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Article: Urinary Spermidine Predicts and Associates with In-Hospital Acute Kidney Injury after Cardiac Surgery

Martin-Lorenzo, Marta / Ramos-Barron, Angeles / Gutierrez-Garcia, Paula / Martin-Blazquez, Ariadna / Santiago-Hernandez, Aranzazu / Rodrigo Calabia, Emilio / Gomez-Alamillo, Carlos / Alvarez-Llamas, Gloria

Antioxidants. 2021 June 02, v. 10, no. 6

2021

Abstract: Acute Kidney Injury (AKI) affects up to 30% of the patients who undergo cardiac surgery (CVS) and is related to higher mortality. We aim to investigate molecular features associated with in-hospital AKI development and determine the predictive value of ... ...

Abstract	Acute Kidney Injury (AKI) affects up to 30% of the patients who undergo cardiac surgery (CVS) and is related to higher mortality. We aim to investigate molecular features associated with in-hospital AKI development and determine the predictive value of these features when analyzed preoperatively. This is a case-control study. From an initial cohort of 110 recruited subjects, a total of 60 patients undergoing cardiac surgery were included: 20 (33%) developed in-hospital AKI (CVS-AKI) and 40 did not (controls, CVS-C). Pre- and post-surgery samples were collected and a prospective study was carried out. A total of 312 serum samples and 258 urine samples were analyzed by nuclear magnetic resonance, mass spectrometry and ELISA. Six features predicted AKI development in pre-surgery samples: urinary kidney functional loss marker kidney injury molecule-1 (uKIM-1), 2-hydroxybutyric acid, 2-hydroxyphenylacetic acid, hippuric acid, phosphoethanolamine and spermidine. Two of them stood out as powerful predictors. Pre-surgery uKIM-1 levels were increased in CVS-AKI vs. CVS-C (AUC = 0.721, p-value = 0.0392) and associated strongly with the outcome (OR = 5.333, p-value = 0.0264). Spermidine showed higher concentration in CVS-AKI (p-value < 0.0001, AUC = 0.970) and had a strong association with the outcome (OR = 69.75, p-value < 0.0001). uKIM-1 and particularly spermidine predict in-hospital AKI associated with CVS in preoperative samples. These findings may aid in preventing postoperative AKI and improve prognosis of CVS.
Keywords	acute kidney injury ; blood serum ; case-control studies ; hippuric acid ; kidneys ; mass spectrometry ; mortality ; nuclear magnetic resonance spectroscopy ; prognosis ; prospective studies ; spermidine ; surgery ; urine
Language	English
Dates of publication	2021-0602
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10060896
Database	NAL-Catalogue (AGRICOLA)

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Article: Urinary Spermidine Predicts and Associates with In-Hospital Acute Kidney Injury after Cardiac Surgery.

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 6

Abstract	Acute Kidney Injury (AKI) affects up to 30% of the patients who undergo cardiac surgery (CVS) and is related to higher mortality. We aim to investigate molecular features associated with in-hospital AKI development and determine the predictive value of these features when analyzed preoperatively. This is a case-control study. From an initial cohort of 110 recruited subjects, a total of 60 patients undergoing cardiac surgery were included: 20 (33%) developed in-hospital AKI (CVS-AKI) and 40 did not (controls, CVS-C). Pre- and post-surgery samples were collected and a prospective study was carried out. A total of 312 serum samples and 258 urine samples were analyzed by nuclear magnetic resonance, mass spectrometry and ELISA. Six features predicted AKI development in pre-surgery samples: urinary kidney functional loss marker kidney injury molecule-1 (uKIM-1), 2-hydroxybutyric acid, 2-hydroxyphenylacetic acid, hippuric acid, phosphoethanolamine and spermidine. Two of them stood out as powerful predictors. Pre-surgery uKIM-1 levels were increased in CVS-AKI vs. CVS-C (AUC = 0.721,
Language	English
Publishing date	2021-06-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10060896
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Article ; Online: Urinary Plasminogen Activator Inhibitor-1: A Biomarker of Acute Tubular Injury.

