transplantation in end-stage chronic kidney disease (ECKD) and (2) the effectiveness and complications of bariatric surgery in patients who had already undergone kidney transplant. METHODS A systematic review and meta-analysis of mortality and complications rates were performed. Thirty studies were reviewed. RESULTS After bariatric surgery, patients with ECKD had similar postoperative weight loss to patients from the general population. Meta-analysis showed post-bariatric surgery rates of 2% (95% CI: 0%-3%) for mortality and 7% (95% CI: 2%-14%) for complications. Approximately one-fifth of the patients had access to a transplant. This rate may be underestimated because of the short duration of follow-up. The lack of control groups did not allow for a conclusion on the role of bariatric surgery in facilitating access to kidney transplantation. In patients who had received a kidney transplant, bariatric surgery seemed to improve renal function but increased graft-rejection risk, possibly because of changes in the bioavailability of immunosuppressant drugs. CONCLUSIONS Bariatric surgery yields significant weight loss in patients with ECKD that improves patients' chances of accessing a transplant but does not guarantee it; however, the risk for complications and death is higher than in other patients. After transplantation, bariatric surgery-induced weight loss appeared to positively impact the function of the grafted kidney, but careful monitoring of immunosuppressant medications is required.
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Role of Diabetes Education Program in Controlling Posttransplant Diabetes in a Recent Renal Transplant Bodybuilder: Case Report and Review of the Literature.
Othman, N, Gheith, O, Al-Otaibi, T, Abdou, H, Halim, MA, Mahmoud, T, Nair, P, Yagan, J, Maher, A, Dahab, M, et al
Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation. 2019;(Suppl 1):169-171
Abstract
Posttransplant diabetes is a common complication of solid-organ transplantation. We present the possible role of diabetes education in improvement of posttransplant diabetes in a 36-year-old bodybuilder who was a kidney transplant recipient. The patient had been abusing some medications to help in bodybuilding. He underwent living unrelated-donor renal transplant with thymoglobulin induction and was maintained on steroids, tacrolimus, and mycophenolate mofetil. Posttransplant diabetes was confirmed by blood tests. His blood sugar was partially controlled by 3 oral agents. The patient participated in our structured diabetes education program. This program was created to cover different items related to diabetes control, including diet, proper exercise, blood sugar monitoring, sick day management, and pathophysiologic roles of diabetes medications. Within 4 months of participation in this program, the patient's blood sugar became well controlled and his diabetes medications started to be minimized. He presently has stable graft function with hemoglobin A1c level around 5.6% on only diet management. Bodybuilders are at risk of deterioration of their kidney function. A proper diabetes education program is recommended to help renal transplant recipients with early posttransplant diabetes mellitus to control their disease. Success requires close evaluation and a multidisciplinary approach.
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5.
Recurrent urinary tract infections caused by Raoultella planticola after kidney transplant.
Harmon, SL, Nadeem, I
Transplant infectious disease : an official journal of the Transplantation Society. 2019;(6):e13196
Abstract
Recurrent urinary tract infections are difficult to manage in patients with a history of kidney transplant and may contribute to graft loss. Few cases describe recurrent urinary tract infections due to Raoultella planticola in this population. We describe the management of recurrent urinary tract infections due to R planticola in a kidney transplant recipient and review other case reports of urinary tract infections due to this organism.
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6.
Simultaneous Living Donor Kidney and Parathyroid Allotransplantation: First Case Report and Review of Literature.
