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  1. Article ; Online: Butyrate promotes kidney resilience through a coordinated kidney protective response in tubular cells.

    Favero, Chiara / Pintor-Chocano, Aranzazu / Sanz, Ana / Ortiz, Alberto / Sanchez-Niño, Maria D

    Biochemical pharmacology

    2024  Volume 224, Page(s) 116203

    Abstract: Acute kidney injury (AKI) is common in hospitalized patients and increases short-term and long-term mortality. Treatment options for AKI are limited. Gut microbiota products such as the short-chain fatty acid butyrate have anti-inflammatory actions that ... ...

    Abstract Acute kidney injury (AKI) is common in hospitalized patients and increases short-term and long-term mortality. Treatment options for AKI are limited. Gut microbiota products such as the short-chain fatty acid butyrate have anti-inflammatory actions that may protect tissues, including the kidney, from injury. However, the molecular mechanisms of tissue protection by butyrate are poorly understood. Treatment with oral butyrate for two weeks prior to folic acid-induced AKI and during AKI improved kidney function and decreased tubular injury and kidney inflammation while stopping butyrate before AKI was not protective. Continuous butyrate preserved the expression of kidney protective factors such as Klotho, PGC-1α and Nlrp6 which were otherwise downregulated. In cultured tubular cells, butyrate blunted the maladaptive tubular cell response to a proinflammatory milieu, preserving the expression of kidney protective factors. Kidney protection afforded by this continuous butyrate schedule was confirmed in a second model of nephrotoxic AKI, cisplatin nephrotoxicity, where the expression of kidney protective factors was also preserved. To assess the contribution of preservation of kidney protective factors to kidney resilience, recombinant Klotho was administered to mice with cisplatin-AKI and shown to preserve the expression of PGC-1α and Nlrp6, decrease kidney inflammation and protect from AKI. In conclusion, butyrate promotes kidney resilience to AKI and decreases inflammation by preventing the downregulation of kidney protective genes such as Klotho. This information may be relevant to optimize antibiotic management during hospitalization.
    Language English
    Publishing date 2024-04-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2024.116203
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Probiotics for kidney disease.

    Favero, Chiara / Ortiz, Alberto / Sanchez-Niño, Maria D

    Clinical kidney journal

    2022  Volume 15, Issue 11, Page(s) 1981–1986

    Abstract: Diet has long been known to influence the course of chronic kidney disease (CKD) and may even result in acute kidney injury (AKI). Diet may influence kidney disease through a direct impact of specific nutrients on the human body through modulation of the ...

    Abstract Diet has long been known to influence the course of chronic kidney disease (CKD) and may even result in acute kidney injury (AKI). Diet may influence kidney disease through a direct impact of specific nutrients on the human body through modulation of the gut microbiota composition or through metabolites generated by the gut microbiota from ingested nutrients. The potential for interaction between diet, microbiota and CKD has fueled research into interventions aimed at modifying the microbiota to treat CKD. These interventions may include diet, probiotics, prebiotics, fecal microbiota transplant and other interventions that modulate the microbiota and its metabolome. A recent report identified
    Language English
    Publishing date 2022-02-28
    Publishing country England
    Document type Editorial
    ZDB-ID 2655800-2
    ISSN 2048-8513 ; 2048-8505
    ISSN (online) 2048-8513
    ISSN 2048-8505
    DOI 10.1093/ckj/sfac056
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: SCARF Genes in COVID-19 and Kidney Disease: A Path to Comorbidity-Specific Therapies.

    Carriazo, Sol / Abasheva, Daria / Duarte, Deborah / Ortiz, Alberto / Sanchez-Niño, Maria Dolores

    International journal of molecular sciences

    2023  Volume 24, Issue 22

    Abstract: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which has killed ~7 million persons worldwide. Chronic kidney disease (CKD) is the most common risk factor for severe COVID-19 and one that most ... ...