Paniagua-Sancho, María / Quiros, Yaremi / Casanova, Alfredo G / Blanco-Gozalo, Víctor / Agüeros-Blanco, Consuelo / Benito-Hernández, Adalberto / Ramos-Barron, María A / Gómez-Alamillo, Carlos / Arias, Manuel / Sancho-Martínez, Sandra M / López-Hernández, Francisco J

American journal of nephrology

2021 Volume 52, Issue 9, Page(s) 714–724

Abstract: Introduction: Acute kidney injury (AKI) is a threatening, multiaetiological syndrome encompassing a variety of forms and damage patterns. AKI lacks sufficiently specific diagnostic tools to evaluate the distinct combination of pathophysiological events ... ...

Abstract	Introduction: Acute kidney injury (AKI) is a threatening, multiaetiological syndrome encompassing a variety of forms and damage patterns. AKI lacks sufficiently specific diagnostic tools to evaluate the distinct combination of pathophysiological events underlying each case, which limits personalized and optimized handling. Therefore, a pathophysiological diagnosis based on new urinary biomarkers is sought for practical (readiness and noninvasiveness) and conceptual reasons, as the urine is a direct product of the kidneys. However, biomarkers found in the urine may also have extrarenal origin, thus conveying pathophysiological information from other organs or tissues. Urinary plasminogen activator inhibitor-1 (PAI-1) has been associated to AKI, although its origin and traffic to the urine are not known. Methods: Herein, we studied the blood or renal origin of urinary PAI-1 (uPAI-1) in experimental AKI in Wistar rats, by means of the in situ renal perfusion method. For this purpose, urine was collected while the kidneys of rats with AKI showing increased uPAI-1 excretion, and controls, were in situ perfused with a saline solution. Results: Our results show that during perfusion, PAI-1 remained in the urine of AKI rats, suggesting that renal cells shed this protein directly to the urine. PAI-1 is also significantly increased in the urine of AKI patients. Its low correlation with other urinary markers such as NGAL or NAG suggests that PAI-1 provides complementary and distinct phenotypical information. Conclusion: In conclusion, uPAI-1 is a biomarker produced by damaged kidneys following AKI, whose precise pathophysiological meaning in AKI needs to be further investigated.
MeSH term(s)	Acute Kidney Injury/urine ; Adult ; Aged ; Animals ; Biomarkers/urine ; Female ; Humans ; Kidney Tubules ; Male ; Middle Aged ; Plasminogen Activator Inhibitor 1/urine ; Rats ; Rats, Wistar
Chemical Substances	Biomarkers ; Plasminogen Activator Inhibitor 1 ; SERPINE1 protein, human
Language	English
Publishing date	2021-09-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604540-6
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000518455
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Article: Urinary KIM-1 Correlates with the Subclinical Sequelae of Tubular Damage Persisting after the Apparent Functional Recovery from Intrinsic Acute Kidney Injury.

Cuesta, Cristina / Fuentes-Calvo, Isabel / Sancho-Martinez, Sandra M / Valentijn, Floris A / Düwel, Annette / Hidalgo-Thomas, Omar A / Agüeros-Blanco, Consuelo / Benito-Hernández, Adalberto / Ramos-Barron, María A / Gómez-Alamillo, Carlos / Arias, Manuel / Nguyen, Tri Q / Goldschmeding, Roel / Martínez-Salgado, Carlos / López-Hernández, Francisco J

Biomedicines

2022 Volume 10, Issue 5

Abstract: Acute kidney injury (AKI) poses an increased risk factor for new AKI episodes, progression to chronic kidney disease, and death. A worsened evolution has been linked to an incomplete renal repair beyond the apparent functional recovery based on plasma ... ...

