(DBR) on the Inflammatory Response Chronic Kidney Disease A Brief Clinical Communication

(DBR) on the Inflammatory Response Chronic Kidney Disease A Brief Clinical Communication | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Short Report (DBR) on the Inflammatory Response Chronic Kidney Disease A Brief Clinical Communication Laura Soldati, Thom E Lobe, Kim Shafer This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4414918/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract To evaluate the effect of the oral administration of a novel probiotic/digestive enzyme supplementation (DBR), on inflammation in CKD patients, the impact on inflammatory markers were assessed at three and six months. When administered twice daily over 6 months, DBR supplementation appears to be effective in decreasing MCP = 1/CCL-2, a pro-inflammatory chemokine responsible for CKD worsening. DBR appears to be a promising adjuvant in CKD treatment Chronic Kidney Disease Probiotics MCP-1/CCL-2 Figures Figure 1 LAY SUMMARY In a prospective study at Milan University in Italy, a cohort of 60 patients with Chronic Kidney Disease (CKD), (Stages III to V) divided into groups were administered DBR, a proprietary probiotic/digestive enzyme combination supplement for either 3 or 6 months, to assess it’s affect on inflammation. When DBR was administered twice daily by mouth for 6 months there was a significant decrease in the levels of the pro-inflammatory cytokine, a Monoclonal Chemoattractant Protein -1 MCP-1/CCL-2 usually associated with a worsening of the CKD. DBR appears to be a promising adjuvant in CKD treatment. Background Chronic Kidney Disease (CKD), defined by the National Kidney Foundation as a condition in which abnormality of kidney structure or function (decline of excretory, endocrine, and metabolic function) occurs with glomerular filtration rate <60 ml/min/1.73m 2 for at least 3 months, affects more than 1 in 7 US adults, or about 35.5 million people, or 14% of the population. 1 Inflammation and oxidative stress play an important role in CKD progression. 2 In the literature, it has been shown that in patients with acute or chronic kidney disease, characterized by high oxidative stress, increased production of IL-6, IL-8, TNF-α, and Monoclonal Chemoattractant Protein -1 MCP-1/CCL-2 often occurs. 3 Also, over the last decade, there has been increased awareness that changes in the quantitative and/or qualitative composition of the gut microbiota are implicated in the occurrence of a systemic inflammatory state, CKD progression, and CKD-related cardiovascular disease (CVD). 4 We know that through corrections of daily habits such as low protein diets, correction of disorders of mineral metabolism and anemia, control of blood pressure and proteinuria, and other lifestyle interventions (smoking cessation and exercise), it is possible to delay the progressive loss of kidney function and/or prevent the development of CKD. 5 We hypothesize that modulation of the intestinal microbiota, by introducing probiotics and digestive enzymes, may be effective in improving clinical outcomes, due to a direct or indirect changes of the inflammatory and oxidative states. Aim The purpose of this study is to evaluate the effect of a novel probiotic/digestive enzyme supplementation (DBR), on inflammation in CKD patients by assessing the impact on inflammatory markers and changes in patterns of intestinal microbiota. PATIENTS, MATERIALS, AND METHODS Thirty patients with CKD (stages III to V), were given twice daily oral supplementation of a proprietary combination of probiotics and digestive enzymes (DBR). The patients were divided into 2 equal groups that received DBR for three (T1) or six months (T2). ELISA kits (Fluorokine, Multianalyte Profiling (MAP), and Luminex) were used to analyze the inflammatory markers of the patients before and after taking DBR. To better evaluate changes in the gut microbiota, 20 healthy age and gender matched control subjects also were recruited as an additional group. Informed consents were obtained for all patients. Results Since inflammation is the basis of chronic kidney disease, the serum concentrations of pro-inflammatory cytokines (CCL-2, IL-1β, IL-6, IL-18, INF-γ, IL-4, IL-12p70, TNF-α) were