Mosaic theory revised: inflammation and salt play central roles in arterial hypertension

Hengel, Felicitas E.; Benitah, Jean-Pierre; Wenzel, Ulrich

doi:10.1038/s41423-022-00851-8

Cited by 29 publications

(25 citation statements)

References 181 publications

(227 reference statements)

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“…Tissue sodium content, as measured via 23 Na MRI, is substantially increased in kidney disease and dialysis patients, with additional conditions that tend to worsen this condition (i.e., ageing, hypertension, cardiac, diabetes, salt diet, dialysate sodium) [ 55 , 56 , 57 , 58 ]. It is also shown in experimental and clinical studies that tissue sodium accumulation contributes via insulin resistance and inflammation to protein–energy wasting [ 56 , 59 , 60 ].…”

Section: Fluid Overload As a Cause Of Protein Energy Malnutrition: Ev...mentioning

confidence: 99%

Fluid Overload and Tissue Sodium Accumulation as Main Drivers of Protein Energy Malnutrition in Dialysis Patients

et al. 2022

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Protein energy malnutrition is recognized as a leading cause of morbidity and mortality in dialysis patients. Protein–energy-wasting process is observed in about 45% of the dialysis population using common biomarkers worldwide. Although several factors are implicated in protein energy wasting, inflammation and oxidative stress mechanisms play a central role in this pathogenic process. In this in-depth review, we analyzed the implication of sodium and water accumulation, as well as the role of fluid overload and fluid management, as major contributors to protein–energy-wasting process. Fluid overload and fluid depletion mimic a tide up and down phenomenon that contributes to inducing hypercatabolism and stimulates oxidation phosphorylation mechanisms at the cellular level in particular muscles. This endogenous metabolic water production may contribute to hyponatremia. In addition, salt tissue accumulation likely contributes to hypercatabolic state through locally inflammatory and immune-mediated mechanisms but also contributes to the perturbation of hormone receptors (i.e., insulin or growth hormone resistance). It is time to act more precisely on sodium and fluid imbalance to mitigate both nutritional and cardiovascular risks. Personalized management of sodium and fluid, using available tools including sodium management tool, has the potential to more adequately restore sodium and water homeostasis and to improve nutritional status and outcomes of dialysis patients.

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Section: Fluid Overload As a Cause Of Protein Energy Malnutrition: Ev...mentioning

confidence: 99%

Fluid Overload and Tissue Sodium Accumulation as Main Drivers of Protein Energy Malnutrition in Dialysis Patients

et al. 2022

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“…Improving these undesirable outcomes depends on a better understanding of the pathogenesis. Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury but that inflammation plays a vital role and contributes to this disease 1,2 . The complement system is an ancient part of innate immunity comprising multiple serum proteins and cellular receptors protecting the host from a hostile microbial environment and maintaining tissue and cell integrity.…”

Section: Introductionmentioning

confidence: 99%

No compliment for complement: Kidney biopsies of patients with malignant nephrosclerosis show no complement activation

Schmidt

Tomas

Huber

et al. 2023

Preprint

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The complement system represents an ancient part of innate immunity and is comprised of multiple serum proteins. In several pathological conditions, including atypical hemolytic syndrome (aHUS), complement activation is contributing to disease progression. Therefore, pharmacological targeting of complement is a viable therapeutic strategy in this population. Recent data suggest complement activation in patients suffering from malignant hypertension and stenosing arteriosclerosis also called malignant nephrosclerosis (MNS). Since MNS and aHUS also share histopathological similarities therapeutic complement inhibition became a discussion in MNS. To eliminate the pitfall of confusing complement trapping with activation in the kidney we used the proximity ligation assay to detect, visualize and quantify assembled complement convertases of the different pathways in renal tissue diagnosed with MNS or aHUS. We compared them to a control group of patients presenting with thin basement membrane syndrome (TBMD). Activation of the alternative and the classical pathways were examined by glomerular and vascular quantification of C3b/Bb and C4b/C2b, respectively. We found an overactivation of the alternative pathway only in patients suffering from aHUS, while complement activation was not altered in MNS when compared with TBMD. Thus our results cannot contribute to the hypothesis that complement inhibition may be an efficient therapeutic strategy for patients presenting end-organ damage due to stenosing arteriosclerosis. The use of complement inhibition in these patients cannot be recommended.

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“…Відповідно до своєї фізіологічної ролі підвищений уміст іонів натрію в організмі провокує патологічні процеси, перш за все артеріальну гіпертензію в більшості людей. Недостатня екскреція іонів натрію нирками призводить до збільшення об'єму позаклітинної рідини при споживанні великої кількості солі та подальшого підвищення артеріального тиску через збільшення серцевого викиду та адаптивне збільшення периферичного опору [1,2]. Гіпернатріємія (ви-УДК 612.…”

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Regulatory mechanisms for maintaining homeostasis of sodium ions

Filipets

Гоженко

Ivanov

et al. 2022

KIDNEYS

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According to general scientific recognition, the content of sodium ions in the body of a healthy person is quite constant, and among the multifaceted biological functions of this electrolyte, participation in maintaining water-salt homeostasis is the most important. Deviations from the normal level of concentration of sodium ions in the blood plasma are the most common electrolyte balance disorders in clinical medicine; however, dysionias still remain a relevant subject of research, in particular, their pathogenetic aspects and the possibilities of pharmacological correction. Sodium as an electrolyte is essential for the volume of extracellular fluid the content of which is inversely related to the urinary excretion of sodium ions. Sodium homeostasis is tightly regulated. In the reactions of ensuring the sodium balance in the body, the kidneys play a leading role, and the changes in their functional state are mediated through the action of the basic neurohumoral regulatory systems. The main renal homeostatic processes — glomerular filtration, tubular reabsorption and secretion — are of decisive importance for the removal of excess ions of sodium or its retention in the body. At the same time, it was found that there are also extrarenal mechanisms that are still being studied. Moreover, a number of studies have suggested that sodium ions can be stored in body tissues without adequate retention of water to buffer the electrolyte. Given the participation of the kidneys in maintaining normal functional and metabolic relationships and in pathological syndromes related to other organs, it is possible to predict the correlation of the activity of established and new markers of extrarenal mechanisms with reducers of water-electrolyte exchange the final effects of which are mediated through changes in the functional state of the kidneys. Evaluation of additional sodium-regulatory systems is a promising current direction for expanding ideas about mechanisms of stability of electrolytes and water.

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Mosaic theory revised: inflammation and salt play central roles in arterial hypertension

Cited by 29 publications

References 181 publications

Fluid Overload and Tissue Sodium Accumulation as Main Drivers of Protein Energy Malnutrition in Dialysis Patients

Fluid Overload and Tissue Sodium Accumulation as Main Drivers of Protein Energy Malnutrition in Dialysis Patients

No compliment for complement: Kidney biopsies of patients with malignant nephrosclerosis show no complement activation

Regulatory mechanisms for maintaining homeostasis of sodium ions

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