Abstract	Acute kidney injury (AKI) poses an increased risk factor for new AKI episodes, progression to chronic kidney disease, and death. A worsened evolution has been linked to an incomplete renal repair beyond the apparent functional recovery based on plasma creatinine (pCr) normalization. However, structural sequelae pass largely unnoticed due to the absence of specific diagnostic tools. The urinary kidney injury molecule 1 (KIM-1) participates in renal tissue damage and repair and is proposed as a biomarker of early and subclinical AKI. Thus, we study in this paper the evolution of KIM-1 urinary excretion alongside renal tissue sequelae after an intrinsic AKI episode induced by cisplatin in Wistar rats. Creatinine clearance, pCr, proteinuria and the fractional excretion of Na
Language	English
Publishing date	2022-05-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10051106
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Article ; Online: Combined use of GM2AP and TCP1-eta urinary levels predicts recovery from intrinsic acute kidney injury.

Blanco-Gozalo, Víctor / Casanova, Alfredo G / Sancho-Martínez, Sandra M / Prieto, Marta / Quiros, Yaremi / Morales, Ana I / Martínez-Salgado, Carlos / Agüeros-Blanco, Consuelo / Benito-Hernández, Adalberto / Ramos-Barron, María A / Gómez-Alamillo, Carlos / Arias, Manuel / López-Hernández, Francisco J

Scientific reports

2020 Volume 10, Issue 1, Page(s) 11599

Abstract: Deficient recovery from acute kidney injury (AKI) has immediate and long-term health, clinical and economic consequences. Pre-emptive recovery estimation may improve nephrology referral, optimize decision making, enrollment in trials, and provide key ... ...

Abstract	Deficient recovery from acute kidney injury (AKI) has immediate and long-term health, clinical and economic consequences. Pre-emptive recovery estimation may improve nephrology referral, optimize decision making, enrollment in trials, and provide key information for subsequent clinical handling and follow-up. For this purpose, new biomarkers are needed that predict outcome during the AKI episode. We hypothesized that damage pattern-specific biomarkers are expected to more closely associate to outcome within distinct subpopulations (i.e. those affected by specific pathological processes determining a specific outcome), as biomarker pleiotropy (i.e. associated to phenomena unrelated to AKI) introduced by unselected, heterogeneous populations may blur statistics. A panel of urinary biomarkers was measured in patients with AKI and their capacity to associate to normal or abnormal recovery was studied in the whole cohort or after sub-classification by AKI etiology, namely pre-renal and intrinsic AKI. A combination of urinary GM2AP and TCP1-eta best associates with recovery from AKI, specifically within the sub-population of renal AKI patients. This two-step strategy generates a multidimensional space in which patients with specific characteristics (i.e. renal AKI patients with good or bad prognosis) can be identified based on a collection of biomarkers working serially, applying pathophysiology-driven criteria to estimate AKI recovery, to facilitate pre-emptive and personalized handling.
MeSH term(s)	Acute Kidney Injury/genetics ; Acute Kidney Injury/pathology ; Acute Kidney Injury/urine ; Biomarkers/urine ; Cell Lineage/genetics ; Chaperonin Containing TCP-1/urine ; Female ; G(M2) Activator Protein/urine ; Humans ; Kidney/pathology ; Male ; Middle Aged
Chemical Substances	Biomarkers ; G(M2) Activator Protein ; TCP1 protein, human ; Chaperonin Containing TCP-1 (EC 3.6.1.-)
Language	English
Publishing date	2020-07-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-68398-0
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Article ; Online: CCL20 blockade increases the severity of nephrotoxic folic acid-induced acute kidney injury.

González-Guerrero, Cristian / Morgado-Pascual, José Luis / Cannata-Ortiz, Pablo / Ramos-Barron, María Angeles / Gómez-Alamillo, Carlos / Arias, Manuel / Mezzano, Sergio / Egido, Jesús / Ruiz-Ortega, Marta / Ortiz, Alberto / Ramos, Adrián M

The Journal of pathology

2018 Volume 246, Issue 2, Page(s) 191–204

Abstract: The chemokine CCL20 activates the CCR6 receptor and has been implicated in the pathogenesis of glomerular injury. However, it is unknown whether it contributes to acute kidney injury (AKI). We identified CCL20 as upregulated in a systems biology strategy ...

