New insights into the pathophysiological mechanisms underlying cardiorenal syndrome

Wang, Jin; Zhang, Weiguang; Wu, Lingling; Mei, Yan; Cui, Shaoyuan; Feng, Zhe; Chen, Xiangmei

doi:10.18632/aging.103354

Cited by 9 publications

(8 citation statements)

References 68 publications

(80 reference statements)

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“…Dysfunction of the heart or kidney could potentially induce dysfunction of the other organ [1,5,6], known as a pathologic condition termed the cardiorenal syndrome [31]. In our sensitivity analysis, GDF-15 and NT-proBNP were mutually adjusted for each other in the multivariate model.…”

Section: Discussionmentioning

confidence: 99%

Growth differentiation factor-15 and incident chronic kidney disease: a population-based cohort study

Bao

Borné

et al. 2021

BMC Nephrol

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Background The relationship between growth differentiation factor 15 (GDF-15) and the development of chronic kidney disease (CKD) is still unclear. We sought to examine whether plasma GDF-15 was related to incident CKD and kidney function decline using a large prospective cohort study. Methods 4318 participants of the Malmö Diet and Cancer Study-Cardiovascular Cohort were examined in 1991-1994. Incidence of CKD was followed prospectively by linkage with national patient registers. Estimated glomerular filtration rate (eGFR) was available for all participants at baseline, and was re-measured in a subgroup of 2744 subjects after 16.6 ± 1.49 years. Incidence of CKD was examined in relation to GDF-15 using Cox regression analysis. Logistic regression was used to examine the association of GDF-15 with eGFR change and eGFR-based CKD. Models were carefully corrected for potential confounders including baseline eGFR, N-terminal pro-B-type natriuretic peptide, and competing risk from death. Results 165 patients developed CKD after 19.2 ± 4.04 years of follow-up. The adjusted hazard ratio (95% confidence interval, CI) for CKD in 4th versus 1st quartile of GDF-15 was 2.37 (1.33, 4.24) (p for trend < 0.01). Each per 1 standard deviation increase in GDF-15 was associated with a decline in eGFR of − 0.97 mL/min/1.73 m2 (95% CI, − 1.49 ~ − 0.45; p < 0.001). GDF-15 was also significantly associated eGFR-based CKD in 2713 subjects with baseline eGFR ≥60 mL/min/1.73 m2. Conclusions GDF-15 predicted incidence of CKD and eGFR decline in the general population, independent of a wide range of potential risk factors and competing risk of death.

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Section: Discussionmentioning

confidence: 99%

Growth differentiation factor-15 and incident chronic kidney disease: a population-based cohort study

Bao

Borné

et al. 2021

BMC Nephrol

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Section: Discussionmentioning

confidence: 99%

Growth Differentiation Factor-15 and Incident Chronic Kidney Disease: A Population-Based Cohort Study

Bao

Borné

et al. 2021

Preprint

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Background The relationship between growth differentiation factor 15 (GDF-15) and the development of chronic kidney disease (CKD) is still unclear. We sought to examine whether plasma GDF-15 was related to incident CKD and kidney function decline using a large prospective cohort study. Methods 4,318 participants of the Malmö Diet and Cancer Study-Cardiovascular Cohort were examined in 1991–1994 and followed prospectively until 2013 for incidence of CKD, as detected from national registers. Estimated glomerular filtration rate (eGFR) was available for all participants at baseline, and was re-measured in a subgroup of 2,744 subjects after 16.6 ± 1.49 years. Incidence of CKD was examined in relation to GDF-15 using Cox regression analysis. Logistic regression was used to examine the association of GDF-15 with eGFR change and eGFR-based CKD. Models were carefully corrected for potential confounders including baseline eGFR, N-terminal pro-B-type natriuretic peptide, and competing risk from death. Results 165 patients developed CKD after 19.2 ± 4.04 years of follow-up. The adjusted hazard ratio (95% confidence interval, CI) for CKD in 4th versus 1st quartile of GDF-15 was 2.37 (1.33, 4.24) (p for trend < 0.01). Each per 1 standard deviation increase in GDF-15 was associated with a decline in eGFR of -0.97 mL/min/1.73 m2 (95% CI, -1.49~-0.45; p < 0.001). GDF-15 was also significantly associated eGFR-based CKD in 2,713 subjects with baseline eGFR ≥ 60 mL/min/1.73 m2. Conclusions GDF-15 predicted incidence of CKD and eGFR decline in the general population, independent of a wide range of potential risk factors and competing risk of death.

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“…AKI-induced damage to the heart is associated with RAAS and sympathetic nervous system activation [61]. The latter increases the energy demand of cardiomyocytes and can perturb the cellular homeostasis, for example, calcium fluxes [62]. RAAS activation indirectly (e.g., due to fluid balance and blood volume regulation) and directly impairs cardiac function following renal injury [62].…”

Section: Association Between Heart and Kidney Damagementioning

confidence: 99%

“…The latter increases the energy demand of cardiomyocytes and can perturb the cellular homeostasis, for example, calcium fluxes [62]. RAAS activation indirectly (e.g., due to fluid balance and blood volume regulation) and directly impairs cardiac function following renal injury [62]. An increase of systemic inflammation has been observed in animal models of ischemic AKI, as recently reviewed [12].…”

Section: Association Between Heart and Kidney Damagementioning

confidence: 99%

Could Repeated Cardio-Renal Injury Trigger Late Cardiovascular Sequelae in Extreme Endurance Athletes?

et al. 2022

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Regular exercise confers multifaceted and well-established health benefits. Yet, transient and asymptomatic increases in markers of cardio-renal injury are commonly observed in ultra-endurance athletes during and after competition. This has raised concerns that chronic recurring insults could cause long-term cardiac and/or renal damage. Indeed, extreme endurance exercise (EEE) over decades has sometimes been linked with untoward cardiac effects, but a causal relation with acute injury markers has not yet been established. Here, we summarize the current knowledge on markers of cardiac and/or renal injury in EEE athletes, outline the possible interplay between cardiac and kidney damage, and explore the roles of various factors in the development of potential exercise-related cardiac damage, including underlying diseases, medication, sex, training, competition, regeneration, mitochondrial dysfunction, oxidative stress, and inflammation. In conclusion, despite the undisputed health benefits of regular exercise, we speculate, based on the intimate link between heart and kidney diseases, that in rare cases excessive endurance sport may induce adverse cardio-renal interactions that under specific, hitherto undefined conditions could result in persistent cardiac damage. We highlight future research priorities and provide decision support for athletes and clinical consultants who are seeking safe strategies for participation in EEE training and competition.

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New insights into the pathophysiological mechanisms underlying cardiorenal syndrome

Cited by 9 publications

References 68 publications

Growth differentiation factor-15 and incident chronic kidney disease: a population-based cohort study

Growth differentiation factor-15 and incident chronic kidney disease: a population-based cohort study

Growth Differentiation Factor-15 and Incident Chronic Kidney Disease: A Population-Based Cohort Study

Could Repeated Cardio-Renal Injury Trigger Late Cardiovascular Sequelae in Extreme Endurance Athletes?

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