    Abstract Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which has killed ~7 million persons worldwide. Chronic kidney disease (CKD) is the most common risk factor for severe COVID-19 and one that most increases the risk of COVID-19-related death. Moreover, CKD increases the risk of acute kidney injury (AKI), and COVID-19 patients with AKI are at an increased risk of death. However, the molecular basis underlying this risk has not been well characterized. CKD patients are at increased risk of death from multiple infections, to which immune deficiency in non-specific host defenses may contribute. However, COVID-19-associated AKI has specific molecular features and CKD modulates the local (kidney) and systemic (lung, aorta) expression of host genes encoding coronavirus-associated receptors and factors (SCARFs), which SARS-CoV-2 hijacks to enter cells and replicate. We review the interaction between kidney disease and COVID-19, including the over 200 host genes that may influence the severity of COVID-19, and provide evidence suggesting that kidney disease may modulate the expression of SCARF genes and other key host genes involved in an effective adaptive defense against coronaviruses. Given the poor response of certain CKD populations (e.g., kidney transplant recipients) to SARS-CoV-2 vaccines and their suboptimal outcomes when infected, we propose a research agenda focusing on CKD to develop the concept of comorbidity-specific targeted therapeutic approaches to SARS-CoV-2 infection or to future coronavirus infections.
    MeSH term(s) Humans ; COVID-19/complications ; COVID-19/genetics ; SARS-CoV-2 ; COVID-19 Vaccines ; Comorbidity ; Renal Insufficiency, Chronic/epidemiology ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/therapy ; Acute Kidney Injury/etiology ; Acute Kidney Injury/genetics
    Chemical Substances COVID-19 Vaccines
    Language English
    Publishing date 2023-11-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242216078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Interaction of Fabry Disease and Diabetes Mellitus: Suboptimal Recruitment of Kidney Protective Factors.

    Sanchez-Niño, Maria D / Ceballos, Maria I / Carriazo, Sol / Pintor-Chocano, Aranzazu / Sanz, Ana B / Saleem, Moin A / Ortiz, Alberto

    International journal of molecular sciences

    2023  Volume 24, Issue 21

    Abstract: Fabry disease is a lysosomal disease characterized by globotriaosylceramide (Gb3) accumulation. It may coexist with diabetes mellitus and both cause potentially lethal kidney end-organ damage. However, there is little information on their interaction ... ...

    Abstract Fabry disease is a lysosomal disease characterized by globotriaosylceramide (Gb3) accumulation. It may coexist with diabetes mellitus and both cause potentially lethal kidney end-organ damage. However, there is little information on their interaction with kidney disease. We have addressed the interaction between Fabry disease and diabetes in data mining of human kidney transcriptomics databases and in Fabry (
    MeSH term(s) Humans ; Mice ; Animals ; Fabry Disease/metabolism ; Protective Factors ; Kidney/metabolism ; Kidney Diseases/genetics ; Kidney Diseases/metabolism ; Renal Insufficiency/metabolism ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Trihexosylceramides/metabolism ; alpha-Galactosidase/genetics
    Chemical Substances Trihexosylceramides ; alpha-Galactosidase (EC 3.2.1.22)
    Language English
    Publishing date 2023-11-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242115853
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Megalin/lipoprotein receptor-related protein 2 autoimmunity and kidney disease.

    Perez-Gomez, Maria V / Sanchez-Niño, Maria D / Ortiz, Alberto

    Clinical kidney journal

    2020  Volume 13, Issue 3, Page(s) 281–286

    Abstract: In this issue ... ...

    Abstract In this issue of
    Language English
    Publishing date 2020-03-19
    Publishing country England
    Document type Editorial
    ZDB-ID 2655800-2
    ISSN 2048-8513 ; 2048-8505
    ISSN (online) 2048-8513
    ISSN 2048-8505
    DOI 10.1093/ckj/sfz171
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Interaction of Fabry Disease and Diabetes Mellitus

    Maria D. Sanchez-Niño / Maria I. Ceballos / Sol Carriazo / Aranzazu Pintor-Chocano / Ana B. Sanz / Moin A. Saleem / Alberto Ortiz

    International Journal of Molecular Sciences, Vol 24, Iss 21, p

    Suboptimal Recruitment of Kidney Protective Factors

    2023  Volume 15853

    Abstract: Fabry disease is a lysosomal disease characterized by globotriaosylceramide (Gb3) accumulation. It may coexist with diabetes mellitus and both cause potentially lethal kidney end-organ damage. However, there is little information on their interaction ... ...

