Mitochondrial DNA Changes in Blood and Urine Display a Specific Signature in Relation to Inflammation in Normoalbuminuric Diabetic Kidney Disease in Type 2 Diabetes Mellitus Patients

Mitochondrial dysfunction is an important mechanism contributing to the development and progression of diabetic kidney disease (DKD). Mitochondrial DNA (mtDNA) levels in blood and urine were evaluated in relation to podocyte injury and proximal tubule (PT) dysfunction, as well as to a specific infla...

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Published inInternational journal of molecular sciences Vol. 24; no. 12; p. 9803
Main Authors Petrica, Ligia, Vlad, Adrian, Gadalean, Florica, Muntean, Danina Mirela, Vlad, Daliborca, Dumitrascu, Victor, Bob, Flaviu, Milas, Oana, Suteanu-Simulescu, Anca, Glavan, Mihaela, Jianu, Dragos Catalin, Ursoniu, Sorin, Balint, Lavinia, Mogos-Stefan, Maria, Ienciu, Silvia, Cretu, Octavian Marius, Popescu, Roxana
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.06.2023
MDPI
Subjects
Albuminuria - urine
Biomarkers
Biomarkers - urine
Blood
Chronic kidney failure
Creatinine
Cytokines
Diabetes
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - genetics
Diabetes therapy
diabetic kidney disease
Diabetic Nephropathies
Diabetic nephropathy
Diabetics
DNA, Mitochondrial - genetics
Glucosaminidase
Humans
Hypotheses
Inflammation
Inflammation - genetics
Inflammatory response
Injuries
Interleukin 10
Interleukin 18
Interleukin-17
Interleukin-18 - genetics
Kidney diseases
Mitochondria
Mitochondria - genetics
Mitochondrial DNA
normoalbuminuria
Oxidative stress
Patients
Peripheral blood
podocyte
proximal tubule
Regression analysis
Type 2 diabetes
Urine
Romania
diabetic kidney disease
inflammation
mitochondrial DNA
podocyte
type 2 diabetes mellitus
normoalbuminuria
proximal tubule
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Abstract Mitochondrial dysfunction is an important mechanism contributing to the development and progression of diabetic kidney disease (DKD). Mitochondrial DNA (mtDNA) levels in blood and urine were evaluated in relation to podocyte injury and proximal tubule (PT) dysfunction, as well as to a specific inflammatory response in normoalbuminuric DKD. A total of 150 type 2 diabetes mellitus (DM) patients (52 normoalbuminuric, 48 microalbuminuric, and 50 macroalbuminuric ones, respectively) and 30 healthy controls were assessed concerning the urinary albumin/creatinine ratio (UACR), biomarkers of podocyte damage (synaptopodin and podocalyxin), PT dysfunction (kidney injury molecule-1 (KIM-1) and -acetyl-β-(D)-glucosaminidase (NAG)), and inflammation (serum and urinary interleukins (IL-17A, IL-18, and IL-10)). MtDNA-CN and nuclear DNA (nDNA) were quantified in peripheral blood and urine via qRT-PCR. MtDNA-CN was defined as the ratio of the number of mtDNA/nDNA copies via analysis of the CYTB/B2M and ND2/B2M ratio. Multivariable regression analysis provided models in which serum mtDNA directly correlated with IL-10 and indirectly correlated with UACR, IL-17A, and KIM-1 (R = 0.626; < 0.0001). Urinary mtDNA directly correlated with UACR, podocalyxin, IL-18, and NAG, and negatively correlated with eGFR and IL-10 (R = 0.631; < 0.0001). Mitochondrial DNA changes in serum and urine display a specific signature in relation to inflammation both at the podocyte and tubular levels in normoalbuminuric type 2 DM patients.
AbstractList Mitochondrial dysfunction is an important mechanism contributing to the development and progression of diabetic kidney disease (DKD). Mitochondrial DNA (mtDNA) levels in blood and urine were evaluated in relation to podocyte injury and proximal tubule (PT) dysfunction, as well as to a specific inflammatory response in normoalbuminuric DKD. A total of 150 type 2 diabetes mellitus (DM) patients (52 normoalbuminuric, 48 microalbuminuric, and 50 macroalbuminuric ones, respectively) and 30 healthy controls were assessed concerning the urinary albumin/creatinine ratio (UACR), biomarkers of podocyte damage (synaptopodin and podocalyxin), PT dysfunction (kidney injury molecule-1 (KIM-1) and N -acetyl-β-(D)-glucosaminidase (NAG)), and inflammation (serum and urinary interleukins (IL-17A, IL-18, and IL-10)). MtDNA-CN and nuclear DNA (nDNA) were quantified in peripheral blood and urine via qRT-PCR. MtDNA-CN was defined as the ratio of the number of mtDNA/nDNA copies via analysis of the CYTB/B2M and ND2/B2M ratio. Multivariable regression analysis provided models in which serum mtDNA directly correlated with IL-10 and indirectly correlated with UACR, IL-17A, and KIM-1 (R 2 = 0.626; p < 0.0001). Urinary mtDNA directly correlated with UACR, podocalyxin, IL-18, and NAG, and negatively correlated with eGFR and IL-10 (R 2 = 0.631; p < 0.0001). Mitochondrial DNA changes in serum and urine display a specific signature in relation to inflammation both at the podocyte and tubular levels in normoalbuminuric type 2 DM patients.