Garcia-Roca, R, Garcia-Aroz, S, Tzvetanov, IG, Giulianotti, PC, Campara, M, Oberholzer, J, Benedetti, E
Transplantation. 2016;(6):1318-21
Abstract
BACKGROUND Congenital hypoparathyroidism can be severely debilitating for patients, leading to renal failure at young age. Parathyroid transplantation may represent a permanent parathyroid replacement therapy. In patients already on immunosuppression for other organ transplant, there is little additional risk involved with parathyroid allotransplantation. METHODS Robotic assisted transaxillary single parathyroidectomy is performed on a living donor also donating a kidney to her sibling. RESULTS Recipient total serum PTH levels became detectable after 3 days from the procedure and maintained for 9 months after transplant with minimal calcium supplementation after the procedure. Literature review and previous results are summarized. CONCLUSIONS Obtaining a parathyroid gland and a kidney from the same donor reduces the exposure to different HLA antigens. The combined procedure using minimally invasive surgery is safe, with the additional cosmetic advantage and convenience for the willing donor. In the setting of need for immunosuppression, additional transplantation to treat the cause is safe and justified in the recipients.
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7.
Rare case of nephrocalcinosis in the distal tubules caused by hereditary renal hypouricaemia 3 months after kidney transplantation.
Okabayashi, Y, Yamamoto, I, Komatsuzaki, Y, Niikura, T, Yamakawa, T, Katsumata, H, Kawabe, M, Katsuma, A, Nakada, Y, Kobayashi, A, et al
Nephrology (Carlton, Vic.). 2016;:67-71
Abstract
We report a rare case of nephrocalcinosis caused by hereditary renal hypouricaemia 3 months after kidney transplantation. A 41-year-old man who underwent living-related kidney transplantation from his father was admitted to our hospital for a protocol biopsy; he had a serum creatinine (S-Cr) of 1.37 mg/dL and no proteinuria. Histologically, there was no evidence of rejection or calcineurin inhibitor toxicity, although scattered nephrocalcinosis was observed in the distal tubules. Perioperatively, the patient had a serum uric acid (S-UA) of 1.9 mg/dL with a fractional excretion of uric acid (FEUA) of 29% (normal, <10%) and UA clearance of 26.8 mL/min (normal, 7.3-14.7 mL/min) 3 days after kidney transplantation. The donor also had a relatively low S-UA of 2.4 mg/dL and high FEUA of 10.3%. Subsequent DNA direct sequencing followed by restriction fragment length polymorphism revealed that both the recipient's and donor's urate transporter 1 (URAT1) gene had a heterozygous nonsense mutation in exon 5 (C889T). Further, the immunoreactivity of antibodies for the C terminus of URAT1 revealed a partial deletion. De Galantha and von Kossa staining revealed that the nephrocalcinosis was due to urate crystals and calcium stones. Therefore, we diagnosed hereditary renal hypouricaemia. We directed the patient to avoid hard exercise, drink plenty of water, and alkalize the urine. The 1-year follow-up allograft biopsy showed no evidence of nephrocalcinosis in the distal tubules. This is the first report of nephrocalcinosis in the distal tubules as a diagnostic clue to hereditary renal hypouricaemia. We also review the related literature.
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8.
Recombinant PTH therapy for severe hypoparathyroidism after kidney transplantation in pre-transplant parathyroidectomized patients: review of the literature and a case report.
Hod, T, Riella, LV, Chandraker, A
Clinical transplantation. 2015;(11):951-7
Abstract
Although transient hypocalcemia following kidney transplantation can occur, severe refractory hypocalcemia is uncommon. We report a case of a 31-yr-old highly sensitized man with end-stage renal disease caused by reflux nephropathy, who received an expanded criteria deceased donor kidney transplant. The post-transplant course was significant for profound hypocalcemia despite treatment with large doses of calcium and vitamin D, in the setting of severe hypoparathyroidism following a subtotal parathyroidectomy three yr prior to the transplant. His course was also complicated by suboptimal allograft function with significant new vascular changes seen in the allograft biopsy by seven wk post-transplant. Teriparatide (recombinant parathyroid hormone) injections were initiated (up to three times daily) with improvement in the vascular changes and a decrease in calcium phosphate calcification in biopsy, as well as reduction in hypercalciuria, restoration of calcium phosphate homeostasis and stabilization of allograft function. We describe six other cases of post-transplant hypoparathyroidism, with five of six having decreased allograft function and three of those five demonstrating significant accelerated vascular changes on biopsy. We discuss the use of teriparatide injections for the treatment of renal transplant recipients with impaired renal function in the setting of hypoparathyroidism.