Abstract	The chemokine CCL20 activates the CCR6 receptor and has been implicated in the pathogenesis of glomerular injury. However, it is unknown whether it contributes to acute kidney injury (AKI). We identified CCL20 as upregulated in a systems biology strategy combining transcriptomics of kidney tissue from experimental toxic folic acid-induced AKI and from stressed cultured tubular cells and have explored the expression and function of CCL20 in experimental and clinical AKI. CCL20 upregulation was confirmed in three models of kidney injury induced by a folic acid overdose, cisplatin or unilateral ureteral obstruction. In injured kidneys, CCL20 was expressed by tubular, endothelial, and interstitial cells, and was also upregulated in human kidneys with AKI. Urinary CCL20 was increased in human AKI and was associated with severity. The function of CCL20 in nephrotoxic folic acid-induced AKI was assessed by using neutralising anti-CCL20 antibodies or CCR6-deficient mice. CCL20/CCR6 targeting increased the severity of kidney failure and mortality. This was associated with more severe histological injury, nephrocalcinosis, capillary rarefaction, and fibrosis, as well as higher expression of tubular injury-associated genes. Surprisingly, mice with CCL20 blockade had a lower tubular proliferative response and a higher number of cells in the G2/M phase, suggesting impaired repair mechanisms. This may be related to a lower influx of Tregs, despite a milder inflammatory response in terms of chemokine expression and infiltration by IL-17
MeSH term(s)	Acute Kidney Injury/chemically induced ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Acute Kidney Injury/prevention & control ; Adult ; Aged ; Animals ; Antibodies, Neutralizing/toxicity ; Case-Control Studies ; Cell Line ; Chemokine CCL20/antagonists & inhibitors ; Chemokine CCL20/genetics ; Chemokine CCL20/immunology ; Chemokine CCL20/metabolism ; Chemotaxis, Leukocyte/drug effects ; Disease Models, Animal ; Female ; Fibrosis ; Folic Acid ; Gene Expression Profiling/methods ; Humans ; Immunity, Innate/drug effects ; Kidney Tubules/drug effects ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Receptors, CCR6/genetics ; Receptors, CCR6/metabolism ; Severity of Illness Index ; Signal Transduction/drug effects ; Systems Biology/methods ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/metabolism ; Th17 Cells/drug effects ; Th17 Cells/metabolism ; Young Adult
Chemical Substances	Antibodies, Neutralizing ; CCL20 protein, human ; CCL20 protein, mouse ; CCR6 protein, human ; CCR6 protein, mouse ; Chemokine CCL20 ; Receptors, CCR6 ; Folic Acid (935E97BOY8)
Language	English
Publishing date	2018-08-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.5132
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Article ; Online: Urine metabolomics insight into acute kidney injury point to oxidative stress disruptions in energy generation and H

Martin-Lorenzo, Marta / Gonzalez-Calero, Laura / Ramos-Barron, Angeles / Sanchez-Niño, Maria D / Gomez-Alamillo, Carlos / García-Segura, Juan Manuel / Ortiz, Alberto / Arias, Manuel / Vivanco, Fernando / Alvarez-Llamas, Gloria

Journal of molecular medicine (Berlin, Germany)

2017 Volume 95, Issue 12, Page(s) 1399–1409

Abstract: Acute kidney injury (AKI) is one of the main complications in acute care medicine and a risk factor for chronic kidney disease (CKD). AKI incidence has increased; however, its diagnosis has limitations and physiopathological mechanisms are underexplored. ...

