Association of blood bicarbonate and pH with mineral metabolism disturbance and outcome after kidney transplantation

Brazier, François; Jouffroy, Jordan; Martinez, Frank; Nguyen–Khoa, Thao; Anglicheau, Dany; Legendre, Christophe; Neuraz, Antoine; Prié, Dominique; Bienaimé, Frank

doi:10.1111/ajt.15686

Cited by 10 publications

(17 citation statements)

References 35 publications

(67 reference statements)

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“…Five studies found a higher percentage or an association of MA in KTRs after deceased donor KTx [4,[22][23][24]58], while in three other studies, no association was found for donor type [41,49,58,59]. Only one study reported on prolonged cold ischemia time and an association with MA 3 months after transplantation [24]. So far, no association with donor age [22,24] or sex was identified [22].…”

Section: Donation and Donormentioning

confidence: 92%

“…Since the 1980s, CNIs are a key component of long-term immunosuppressive regimen after organ transplantation. Several studies could demonstrate an association of CNIs with the occurrence of chronic MA, with some evidence that it occurs more frequently with tacrolimus than cyclosporine A [22,24,41,47,48]. This effect seems to be dose dependent [49,50].…”

Section: Calcineurin Inhibitorsmentioning

confidence: 99%

“…However, in a small biopsy study, lower expression of the vacuolar proton pump after transplantation was found independent of acute rejection episodes [57]. In addition, in larger studies, no associations of acute rejections and MA were detected [22,24,41,58].…”

Section: Calcineurin Inhibitorsmentioning

confidence: 99%

“…Donation and donor-associated factors may play a role in the development of chronic MA -in particular since the incidence of MA early after transplantation is highest -but there is a paucity of evidence so far [4]. Five studies found a higher percentage or an association of MA in KTRs after deceased donor KTx [4,[22][23][24]58], while in three other studies, no association was found for donor type [41,49,58,59]. Only one study reported on prolonged cold ischemia time and an association with MA 3 months after transplantation [24].…”

Section: Donation and Donormentioning

confidence: 99%

“…Consequently, the KDIGO guidelines suggest bicarbonate substitution in CKD patients if serum bicarbonate concentration is <22 mmol/L [1]. In contrast to CKD patients, only few retrospective studies have been published on the impact of MA on graft function and mortality in KTRs [22][23][24][25][26]. Thus, although the first description of MA after KTx was more than half a century ago, there is still a lack of guidelines on how to deal with chronic MA in KTRs [27].…”

Section: Introductionmentioning

confidence: 99%

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Causes and Consequences of Metabolic Acidosis in Patients after Kidney Transplantation

Ritter

Mohebbi

2020

Kidney Blood Press Res

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Background: Metabolic acidosis (MA) is a common complication in kidney transplantation (KTx). It is more prevalent in KTx than in CKD, and it occurs at higher glomerular filtration rates. The pathophysiologic understanding of MA in KTx and its clinical impact has been highlighted by few recent studies. However, no guidelines exist yet for the treatment of MA after KTx. Summary: MA in KTx seems to share pathophysiologic mechanisms with CKD, such as impaired ammoniagenesis. Additional kidney transplant-specific factors seem to alter not only the prevalence but also the phenotype of MA, which typically shows features of renal tubular acidosis. There is evidence that calcineurin inhibitors, immunological factors, process of donation, donor characteristics, and diet may contribute to MA occurrence. According to several mainly observational studies, MA seems to play a role in disturbed bone metabolism, cardiovascular morbidity, declining graft function, and mortality. A better understanding of the pathophysiology and evidence from randomized controlled trials, in particular, are needed to clarify the role of MA and the potential benefit of alkali treatment in KTx. Alkali therapy might not only be beneficial but also cost effective and safe. Key Messages: MA seems to be associated with several negative outcomes in KTx. A deeper understanding of the pathophysiology and clinical consequences of MA in KTx is crucial. Clinical trials will have to determine the potential benefits of alkali therapy.

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Section: Donation and Donormentioning

confidence: 92%

Section: Calcineurin Inhibitorsmentioning

confidence: 99%

Section: Calcineurin Inhibitorsmentioning

confidence: 99%

Section: Donation and Donormentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Causes and Consequences of Metabolic Acidosis in Patients after Kidney Transplantation

Ritter

Mohebbi

2020

Kidney Blood Press Res

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Kidney metabolism and acid–base control: back to the basics

Silva

Mohebbi²

2022

Pflugers Arch - Eur J Physiol

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Kidneys are central in the regulation of multiple physiological functions, such as removal of metabolic wastes and toxins, maintenance of electrolyte and fluid balance, and control of pH homeostasis. In addition, kidneys participate in systemic gluconeogenesis and in the production or activation of hormones. Acid–base conditions influence all these functions concomitantly. Healthy kidneys properly coordinate a series of physiological responses in the face of acute and chronic acid–base disorders. However, injured kidneys have a reduced capacity to adapt to such challenges. Chronic kidney disease patients are an example of individuals typically exposed to chronic and progressive metabolic acidosis. Their organisms undergo a series of alterations that brake large detrimental changes in the homeostasis of several parameters, but these alterations may also operate as further drivers of kidney damage. Acid–base disorders lead not only to changes in mechanisms involved in acid–base balance maintenance, but they also affect multiple other mechanisms tightly wired to it. In this review article, we explore the basic renal activities involved in the maintenance of acid–base balance and show how they are interconnected to cell energy metabolism and other important intracellular activities. These intertwined relationships have been investigated for more than a century, but a modern conceptual organization of these events is lacking. We propose that pH homeostasis indissociably interacts with central pathways that drive progression of chronic kidney disease, such as inflammation and metabolism, independent of etiology.

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Metabolic acidosis in chronic kidney disease: mere consequence or also culprit?

Kuhn,

Mohebbi,

Ritter

2024

Pflugers Arch - Eur J Physiol

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Metabolic acidosis is a frequent complication in non-transplant chronic kidney disease (CKD) and after kidney transplantation. It occurs when net endogenous acid production exceeds net acid excretion. While nephron loss with reduced ammoniagenesis is the main cause of acid retention in non-transplant CKD patients, additional pathophysiological mechanisms are likely inflicted in kidney transplant recipients. Functional tubular damage by calcineurin inhibitors seems to play a key role causing renal tubular acidosis. Notably, experimental and clinical studies over the past decades have provided evidence that metabolic acidosis may not only be a consequence of CKD but also a driver of disease. In metabolic acidosis, activation of hormonal systems and the complement system resulting in fibrosis have been described. Further studies of changes in renal metabolism will likely contribute to a deeper understanding of the pathophysiology of metabolic acidosis in CKD. While alkali supplementation in case of reduced serum bicarbonate < 22 mmol/l has been endorsed by CKD guidelines for many years to slow renal functional decline, among other considerations, beneficial effects and thresholds for treatment have lately been under intense debate. This review article discusses this topic in light of the most recent results of trials assessing the efficacy of dietary and pharmacological interventions in CKD and kidney transplant patients.

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Association of blood bicarbonate and pH with mineral metabolism disturbance and outcome after kidney transplantation

Cited by 10 publications

References 35 publications

Causes and Consequences of Metabolic Acidosis in Patients after Kidney Transplantation

Causes and Consequences of Metabolic Acidosis in Patients after Kidney Transplantation

Kidney metabolism and acid–base control: back to the basics

Metabolic acidosis in chronic kidney disease: mere consequence or also culprit?

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