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9.
Mammalian Target of Rapamycin Inhibitors and Nephrotoxicity: Fact or Fiction.
Barbari, A, Maawad, M, Kfoury Kassouf, H, Kamel, G
Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation. 2015;(5):377-86
Abstract
Mammalian target of rapamycin inhibitors, such as rapamycin and more recently everolimus, have substituted calcineurin inhibitors in many minimization strategies. Despite their acclaimed renal safety profile, several lines of evidence are emerging on their potential nephrotoxic effect. Predisposing conditions for nephrotoxicity involve a complex interplay between several environmental and genetic factors in the donor-recipient pair. Renal injury may be enhanced by pharmacodynamic interactions when combined with other drugs such as calcineurin inhibitors or nutrients that are predominantly related to an increase in local tissue exposure. These toxic interactions may occur within adequate doses and therapeutic blood levels. This explains the occurrence of nephrotoxicity in some but not all cases. Here, we postulated that activity of a low permeability glycoprotein efflux pump related to low protein expression and/or inhibition enhanced immunosuppressive drug entry in different cells. A rise in intracellular drug concentration increases bioactivity, leading to greater immunosuppression and more immune-related, nonrenal adverse events in the recipient and increased nephrotoxicity in the kidney graft. Under specific isolated or combined environmental and/or genetic conditions in both the recipient and donor affecting the glycoprotein efflux pump and/or the mammalian target of rapamycin pathway, these renal injuries may be aggravated by heightened drug tissue concentrations despite adherence to therapeutic drug and blood levels. Mammalian target of rapamycin inhibitors may induce predominantly a dose-dependent renal epithelial cell injury affecting either the glomerular or the renal tubular epithelial cells, leading to cell death and apoptosis. Epithelial mesenchymal transition mediated interstitial fibrosis and tubular atrophy observed with these drugs may be the result of a cumulative toxic renal tubular injury induced by the direct insult of the drug itself and/or podocytopathy-associated proteinuria. The resulting glomerular tubular damage will ultimately lead to graft failure and loss, if exposure persists.
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10.
Does basiliximab induction trigger lifethreatening ARDS and shock in young patients after kidney transplantation?
Massart, A, Heenen, S, Bejjani, G, Hoang, AD, Mikhalski, D, Broeders, E, Creteur, J, Backer, DD, Abramowicz, D
Clinical nephrology. 2015;(1):61-70
Abstract
BACKGROUND Kidney disease Improving Global Outcomes (KDIGO) guidelines strongly recommend administering an anti-IL-2R mAb (i.e., basiliximab) for induction in all kidney transplant recipients. We describe a life-threatening episode of shock following basiliximab injection and review the literature. METHODS AND RESULTS A 20-year-old male was given tacrolimus, methylprednisolone, mycophenolate, and basiliximab, 20 mg in the context of living-related kidney transplantation. On post-operative Day 1 (POD 1), he developed acute respiratory distress syndrome (ARDS), shock, multiple organ failure, and had a cardiac arrest. After effective resuscitation, he received rescue therapies (NO inhalation, extra-corporeal membrane oxygenation, and CVVHD) but lost the graft as the result of cortical necrosis. We conducted PubMed searches that yielded 7 similar cases; 6 required invasive ventilation. Three patients developed cardiac arrest, 3 required major inotropic support, and 2 developed MOF and myocardial depression. All but 1 patient recovered rapidly within a few days. There was no evidence for infectious, allergic, or over-hydration concerns. Although the direct causal role of basiliximab cannot be formally proven, the fact that ARDS at the time of induction therapy with other immunosuppressive agents is otherwise extremely rare suggests a direct role for basiliximab. CONCLUSIONS Basiliximab could be associated with shock and ARDS.