measured. Analysis shows that, after six months of treatment with DBR, CCL-2 levels decreased significantly (p-value 0.072; Figure 1). There were no significant differences noted in any other pro-inflammatory cytokines measured. Through the analysis of alpha-diversity, the Shannon indices obtained for the population’s groups were compared, resulting in statistically significant differences between controls and T0 (3,2 0,35, p-value=0,0321) and between controls and T2 (2,8 0,62, p-value = 0,0256). DISCUSSION CCl-2 appears to play an important role in renal inflammatory disease. Blockade of CCL-2 in several models of renal disease has ameliorated the disease, suggesting that inhibition of CCL-2 is a promising and valid strategy to treat patients with renal inflammatory disease 3 Several novel therapies have recently been shown to reduce both the kidney expression of CCL-2 and diabetic renal inflammation in animal models by targeting renal oxidative stress. However, the suppression of the inflammatory response was only partially affected by these treatments, indicating the need for more specific blockade of CCL-2 such as occurs with DBR. 6 Probiotics are know to retard the renal failure progression and decrease inflammatory markers such as plasma IS, pCS levels 4 , 6 , 7 , but the mechanisms are not clear. As a result, oral supplementation of probiotics in CKD patients, may exert a nephroprotective effect 7 . In a study of 888 patients with CKD divided into two groups, one consuming plain yogurt and one consuming yogurt with added probiotics, CRP levels dropped significantly in both groups compared to controls who consumed no yogurt. These findings were not dose dependent and appeared to be independent of age, sex, body mass index, CKD stage, cardiovascular disease, and fiber and protein consumption or total energy intake. 8 However, the administration of DBR alone has shown a documented reduction in CCL-2 production correlating with decreased oxidative stress and improvement renal function in patients with CKD. CONCLUSION When administered twice daily over 6 months, DBR supplementation appears to be effective in decreasing MCP = 1/CCL-2, a pro-inflammatory chemokine responsible for CKD worsening. DBR is a promising adjuvant in CKD treatment. Declarations Ethical Statements: Ethical Approval for this study was granted by the University of Milan. Consent to Participate and Consent to Publish was obtained by the University of Milan for each subject in the study. Competing interests Neither Drs Soldati or Lobe have any competing interests related to this study. Kim Shafer is the CEO of Daily Body Restore, LLC. Funding: This study was sponsored by Daily Body Restore, LLC, Michigan, USA through contract number: CTE_INT17LSOLD_01 with the University of Milan, Milan, Italy References Group CW. Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International 2013 : 1-150. H. Fujii KN, and M. Fukagawa. Role of Oxidative Stress and Indoxyl Sulfate in Progression of Cardiovascular Disease in Chronic Kidney Disease. Therapeutic Apheresis and Dialysis 2011; 15: 125– 128. Haller H, et al. Monocyte chemoattractant protein-1 and the kidney. Curr Opin Nephrol Hypertens 2016; 25: 42-49. al EC-Re. Impact of Altered Intestinal Microbiota on Chronic Kidney Disease Progression. Toxins 2018; 10: 300. E. Riccio ADN, and A. Pisani (ed). Nutritional treatment in chronic kidney disease: the concept of nephroprotectio . 2015. 161–167pp. Tesch GH. MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy. Amer J Physiol - Renal Physiol 2008; 294: F697-F701. Khiabani SA. ea. Chronic kidney disease and gut microbiota. Heliyon 2023; 9: e18991. Institut National de la Santé Et de la Recherche Médicale F. Chronic Kidney Disease - Renal Epidemiology and Information Network (CKD-REIN. 2019. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-4414918","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Short Report","associatedPublications":[],"authors":[{"id":306710964,"identity":"372b4655-77c2-441b-a965-ce2d03175322","order_by":0,"name":"Laura Soldati","email":"","orcid":"","institution":"University of Milan","correspondingAuthor":false,"prefix":"","firstName":"Laura","middleName":"","lastName":"Soldati","suffix":""},{"id":306710965,"identity":"be552687-4ad5-47ab-8b2e-a07213582c3f","order_by":1,"name":"Thom E Lobe","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAmUlEQVRIiWNgGAWjYDACdgY2BoYKBh4QW4IoHTzMIC1nSNbC2AbhEKfFnpn52IOP8w7L8DcwH7zNQ5wtbOmGM7cd5pE4wJZsTaQWHjNpXqAWAwYgg3gtf+eAtPB/I0ELYwPYFjYitRwG+qXnWDqPxGE2Y8s5xGhhb28+9uBHjbU9f3vzwxtviNGCAMykKR8Fo2AUjIJRgA8AAF5II7bsyOGEAAAAAElFTkSuQmCC","orcid":"","institution":"University of Illinois at Chicago","correspondingAuthor":true,"prefix":"","firstName":"Thom","middleName":"E","lastName":"Lobe","suffix":""},{"id":306710966,"identity":"eaf9e0f7-eba4-43ec-b62d-45f4e042092c","order_by":2,"name":"Kim Shafer","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Kim","middleName":"","lastName":"Shafer","suffix":""}],"badges":[],"createdAt":"2024-05-13 18:38:32","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-4414918/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-4414918/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":57727960,"identity":"ca3843a6-6a27-4c88-9abf-f731c835f863","added_by":"auto","created_at":"2024-06-04 21:40:37","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":19589,"visible":true,"origin":"","legend":"\u003cp\u003eLevels of pro-inflammatory chemokine CCL-2/MCP-1 in CKD patients. CKD T0: CKD patients at baseline; CKD T2: CKD patients after 6 months of DBR supplementation.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-4414918/v1/59afb051648541cbced006d9.png"},{"id":73247180,"identity":"3114b35a-ed75-4021-86b8-24114ac65fc2","added_by":"auto","created_at":"2025-01-08 07:09:28","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":220393,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4414918/v1/f26b8739-f5d8-41d0-8891-4c60df5bffa2.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"(DBR) on the Inflammatory Response Chronic Kidney Disease A Brief Clinical Communication","fulltext":[{"header":"LAY SUMMARY","content":"\u003cp\u003eIn a prospective study at Milan University in Italy, a cohort of 60 patients with Chronic Kidney Disease (CKD), (Stages III to V) divided into groups were administered DBR, a proprietary probiotic/digestive enzyme combination supplement for either 3 or 6 months, to assess it\u0026rsquo;s affect on inflammation. When DBR was administered twice daily by mouth for 6 months there was a significant decrease in the levels of the pro-inflammatory cytokine, a Monoclonal Chemoattractant Protein -1 MCP-1/CCL-2 usually associated with a worsening of the CKD. \u0026nbsp;DBR appears to be a promising adjuvant in CKD treatment. \u0026nbsp;\u003c/p\u003e\n"},{"header":"Background","content":"\u003cp\u003eChronic Kidney Disease (CKD), defined by the National Kidney Foundation as a condition in which abnormality of kidney structure or function (decline of excretory, endocrine, and metabolic function) occurs with glomerular filtration rate \u0026lt;60 ml/min/1.73m\u003csup\u003e2\u003c/sup\u003e for at least 3 months, affects more than 1 in 7 US adults, or about 35.5 million people, or 14% of the population.\u003csup\u003e1\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eInflammation and oxidative stress play an important role in CKD progression.\u003csup\u003e2\u003c/sup\u003e In the literature, it has been shown that in patients with acute or chronic kidney disease, characterized by high oxidative stress, increased production of IL-6, IL-8, TNF-\u0026alpha;, and Monoclonal Chemoattractant Protein -1 MCP-1/CCL-2 often occurs.\u003csup\u003e3\u003c/sup\u003e Also, over the last decade, there has been increased awareness that changes in the quantitative and/or qualitative composition of the gut microbiota are implicated in the occurrence of a systemic inflammatory state, CKD progression, and CKD-related cardiovascular disease (CVD).\u003csup\u003e4\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eWe know that through corrections of daily habits such as low protein diets, correction of disorders of mineral metabolism and anemia, control of blood pressure and proteinuria, and other lifestyle interventions (smoking cessation and exercise), it is possible to delay the progressive loss of kidney function and/or prevent the development of CKD.