Long-term effects of hypercalcemia in kidney transplant recipients with persistent hyperparathyroidism

Ramirez-Sandoval, Juan Carlos; Marino, Lluvia; Cojuc-Konigsberg, Gabriel; Reul-Linares, Estefania; Pichardo-Cabrera, Nathalie Desire; Cruz, Cristino; Hernández-Paredes, Elisa Naomi; Berman-Parks, Nathan; Vidal-Ruíz, Vanessa; Estrada-Linares, Jonathan Mauricio; Reza-Albarrán, Alfredo Adolfo; Correa-Rotter, Ricardo; Morales-Buenrostro, Luis Eduardo

doi:10.1007/s40620-023-01815-5

Cited by 2 publications

(2 citation statements)

References 31 publications

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“…In their study, this association did not reach statistical significance [ 45 ]. Hypercalcemia should not be underestimated, as 62% of kidney transplant patients presented with persistent hypercalcemia [ 46 ]. The risk of hypercalcemia can be decreased with calcimimetics.…”

Section: Discussionmentioning

confidence: 99%

Exploring Acute Pancreatitis in Kidney Transplant Recipients: A Multicentre Retrospective Cohort Analysis of Incidence, Causes, and Clinical Outcomes

Basic-Jukic,

Androvic,

Beck

et al. 2024

JCM

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Background: The aim of this multicentre retrospective study is to determine the incidence, etiology, clinical characteristics, and outcomes of kidney transplant recipients diagnosed and treated for acute pancreatitis. Methods: We analyzed data from kidney transplant recipients who received kidney allografts between October 1973 and December 2023 and were diagnosed and treated for acute pancreatitis. Results: Of 2482 patients who received kidney allografts, 10 (0.4%) (5 male) were diagnosed with acute pancreatitis, with a mean age of 48.6 years. Patients were diagnosed with acute pancreatitis between 3 weeks and 24 years after the transplantation. Possible etiologies included cholecystolithiasis, COVID-19, hypercalcemia, postprocedural, use of cannabis, trimetoprim-sulphometoxasole, statins, sirolimus, tacrolimus and obesity. There was no suspected etiology in two patients. Patients were treated with aggressive hydration, pain alleviation and antibiotics if indicated. Four patients developed complications. Local complications included peripancreatic collections, pseudocyst, and abscesses formation, while systemic complications occurred in the form of Cytomegalovirus (CMV) reactivation and urinary tract infection. All patients survived with preserved kidney allograft function. Conclusions: Acute pancreatitis in kidney transplant recipients is rare. However, it may be linked to significant morbidity and mortality. While symptoms may be nonspecific and brought on by a variety of viral and non-infectious illnesses, as well as adverse effects from immunosuppressive medications, a high degree of awareness is required.

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Section: Discussionmentioning

confidence: 99%

Exploring Acute Pancreatitis in Kidney Transplant Recipients: A Multicentre Retrospective Cohort Analysis of Incidence, Causes, and Clinical Outcomes

Basic-Jukic,

Androvic,

Beck

et al. 2024

JCM

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“…detected that tertiary hyperparathyroidism after transplantation was associated with a higher eGFR, 28 which has been suggested to be a hyperfiltration effect of hypercalcemia. 29 In a reciprocal manner, the treatment of tertiary hyperparathyroidism with parathyroidectomy 30 or cinacalcet 31 has shown a mild decrease in eGFR of KTR.…”

Section: F I G U R Ementioning

confidence: 99%

Impact of hyperparathyroidism on allograft histology and function after kidney transplantation: Rethinking its causal role in graft dysfunction

Cojuc‐Konigsberg,

Tinajero‐Sánchez,

Canaviri‐Flores

et al. 2024

Clinical Transplantation

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IntroductionThe causal relationship between hyperparathyroidism and kidney graft dysfunction remains inconclusive. Applying Bradford‐Hill's temporality and consistency causation principles, we assessed the effect of parathyroid hormone (iPTH) on graft histology and eGFR trajectory on kidney transplant recipients (KTRs) with normal time‐zero graft biopsies.MethodsRetrospective cohort study evaluating the effect of hyperparathyroidism on interstitial fibrosis and tubular atrophy (IF/TA) development in 1232 graft biopsies. Pre‐transplant hyperparathyroidism was categorized by KDIGO or KDOQI criteria, and post‐transplant hyperparathyroidism by iPTH >1× and >2× the URL 1 year after transplantation.ResultsWe included 325 KTRs (56% female, age 38 ± 13 years, follow‐up 4.2 years [IQR: 2.7‐5.8]). Based on pre‐transplant iPTH levels, 26% and 66% exceeded the KDIGO and KDOQI targets, respectively. There were no significant differences in the development of >25% IF/TA between KTRs with pre‐transplant iPTH levels above and within target range according to KDIGO (53% vs. 62%, P = .16, HR.94 [95% CI:.67–1.32]) and KDOQI (60% vs. 60%, P = 1.0, HR 1.19 [95% CI:.88–1.60]) criteria. Similarly, there were no differences when using 1 year post‐transplant iPTH cut‐offs > 88 pg/mL (58% vs. 64%, P = .33) and > 176 pg/mL (55% vs. 62%, P = .19). After adjusting for confounders, no significant differences were observed in eGFR trajectories among the iPTH strata.ConclusionIn young KTRs who received a healthy graft, no association was found between increased pre‐ and post‐transplant iPTH levels and graft dysfunction, as assessed histologically and through eGFR trajectory. The concept of hyperparathyroidism as a risk factor for graft dysfunction in recipients at low risk requires reevaluation.

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Long-term effects of hypercalcemia in kidney transplant recipients with persistent hyperparathyroidism

Cited by 2 publications

References 31 publications

Exploring Acute Pancreatitis in Kidney Transplant Recipients: A Multicentre Retrospective Cohort Analysis of Incidence, Causes, and Clinical Outcomes

Exploring Acute Pancreatitis in Kidney Transplant Recipients: A Multicentre Retrospective Cohort Analysis of Incidence, Causes, and Clinical Outcomes

Impact of hyperparathyroidism on allograft histology and function after kidney transplantation: Rethinking its causal role in graft dysfunction

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