    Abstract Fabry disease is a lysosomal disease characterized by globotriaosylceramide (Gb3) accumulation. It may coexist with diabetes mellitus and both cause potentially lethal kidney end-organ damage. However, there is little information on their interaction with kidney disease. We have addressed the interaction between Fabry disease and diabetes in data mining of human kidney transcriptomics databases and in Fabry ( Gla -/-) and wild type mice with or without streptozotocin-induced diabetes. Data mining was consistent with differential expression of genes encoding enzymes from the Gb3 metabolic pathway in human diabetic kidney disease, including upregulation of UGCG , the gene encoding the upstream and rate-limiting enzyme glucosyl ceramide synthase. Diabetic Fabry mice displayed the most severe kidney infiltration by F4/80+ macrophages, and a lower kidney expression of kidney protective genes ( Pgc1α and Tfeb ) than diabetic wild type mice, without a further increase in kidney fibrosis. Moreover, only diabetic Fabry mice developed kidney insufficiency and these mice with kidney insufficiency had a high expression of Ugcg . In conclusion, we found evidence of interaction between diabetes and Fabry disease that may increase the severity of the kidney phenotype through modulation of the Gb3 synthesis pathway and downregulation of kidney protective genes.
    Keywords fabry disease ; diabetes mellitus ; kidney ; chronic kidney disease ; inflammation ; fibrosis ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 616 ; 570
    Language English
    Publishing date 2023-11-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Albuminuria Downregulation of the Anti-Aging Factor Klotho: The Missing Link Potentially Explaining the Association of Pathological Albuminuria with Premature Death.

    Fernández-Fernández, Beatriz / Valiño-Rivas, Lara / Sánchez-Niño, Maria D / Ortiz, Alberto

    Advances in therapy

    2020  Volume 37, Issue Suppl 2, Page(s) 62–72

    Abstract: Ten percent of the adult population has chronic kidney disease (CKD), which is diagnosed when the glomerular filtration rate (GFR) is below 60 mL/min per 1.73 ... ...

    Abstract Ten percent of the adult population has chronic kidney disease (CKD), which is diagnosed when the glomerular filtration rate (GFR) is below 60 mL/min per 1.73 m
    MeSH term(s) Adult ; Age Factors ; Aged ; Aged, 80 and over ; Aging/genetics ; Aging/physiology ; Albuminuria/genetics ; Albuminuria/metabolism ; Albuminuria/physiopathology ; Disease Progression ; Down-Regulation/genetics ; Female ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Humans ; Male ; Middle Aged ; Mortality, Premature
    Chemical Substances Glucuronidase (EC 3.2.1.31)
    Language English
    Publishing date 2020-03-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 632651-1
    ISSN 1865-8652 ; 0741-238X
    ISSN (online) 1865-8652
    ISSN 0741-238X
    DOI 10.1007/s12325-019-01180-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Does wealth make health? Cherchez la renal replacement therapy.

    Sanchez-Niño, Maria D / Ortiz, Alberto

    Clinical kidney journal

    2017  Volume 10, Issue 1, Page(s) 45–48

    Abstract: In this issue ... ...

    Abstract In this issue of
    Language English
    Publishing date 2017-01-25
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2655800-2
    ISSN 2048-8513 ; 2048-8505
    ISSN (online) 2048-8513
    ISSN 2048-8505
    DOI 10.1093/ckj/sfw149
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Time-Dependent Changes of Klotho and FGF-23 Levels after Kidney Transplantation: Role of Cold Ischemia Time, Renal Function and Graft Inflammation.

    Vazquez-Sanchez, Teresa / Sanchez-Niño, Maria Dolores / Ruiz-Esteban, Pedro / López, Veronica / León, Myriam / Caballero, Abelardo / Ruiz-Escalera, Juan Francisco / Ortiz, Alberto / Torres, Armando / Rodriguez, Mariano / Hernandez, Domingo

    Journal of clinical medicine

    2023  Volume 12, Issue 13

    Abstract: We investigated the evolution of serum klotho (s-Kl) and FGF-23 during the first two years post-kidney transplantation (KT), considering the cold ischemia time (CIT), glomerular filtration rate (GFR) and graft subclinical inflammation (SCI). We undertook ...

