Safety and efficacy of patiromer use with tacrolimus in kidney transplant recipients

Rattanavich, Rungwasee; Malone, Andrew F.; Alhamad, Tarek

doi:10.1111/tri.13369

Cited by 11 publications

(5 citation statements)

References 2 publications

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“…The availability of the novel oral antihyperkalemic agents (patiromer and sodium zirconium cyclosilicate) may offer the opportunity to test the potential benefits of RAASi in the post-KT settings in a controlled fashion [32,33]. It must be mentioned that there are limited data on the risk/benefit profiles of the novel antihyperkalemic agents in the post-KT setting, although small single center experiences have reported the ability to maintain target therapeutic tacrolimus levels with concomitant use of these drugs when administered as per labeling specifications [34].…”

Section: Hypertension As a Risk Factormentioning

confidence: 99%

Cardiovascular disease in the kidney transplant recipient: epidemiology, diagnosis and management strategies

Rangaswami

Mathew

Parasuraman

et al. 2019

Nephrology Dialysis Transplantation

127

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Section: Hypertension As a Risk Factormentioning

confidence: 99%

Cardiovascular disease in the kidney transplant recipient: epidemiology, diagnosis and management strategies

Rangaswami

Mathew

Parasuraman

et al. 2019

Nephrology Dialysis Transplantation

127

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“…Tacrolimus (TAC, also known as FK506), a new immunosuppressive drug, has lower nephrotoxicity than cyclosporine, which has been widely used in post–kidney transplantation and immune‐related chronic kidney disease by suppression of nuclear factor of activated T cell (NFAT) dephosphorylation and transcriptional activation of NFAT target genes 12‐14 . Recently, TAC was attempted to be used in experimental DN patients and animal models.…”

Section: Introductionmentioning

confidence: 99%

Tacrolimus ameliorates tubulointerstitial inflammation in diabetic nephropathy via inhibiting the NFATc1/TRPC6 pathway

Zhang

Wang

Liu

et al. 2020

J Cellular Molecular Medi

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Tubulointerstitial inflammation is crucial for the progression of diabetic nephropathy (DN), and tubular cells act as a driving force in the inflammatory cascade. Emerging data suggested that tacrolimus (TAC) ameliorates podocyte injury and macrophage infiltration in streptozotocin (STZ) mice. However, the effect of TAC on tubulointerstitial inflammation remains unknown. We found that albuminuria and tubulointerstitial damage improved in db/db mice treated with TAC. Macrophage infiltration and expression of IL‐6, TNF‐α, fibronectin, collagen 1 and cleaved caspase 3 were inhibited as well. In addition, the expression of nuclear factor of activated T cell 1 (NFATc1) and transient receptor potential channel 6 (TRPC6) was up‐regulated in the kidneys of DN patients and correlated with tubular injury and inflammation. The expression of NFATc1 and TRPC6 also increased in the kidneys of db/db mice and HK‐2 cells with high glucose (HG), while TAC inhibited these effects. HG‐induced inflammatory markers and apoptosis were reversed by TAC and NFATc1 siRNA in HK‐2 cells, which was abolished by TRPC6 plasmid. Furthermore, HG‐induced TRPC6 expression was inhibited by NFATc1 siRNA, while NFATc1 nuclear translocation was inhibited by TAC, but was restored by TRPC6 plasmid in HK‐2 cells under HG conditions. These findings suggest that TAC ameliorates tubulointerstitial inflammation in DN through NFATc1/TRPC6 feedback loop.

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“…Rattanavich et al [52] reported on two kidney transplant patients on tacrolimus who were treated with patiromer for hyperkalaemia. The study revealed that the use of patiromer is effective in treating hyperkalaemia and does not affect tacrolimus trough levels when administered at least 3 h after the tacrolimus dose.…”

Section: Patiromermentioning

confidence: 99%

Novel approaches to management of hyperkalaemia in kidney transplantation

Rizk

Quan

Gabardi

et al. 2021

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of reviewMedications used frequently after kidney transplantation, including calcineurin inhibitors, angiotensinconverting enzyme inhibitors, angiotensin receptor blockers, beta blockers and antimicrobials, are considered the leading culprit for posttransplant hyperkalaemia in recipients with a well functioning allograft. Other risk factors include comorbidities such as diabetes, hypertension and heart failure; and consumption of a potassium-enriched diet. We review the mechanisms for hyperkalaemia following kidney transplantation that are addressed using nonpharmacological and pharmacological interventions. We also discuss emerging therapeutic approaches for the management of recurrent hyperkalaemia in solid organ transplantation, including newer potassium binding therapies. Recent findingsPatiromer and sodium zirconium cyclosilicate are emerging potassium binders approved for the treatment of hyperkalaemia. Patiromer is a polymer that exchanges potassium for calcium ions. In contrast, sodium zirconium cyclosilicate is a nonpolymer compound that exchanges potassium for sodium and hydrogen ions. Both agents are efficacious in the treatment of chronic or recurrent hyperkalaemia and may result in fewer gastrointestinal side effects than older potassium binders such as sodium polystyrene sulfonate and calcium polystyrene sulfonate. Large-scale clinical studies have not been performed in kidney transplant patients. Patiromer may increase serum concentrations of tacrolimus, but not cyclosporine. Sodium zirconium cyclosilicate does not appear to compromise tacrolimus pharmacokinetics, although it may have a higher sodium burden.

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Safety and efficacy of patiromer use with tacrolimus in kidney transplant recipients

Cited by 11 publications

References 2 publications

Cardiovascular disease in the kidney transplant recipient: epidemiology, diagnosis and management strategies

Cardiovascular disease in the kidney transplant recipient: epidemiology, diagnosis and management strategies

Tacrolimus ameliorates tubulointerstitial inflammation in diabetic nephropathy via inhibiting the NFATc1/TRPC6 pathway

Novel approaches to management of hyperkalaemia in kidney transplantation

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