Mitochondrial dysfunction is an important mechanism contributing to the development and progression of diabetic kidney disease (DKD). Mitochondrial DNA (mtDNA) levels in blood and urine were evaluated in relation to podocyte injury and proximal tubule (PT) dysfunction, as well as to a specific inflammatory response in normoalbuminuric DKD. A total of 150 type 2 diabetes mellitus (DM) patients (52 normoalbuminuric, 48 microalbuminuric, and 50 macroalbuminuric ones, respectively) and 30 healthy controls were assessed concerning the urinary albumin/creatinine ratio (UACR), biomarkers of podocyte damage (synaptopodin and podocalyxin), PT dysfunction (kidney injury molecule-1 (KIM-1) and N-acetyl-β-(D)-glucosaminidase (NAG)), and inflammation (serum and urinary interleukins (IL-17A, IL-18, and IL-10)). MtDNA-CN and nuclear DNA (nDNA) were quantified in peripheral blood and urine via qRT-PCR. MtDNA-CN was defined as the ratio of the number of mtDNA/nDNA copies via analysis of the CYTB/B2M and ND2/B2M ratio. Multivariable regression analysis provided models in which serum mtDNA directly correlated with IL-10 and indirectly correlated with UACR, IL-17A, and KIM-1 (R2 = 0.626; p < 0.0001). Urinary mtDNA directly correlated with UACR, podocalyxin, IL-18, and NAG, and negatively correlated with eGFR and IL-10 (R2 = 0.631; p < 0.0001). Mitochondrial DNA changes in serum and urine display a specific signature in relation to inflammation both at the podocyte and tubular levels in normoalbuminuric type 2 DM patients.
Mitochondrial dysfunction is an important mechanism contributing to the development and progression of diabetic kidney disease (DKD). Mitochondrial DNA (mtDNA) levels in blood and urine were evaluated in relation to podocyte injury and proximal tubule (PT) dysfunction, as well as to a specific inflammatory response in normoalbuminuric DKD. A total of 150 type 2 diabetes mellitus (DM) patients (52 normoalbuminuric, 48 microalbuminuric, and 50 macroalbuminuric ones, respectively) and 30 healthy controls were assessed concerning the urinary albumin/creatinine ratio (UACR), biomarkers of podocyte damage (synaptopodin and podocalyxin), PT dysfunction (kidney injury molecule-1 (KIM-1) and N-acetyl-β-(D)-glucosaminidase (NAG)), and inflammation (serum and urinary interleukins (IL-17A, IL-18, and IL-10)). MtDNA-CN and nuclear DNA (nDNA) were quantified in peripheral blood and urine via qRT-PCR. MtDNA-CN was defined as the ratio of the number of mtDNA/nDNA copies via analysis of the CYTB/B2M and ND2/B2M ratio. Multivariable regression analysis provided models in which serum mtDNA directly correlated with IL-10 and indirectly correlated with UACR, IL-17A, and KIM-1 (R[sup.2] = 0.626; p < 0.0001). Urinary mtDNA directly correlated with UACR, podocalyxin, IL-18, and NAG, and negatively correlated with eGFR and IL-10 (R[sup.2] = 0.631; p < 0.0001). Mitochondrial DNA changes in serum and urine display a specific signature in relation to inflammation both at the podocyte and tubular levels in normoalbuminuric type 2 DM patients.