\u003csup\u003e5\u003c/sup\u003e We hypothesize that modulation of the intestinal microbiota, by introducing probiotics and digestive enzymes, may be effective in improving clinical outcomes, due to a direct or indirect changes of the inflammatory and oxidative states.\u003c/p\u003e\n\u003ch3\u003eAim\u003c/h3\u003e\n\u003cp\u003eThe purpose of this study is to evaluate the effect of a novel probiotic/digestive enzyme supplementation (DBR), on inflammation in CKD patients by assessing the impact on inflammatory markers and changes in patterns of intestinal microbiota.\u003c/p\u003e\n"},{"header":"PATIENTS, MATERIALS, AND METHODS","content":"\u003cp\u003eThirty patients with CKD (stages III to V), were given twice daily oral supplementation of a proprietary combination of probiotics and digestive enzymes (DBR). The patients were divided into 2 equal groups that received DBR for three (T1) or six months (T2).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eELISA kits (Fluorokine, Multianalyte Profiling (MAP), and Luminex) were used to analyze the inflammatory markers of the patients before and after taking DBR.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTo better evaluate changes in the gut microbiota, 20 healthy age and gender matched control subjects also were recruited as an additional group.\u003c/p\u003e\n\u003cp\u003eInformed consents were obtained for all patients.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eSince inflammation is the basis of chronic kidney disease, the serum concentrations of pro-inflammatory cytokines (CCL-2, IL-1\u0026beta;, IL-6, IL-18, INF-\u0026gamma;, IL-4, IL-12p70, TNF-\u0026alpha;) were measured. Analysis shows that, after six months of treatment with DBR, CCL-2 levels decreased significantly (p-value 0.072; Figure 1). There were no significant differences noted in any other pro-inflammatory cytokines measured.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThrough the analysis of alpha-diversity, the Shannon indices obtained for the population\u0026rsquo;s groups were compared, resulting in statistically significant differences between controls and T0 (3,2 0,35, p-value=0,0321) and between controls and T2 (2,8 0,62, p-value = 0,0256).\u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eCCl-2 appears to play an important role in renal inflammatory disease. Blockade of CCL-2 in several models of renal disease has ameliorated the disease, suggesting that inhibition of CCL-2 is a promising and valid strategy to treat patients with renal inflammatory disease \u003csup\u003e\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eSeveral novel therapies have recently been shown to reduce both the kidney expression of CCL-2 and diabetic renal inflammation in animal models by targeting renal oxidative stress. However, the suppression of the inflammatory response was only partially affected by these treatments, indicating the need for more specific blockade of CCL-2 such as occurs with DBR. \u003csup\u003e\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eProbiotics are know to retard the renal failure progression and decrease inflammatory markers such as plasma IS, pCS levels \u003csup\u003e\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e, but the mechanisms are not clear. As a result, oral supplementation of probiotics in CKD patients, may exert a nephroprotective effect \u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e. In a study of 888 patients with CKD divided into two groups, one consuming plain yogurt and one consuming yogurt with added probiotics, CRP levels dropped significantly in both groups compared to controls who consumed no yogurt. These findings were not dose dependent and appeared to be independent of age, sex, body mass index, CKD stage, cardiovascular disease, and fiber and protein consumption or total energy intake.\u003csup\u003e\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eHowever, the administration of DBR alone has shown a documented reduction in CCL-2 production correlating with decreased oxidative stress and improvement renal function in patients with CKD.\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eWhen administered twice daily over 6 months, DBR supplementation appears to be effective in decreasing MCP\u0026thinsp;=\u0026thinsp;1/CCL-2, a pro-inflammatory chemokine responsible for CKD worsening. DBR is a promising adjuvant in CKD treatment.