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Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes

(1) Background: Little research is conducted on the link between diabetic kidney disease (DKD) progression and diabetic gastroenteropathy in type 1 diabetes (T1D). (2) Methods. We performed a cross-sectional study with 100 T1D patients; 27 of them had progressive DKD, defined as an estimated glomeru...

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Autores principales: Fedulovs, Aleksejs, Tzivian, Lilian, Zalizko, Polina, Ivanova, Santa, Bumane, Renāte, Janeviča, Jana, Krūzmane, Lelde, Krustins, Eduards, Sokolovska, Jelizaveta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10604159/
https://www.ncbi.nlm.nih.gov/pubmed/37893052
http://dx.doi.org/10.3390/biomedicines11102679
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author Fedulovs, Aleksejs
Tzivian, Lilian
Zalizko, Polina
Ivanova, Santa
Bumane, Renāte
Janeviča, Jana
Krūzmane, Lelde
Krustins, Eduards
Sokolovska, Jelizaveta
author_facet Fedulovs, Aleksejs
Tzivian, Lilian
Zalizko, Polina
Ivanova, Santa
Bumane, Renāte
Janeviča, Jana
Krūzmane, Lelde
Krustins, Eduards
Sokolovska, Jelizaveta
author_sort Fedulovs, Aleksejs
collection PubMed
description (1) Background: Little research is conducted on the link between diabetic kidney disease (DKD) progression and diabetic gastroenteropathy in type 1 diabetes (T1D). (2) Methods. We performed a cross-sectional study with 100 T1D patients; 27 of them had progressive DKD, defined as an estimated glomerular filtration rate (eGFR) decline ≥3 mL/min/year or increased albuminuria stage, over a mean follow-up time of 5.89 ± 1.73 years. A newly developed score with 17 questions on gastrointestinal (GI) symptoms was used. Faecal calprotectin was measured by ELISA. Lower GI endoscopies were performed in 21 patients. (3) Results: The gastrointestinal symptom score demonstrated high reliability (Cronbach’s α = 0.78). Patients with progressive DKD had higher GI symptom scores compared to those with stable DKD (p = 0.019). The former group demonstrated more frequent bowel movement disorders (p < 0.01). The scores correlated negatively with eGFR (r = −0.335; p = 0.001), positively with albuminuria (r = 0.245; p = 0.015), Hba1c (r = 0.305; p = 0.002), and diabetes duration (r = 0.251; p = 0.012). Faecal calprotectin levels did not differ between DKD groups significantly. The most commonly reported histopathological findings of enteric mucosa were infiltration with eosinophils, lymphocytes, plasmacytes, the presence of lymphoid follicles, and lymphoid aggregates. Conclusion: The progression of DKD is positively correlated with gastrointestinal symptoms; however, more research is needed to clarify the causal relationships of the gut-kidney axis in T1D.
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spelling pubmed-106041592023-10-28 Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes Fedulovs, Aleksejs Tzivian, Lilian Zalizko, Polina Ivanova, Santa Bumane, Renāte Janeviča, Jana Krūzmane, Lelde Krustins, Eduards Sokolovska, Jelizaveta Biomedicines Article (1) Background: Little research is conducted on the link between diabetic kidney disease (DKD) progression and diabetic gastroenteropathy in type 1 diabetes (T1D). (2) Methods. We performed a cross-sectional study with 100 T1D patients; 27 of them had progressive DKD, defined as an estimated glomerular filtration rate (eGFR) decline ≥3 mL/min/year or increased albuminuria stage, over a mean follow-up time of 5.89 ± 1.73 years. A newly developed score with 17 questions on gastrointestinal (GI) symptoms was used. Faecal calprotectin was measured by ELISA. Lower GI endoscopies were performed in 21 patients. (3) Results: The gastrointestinal symptom score demonstrated high reliability (Cronbach’s α = 0.78). Patients with progressive DKD had higher GI symptom scores compared to those with stable DKD (p = 0.019). The former group demonstrated more frequent bowel movement disorders (p < 0.01). The scores correlated negatively with eGFR (r = −0.335; p = 0.001), positively with albuminuria (r = 0.245; p = 0.015), Hba1c (r = 0.305; p = 0.002), and diabetes duration (r = 0.251; p = 0.012). Faecal calprotectin levels did not differ between DKD groups significantly. The most commonly reported histopathological findings of enteric mucosa were infiltration with eosinophils, lymphocytes, plasmacytes, the presence of lymphoid follicles, and lymphoid aggregates. Conclusion: The progression of DKD is positively correlated with gastrointestinal symptoms; however, more research is needed to clarify the causal relationships of the gut-kidney axis in T1D. MDPI 2023-09-29 /pmc/articles/PMC10604159/ /pubmed/37893052 http://dx.doi.org/10.3390/biomedicines11102679 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Fedulovs, Aleksejs
Tzivian, Lilian
Zalizko, Polina
Ivanova, Santa
Bumane, Renāte
Janeviča, Jana
Krūzmane, Lelde
Krustins, Eduards
Sokolovska, Jelizaveta
Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes
title Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes
title_full Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes
title_fullStr Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes
title_full_unstemmed Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes
title_short Progression of Diabetic Kidney Disease and Gastrointestinal Symptoms in Patients with Type I Diabetes
title_sort progression of diabetic kidney disease and gastrointestinal symptoms in patients with type i diabetes
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10604159/
https://www.ncbi.nlm.nih.gov/pubmed/37893052
http://dx.doi.org/10.3390/biomedicines11102679
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