Association between copeptin and declining glomerular filtration rate in people with newly diagnosed diabetes. The Skaraborg Diabetes Register

Pikkemaat, Miriam; Melander, Olle; Boström, Kristina Bengtsson

doi:10.1016/j.jdiacomp.2015.07.006

Cited by 41 publications

(31 citation statements)

References 21 publications

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“…In 1,328 patients with newly diagnosed type 2 diabetes (the Dutch ZODIAC prospective study), the upper quartile of plasma copeptin concentration was associated with a faster decline of estimated glomerular filtration rate (eGFR) and with a greater increase of the urinary albumin-to-creatinine ratio during a 6.5-year follow-up [4]. In agreement with these findings, high copeptin was associated with a decline of kidney function (assessed by the eGFR) in another cohort of newly diagnosed type 2 diabetic patients (the Skaraborg-Diabetes Register) [14]. Velho et al [15] analyzed data of 3,101 French type 2 diabetic patients from the DIABHYCAR cohort.…”

Section: High Copeptin and Diabetic Nephropathy: Epidemiological Datasupporting

confidence: 58%

Vasopressin and Diabetic Kidney Disease

Boustany¹

2018

Ann Nutr Metab

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Background: Diabetic nephropathy has become the most common cause of chronic kidney disease (CKD). Despite the progress accomplished in therapy, the prevalence of renal disorders remains high. Some modifiable factors driving the increase in incidence of CKD, in diabetes and other settings, might have been overlooked. Consistent evidence supports a role for vasopressin, hydration state, and urine concentration in kidney health. Summary: Plasma vasopressin is elevated in diabetes, even if metabolic control is good. Several epidemiological studies have pointed to a positive association between markers of vasopressin secretion (24-h fluid intake, urine volume, plasma copeptin concentration) and renal function decline in both the community and populations at high risk of CKD, namely, diabetic patients. Research involving animal models also supports a critical causal role of the V2 receptor antidiuretic effects of vasopressin in the early signs of kidney disease associated with type 1 or type 2 diabetes. Key Messages: Data supporting the detrimental effects of chronic vasopressin action on the kidney is consistent in animal models and human observational studies. Since vasopressin secretion can be modulated by water intake, and its actions by selective receptor antagonists, the vasopressin-hydration system could be a potential therapeutic target for the prevention and treatment of diabetic nephropathy. Intervention studies are needed to examine the relevance of lifestyle or pharmacological interventions.

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Section: High Copeptin and Diabetic Nephropathy: Epidemiological Datasupporting

confidence: 58%

Vasopressin and Diabetic Kidney Disease

Boustany¹

2018

Ann Nutr Metab

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“…Interestingly, high copeptin is also associated with a broad range of other diseases such as heart failure [28], vascular dementia [27], cognitive impairment [29], microalbuminuria [25], chronic kidney disease [17, 30], inflammatory bowel disease [31], cancer [32], and premature mortality [24]. …”

Section: Association Of Vasopressin (Copeptin) Levels With Risk and Omentioning

confidence: 99%

Two Liters a Day Keep the Doctor Away? Considerations on the Pathophysiology of Suboptimal Fluid Intake in the Common Population

Läng

Guelinckx

Lemetais

et al. 2017

Kidney Blood Press Res

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Suboptimal fluid intake may require enhanced release of antidiuretic hormone (ADH) or vasopressin for the maintenance of adequate hydration. Enhanced copeptin levels (reflecting enhanced vasopressin levels) in 25% of the common population are associated with enhanced risk of metabolic syndrome with abdominal obesity, type 2 diabetes, hypertension, coronary artery disease, heart failure, vascular dementia, cognitive impairment, microalbuminuria, chronic kidney disease, inflammatory bowel disease, cancer, and premature mortality. Vasopressin stimulates the release of glucocorticoids which in turn up-regulate the serum- and glucocorticoid-inducible kinase 1 (SGK1). Moreover, dehydration upregulates the transcription factor NFAT5, which in turn stimulates SGK1 expression. SGK1 is activated by insulin, growth factors and oxidative stress via phosphatidylinositide-3-kinase, 3-phosphoinositide-dependent kinase PDK1 and mTOR. SGK1 is a powerful stimulator of Na⁺/K⁺-ATPase, carriers (e.g. the Na⁺,K⁺,2Cl^- cotransporter NKCC, the NaCl cotransporter NCC, the Na⁺/H⁺ exchanger NHE3, and the Na⁺ coupled glucose transporter SGLT1), and ion channels (e.g. the epithelial Na⁺ channel ENaC, the Ca²⁺ release activated Ca²⁺ channel Orai1 with its stimulator STIM1, and diverse K⁺ channels). SGK1 further participates in the regulation of the transcription factors nuclear factor kappa-B NFκB, p53, cAMP responsive element binding protein (CREB), activator protein-1, and forkhead transcription factor FKHR-L1 (FOXO3a). Enhanced SGK1 activity fosters the development of hypertension, obesity, diabetes, thrombosis, stroke, inflammation including inflammatory bowel disease and autoimmune disease, cardiac fibrosis, proteinuria, renal failure as well as tumor growth. The present brief review makes the case that suboptimal fluid intake in the common population may enhance vasopressin and glucocorticoid levels thus up-regulating SGK1 expression and favouring the development of SGK1 related pathologies.

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“…Cross-sectional and prospective studies in the general population have shown associations between plasma copeptin and albuminuria or renal function decline (Meijer et al, 2010;Enhorning et al, 2013;Roussel et al, 2015). High circulating copeptin concentration was also associated with the development and progression of diabetic nephropathy in patients with type 2 diabetes (Boertien et al, 2013;Velho et al, 2013;Hu et al, 2015;Pikkemaat et al, 2015;Zhu et al, 2016), and with prevalence of ESRD in subjects with long-standing type 1 diabetes (Bjornstad et al, 2016;Velho et al, 2016). Experimental data suggests a causal role of vasopressin in renal dysfunction through activation of the V2-receptor (V2R).…”

Section: Introductionmentioning

confidence: 99%

Antagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes

Boustany

Taveau

Chollet

et al. 2017

Journal of Diabetes and its Complications

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Methods: Male obese diabetic db/db mice were treated for 12 weeks with a selective V2R antagonist (SR121463) and compared to non-treated db/db and non-diabetic db/m mice. All animals were previously uninephrectomized.Results: The V2R antagonist did not alter glycaemia or glycosuria in db/db mice. It induced a two-fold increase in urine output and a 52% decrease in urine osmolality compared to nontreated db/db mice. After four weeks of treatment urinary albumin to creatinine ratio was 50% lower in treated mice compared to non-treated mice, and remained significantly lower until end of experiment. Glomerular filtration rate increased significantly over time in non-treated db/db mice but remained stable in treated mice.Conclusions: This study shows that vasopressin contributes to albuminuria and glomerular hyperfiltration via V2R in a mouse model of type 2 diabetes. It documents causality behind the association of vasopressin with renal disease observed in diabetic patients.

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Association between copeptin and declining glomerular filtration rate in people with newly diagnosed diabetes. The Skaraborg Diabetes Register

Cited by 41 publications

References 21 publications

Vasopressin and Diabetic Kidney Disease

Vasopressin and Diabetic Kidney Disease

Two Liters a Day Keep the Doctor Away? Considerations on the Pathophysiology of Suboptimal Fluid Intake in the Common Population

Antagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes

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