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthical Statements:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eEthical Approval for this study was granted by the University of Milan.\u0026nbsp;\u003c/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eConsent to Participate\u003c/strong\u003e and \u003cstrong\u003eConsent to Publish\u003c/strong\u003e was obtained by the University of Milan for each subject in the study.\u0026nbsp;\u003c/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e \u0026nbsp;\u003c/p\u003e\n\u003cp\u003eNeither Drs Soldati or Lobe have any competing interests related to this study. Kim Shafer is the CEO of Daily Body Restore, LLC.\u003c/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eFunding:\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was sponsored by Daily Body Restore, LLC, Michigan, USA through\u0026nbsp;contract number:\u0026nbsp;CTE_INT17LSOLD_01 with the University of Milan, Milan, Italy\u003c/p\u003e\n\n\n"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eGroup CW. Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. \u003cem\u003eKidney International\u003c/em\u003e 2013\u003cstrong\u003e: \u003c/strong\u003e1-150.\u003c/li\u003e\n \u003cli\u003eH. Fujii KN, and M. Fukagawa. Role of Oxidative Stress and Indoxyl Sulfate in Progression of Cardiovascular Disease in Chronic Kidney Disease. \u003cem\u003eTherapeutic Apheresis and Dialysis\u003c/em\u003e 2011; \u003cstrong\u003e15: \u003c/strong\u003e125\u0026ndash; 128.\u003c/li\u003e\n \u003cli\u003eHaller H, et al. Monocyte chemoattractant protein-1 and the kidney. \u003cem\u003eCurr Opin Nephrol Hypertens\u003c/em\u003e 2016; \u003cstrong\u003e25: \u003c/strong\u003e42-49.\u003c/li\u003e\n \u003cli\u003eal EC-Re. Impact of Altered Intestinal Microbiota on Chronic Kidney Disease Progression. \u003cem\u003eToxins\u003c/em\u003e 2018; \u003cstrong\u003e10: \u003c/strong\u003e300.\u003c/li\u003e\n \u003cli\u003eE. Riccio ADN, and A. Pisani (ed). \u003cem\u003eNutritional treatment in chronic kidney disease: the concept of nephroprotectio\u003c/em\u003e. 2015. 161\u0026ndash;167pp.\u003c/li\u003e\n \u003cli\u003eTesch GH. MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy. \u003cem\u003eAmer J Physiol - Renal Physiol\u003c/em\u003e 2008; \u003cstrong\u003e294: \u003c/strong\u003eF697-F701.\u003c/li\u003e\n \u003cli\u003eKhiabani SA. ea. Chronic kidney disease and gut microbiota. \u003cem\u003eHeliyon\u003c/em\u003e 2023; \u003cstrong\u003e9: \u003c/strong\u003ee18991.\u003c/li\u003e\n \u003cli\u003eInstitut National de la Sant\u0026eacute; Et de la Recherche M\u0026eacute;dicale F. Chronic Kidney Disease - Renal Epidemiology and Information Network (CKD-REIN. 2019.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Chronic Kidney Disease, Probiotics, MCP-1/CCL-2","lastPublishedDoi":"10.21203/rs.3.rs-4414918/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4414918/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eTo evaluate the effect of the oral administration of a novel probiotic/digestive enzyme supplementation (DBR), on inflammation in CKD patients, the impact on inflammatory markers were assessed at three and six months. When administered twice daily over 6 months, DBR supplementation appears to be effective in decreasing MCP = 1/CCL-2, a pro-inflammatory chemokine responsible for CKD worsening. DBR appears to be a promising adjuvant in CKD treatment\u003c/p\u003e","manuscriptTitle":"(DBR) on the Inflammatory Response Chronic Kidney Disease A Brief Clinical Communication","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-06-04 21:40:32","doi":"10.21203/rs.3.rs-4414918/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"eadbcd0d-8e70-4563-8f58-601e2864f997","owner":[],"postedDate":"June 4th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-01-08T07:09:08+00:00","versionOfRecord":[],"versionCreatedAt":"2024-06-04 21:40:32","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-4414918","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4414918","identity":"rs-4414918","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}