    Abstract We investigated the evolution of serum klotho (s-Kl) and FGF-23 during the first two years post-kidney transplantation (KT), considering the cold ischemia time (CIT), glomerular filtration rate (GFR) and graft subclinical inflammation (SCI). We undertook a prospective, cohort, multicenter study of consecutive patients between April 2018 and January 2021 (with follow-up at 24 months). Subgroups were analyzed according to the median CIT (<14 vs. ≥14 h), the median GFR (≤40 vs. >40 mL/min/1.73 m
    Language English
    Publishing date 2023-07-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm12134486
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The transcription factor Fosl1 preserves Klotho expression and protects from acute kidney injury.

    Cuarental, Leticia / Ribagorda, Marta / Ceballos, Maria I / Pintor-Chocano, Aranzazu / Carriazo, Sol M / Dopazo, Ana / Vazquez, Enrique / Suarez-Alvarez, Beatriz / Cannata-Ortiz, Pablo / Sanz, Ana B / Ortiz, Alberto / Sanchez-Niño, Maria D

    Kidney international

    2022  Volume 103, Issue 4, Page(s) 686–701

    Abstract: Increased expression of AP-1 transcription factor components has been reported in acute kidney injury (AKI). However, the role of specific components, such as Fosl1, in tubular cells or AKI is unknown. Upstream regulator analysis of murine nephrotoxic ... ...

    Abstract Increased expression of AP-1 transcription factor components has been reported in acute kidney injury (AKI). However, the role of specific components, such as Fosl1, in tubular cells or AKI is unknown. Upstream regulator analysis of murine nephrotoxic AKI transcriptomics identified AP-1 as highly upregulated. Among AP-1 canonical components, Fosl1 was found to be upregulated in two transcriptomics datasets from nephrotoxic murine AKI induced by folic acid or cisplatin and from proximal tubular cells exposed to TWEAK, a cytokine mediator of AKI. Fosl1 was minimally expressed in the kidneys of control uninjured mice. Increased Fosl1 protein was localized to proximal tubular cell nuclei in AKI. In human AKI, FOSL1 was found present in proximal tubular cells in kidney sections and in urine along with increased urinary FOSL1 mRNA. Selective Fosl1 deficiency in proximal tubular cells (Fosl1Δtub) increased the severity of murine cisplatin- or folate-induced AKI as characterized by lower kidney function, more severe kidney inflammation and Klotho downregulation. Indeed, elevated AP-1 activity was observed after cisplatin-induced AKI in Fosl1Δtub mice compared to wild-type mice. More severe Klotho downregulation preceded more severe kidney dysfunction. The Klotho promoter was enriched in Fosl1 binding sites and Fosl1 bound to the Klotho promoter in cisplatin-AKI. In cultured proximal tubular cells, Fosl1 targeting increased the proinflammatory response and downregulated Klotho. In vivo, recombinant Klotho administration protected Fosl1Δtub mice from cisplatin-AKI. Thus, increased proximal tubular Fosl1 expression during AKI is an adaptive response, preserves Klotho, and limits the severity of tubular cell injury and AKI.
    MeSH term(s) Animals ; Humans ; Mice ; Acute Kidney Injury/chemically induced ; Acute Kidney Injury/genetics ; Acute Kidney Injury/prevention & control ; Cells, Cultured ; Cisplatin/toxicity ; Kidney/metabolism ; Mice, Inbred C57BL ; Transcription Factor AP-1/genetics ; Transcription Factor AP-1/metabolism ; Klotho Proteins/metabolism
    Chemical Substances Cisplatin (Q20Q21Q62J) ; Transcription Factor AP-1 ; fos-related antigen 1 ; Klotho Proteins (EC 3.2.1.31)
    Language English
    Publishing date 2022-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2022.11.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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