Mitochondrial dysfunction is an important mechanism contributing to the development and progression of diabetic kidney disease (DKD). Mitochondrial DNA (mtDNA) levels in blood and urine were evaluated in relation to podocyte injury and proximal tubule (PT) dysfunction, as well as to a specific inflammatory response in normoalbuminuric DKD. A total of 150 type 2 diabetes mellitus (DM) patients (52 normoalbuminuric, 48 microalbuminuric, and 50 macroalbuminuric ones, respectively) and 30 healthy controls were assessed concerning the urinary albumin/creatinine ratio (UACR), biomarkers of podocyte damage (synaptopodin and podocalyxin), PT dysfunction (kidney injury molecule-1 (KIM-1) and -acetyl-β-(D)-glucosaminidase (NAG)), and inflammation (serum and urinary interleukins (IL-17A, IL-18, and IL-10)). MtDNA-CN and nuclear DNA (nDNA) were quantified in peripheral blood and urine via qRT-PCR. MtDNA-CN was defined as the ratio of the number of mtDNA/nDNA copies via analysis of the CYTB/B2M and ND2/B2M ratio. Multivariable regression analysis provided models in which serum mtDNA directly correlated with IL-10 and indirectly correlated with UACR, IL-17A, and KIM-1 (R = 0.626; < 0.0001). Urinary mtDNA directly correlated with UACR, podocalyxin, IL-18, and NAG, and negatively correlated with eGFR and IL-10 (R = 0.631; < 0.0001). Mitochondrial DNA changes in serum and urine display a specific signature in relation to inflammation both at the podocyte and tubular levels in normoalbuminuric type 2 DM patients.
Audience Academic
Author Vlad, Adrian
Gadalean, Florica
Vlad, Daliborca
Dumitrascu, Victor
Balint, Lavinia
Mogos-Stefan, Maria
Glavan, Mihaela
Muntean, Danina Mirela
Popescu, Roxana
Petrica, Ligia
Ursoniu, Sorin
Suteanu-Simulescu, Anca
Jianu, Dragos Catalin
Ienciu, Silvia
Cretu, Octavian Marius
Bob, Flaviu
Milas, Oana
AuthorAffiliation 4 Center for Translational Research and Systems Medicine, Faculty of Medicine, “Victor Babes” University of Medicine and Pharmacy, No. 2, Eftimie Murgu Sq., 300041 Timisoara, Romania
2 Centre for Molecular Research in Nephrology and Vascular Disease, Faculty of Medicine, “Victor Babes” University of Medicine and Pharmacy, No. 2, Eftimie Murgu Sq., 300041 Timisoara, Romania; vlad.adrian@umft.ro (A.V.); daninamuntean@umft.ro (D.M.M.); vlad.daliborca@umft.ro (D.V.); dumitrascu.victor@umft.ro (V.D.); jianu.dragos@umft.ro (D.C.J.); sursoniu@umft.ro (S.U.); popescu.roxana@umft.ro (R.P.)
12 Emergency Clinical Municipal Hospital Timisoara, 300041 Timisoara, Romania
1 Department of Internal Medicine II, Division of Nephrology, “Victor Babes” University of Medicine and Pharmacy, No. 2, Eftimie Murgu Sq., 300041 Timisoara, Romania or petrica.ligia@umft.ro (L.P.); bob.flaviu@umft.ro (F.B.); oana.milas@yahoo.com (O.M.); anca.simulescu@yahoo.com (A.S.-S.); mihaelapatruica@gmail.com (M.G.); lavinia.bali
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/37372951$$D View this record in MEDLINE/PubMed
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Issue 12
Keywords diabetic kidney disease
inflammation
mitochondrial DNA
podocyte
type 2 diabetes mellitus
normoalbuminuria
proximal tubule
Language English
License 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/).
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Snippet Mitochondrial dysfunction is an important mechanism contributing to the development and progression of diabetic kidney disease (DKD). Mitochondrial DNA (mtDNA)...
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SubjectTerms Albuminuria - urine
Biomarkers
Biomarkers - urine
Blood
Chronic kidney failure
Creatinine
Cytokines
Diabetes
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - genetics
Diabetes therapy
diabetic kidney disease
Diabetic Nephropathies
Diabetic nephropathy
Diabetics
DNA, Mitochondrial - genetics
Glucosaminidase
Humans
Hypotheses
Inflammation
Inflammation - genetics
Inflammatory response
Injuries
Interleukin 10
Interleukin 18
Interleukin-17
Interleukin-18 - genetics
Kidney diseases
Mitochondria
Mitochondria - genetics
Mitochondrial DNA
normoalbuminuria
Oxidative stress
Patients
Peripheral blood
podocyte
proximal tubule
Regression analysis
Type 2 diabetes
Urine
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Title Mitochondrial DNA Changes in Blood and Urine Display a Specific Signature in Relation to Inflammation in Normoalbuminuric Diabetic Kidney Disease in Type 2 Diabetes Mellitus Patients
URI https://www.ncbi.nlm.nih.gov/pubmed/37372951
https://www.proquest.com/docview/2829821366
https://search.proquest.com/docview/2830666297
https://pubmed.ncbi.nlm.nih.gov/PMC10298001
https://doaj.org/article/c3b2da414e00448e91ff3ead2b767c74
Volume 24
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