Abstract	Acute kidney injury (AKI) is one of the main complications in acute care medicine and a risk factor for chronic kidney disease (CKD). AKI incidence has increased; however, its diagnosis has limitations and physiopathological mechanisms are underexplored. We investigated urine samples, aiming to identify major metabolite changes during human AKI evolution. Metabolic signatures found were further explored for a potential link to severity of injury. Twenty-four control subjects and 38 hospitalized patients with AKI were recruited and urine samples were collected at the time of diagnosis, during follow-up and at discharge. Nuclear magnetic resonance (NMR) was used in a first discovery phase for identifying potential metabolic differences. Target metabolites of interest were confirmed by liquid chromatography-mass spectrometry (LC-MS/MS) in an independent group. Underlying metabolic defects were further explored by kidney transcriptomics of murine toxic AKI. Urinary 2-hydroxybutyric acid, pantothenic acid, and hippuric acid were significantly downregulated and urinary N-acetylneuraminic acid, phosphoethanolamine, and serine were upregulated during AKI. Hippuric acid, phosphoethanolamine, and serine showed further downregulation/upregulation depending on the metabolite in acute tubular necrosis (ATN) AKI compared to prerenal AKI. Kidney transcriptomics disclosed decreased expression of cystathionase, cystathionine-β-synthase, and ethanolamine-phosphate cytidylyltransferase, and increased N-acetylneuraminate synthase as the potentially underlying cause of changes in urinary metabolites. A urinary metabolite panel identified AKI patients and provided insight into intrarenal events. A urine fingerprint made up of six metabolites may be related to pathophysiological changes in oxidative stress, energy generation, and H Key messages: The urinary metabolome reflects AKI evolution and severity of injury. Kidney transcriptomics revealed enzymatic expression changes. Enzymatic expression changes may be the potentially underlying cause of changes in urine metabolites. Identified metabolite changes link oxidative stress, energy generation, and H
MeSH term(s)	Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Acute Kidney Injury/urine ; Adult ; Aged ; Aged, 80 and over ; Energy Metabolism ; Female ; Gene Expression Regulation ; Humans ; Hydrogen Sulfide/metabolism ; Linear Models ; Male ; Metabolomics ; Middle Aged ; Oxidative Stress ; ROC Curve ; Severity of Illness Index ; Transcriptome/genetics
Chemical Substances	Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2017-10-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-017-1594-5
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Article ; Online: Urinary Kininogen-1 and Retinol binding protein-4 respond to Acute Kidney Injury: predictors of patient prognosis?

Gonzalez-Calero, Laura / Martin-Lorenzo, Marta / Ramos-Barron, Angeles / Ruiz-Criado, Jorge / Maroto, Aroa S / Ortiz, Alberto / Gomez-Alamillo, Carlos / Arias, Manuel / Vivanco, Fernando / Alvarez-Llamas, Gloria

Scientific reports

2016 Volume 6, Page(s) 19667

Abstract: Implementation of therapy for acute kidney injury (AKI) depends on successful prediction of individual patient prognosis. Clinical markers as serum creatinine (sCr) have limitations in sensitivity and early response. The aim of the study was to identify ... ...

Abstract	Implementation of therapy for acute kidney injury (AKI) depends on successful prediction of individual patient prognosis. Clinical markers as serum creatinine (sCr) have limitations in sensitivity and early response. The aim of the study was to identify novel molecules in urine which show altered levels in response to AKI and investigate their value as predictors of recovery. Changes in the urinary proteome were here investigated in a cohort of 88 subjects (55 AKI patients and 33 healthy donors) grouped in discovery and validation independent cohorts. Patients' urine was collected at three time points: within the first 48 h after diagnosis(T1), at 7 days of follow-up(T2) and at discharge of Nephrology(T3). Differential gel electrophoresis was performed and data were confirmed by Western blot (WB), liquid chromatography/mass spectrometry (LC-MS/MS) and enzyme-linked immunosorbent assay (ELISA). Retinol binding protein 4 (RBP4) and kininogen-1 (KNG1) were found significantly altered following AKI. RBP4 increased at T1, and progressively decreased towards normalization. Maintained decrease was observed for KNG1 from T1. Individual patient response along time revealed RBP4 responds to recovery earlier than sCr. In conclusion, KNG1 and RBP4 respond to AKI. By monitoring RBP4, patient's recovery can be anticipated pointing to a role of RBP4 in prognosis evaluation.
MeSH term(s)	Acute Kidney Injury/diagnosis ; Acute Kidney Injury/etiology ; Acute Kidney Injury/urine ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biomarkers ; Comorbidity ; Creatinine/blood ; Female ; Humans ; Kininogens/urine ; Male ; Middle Aged ; Prognosis ; ROC Curve ; Retinol-Binding Proteins, Plasma/urine ; Young Adult
Chemical Substances	Biomarkers ; KNG1 protein, human ; Kininogens ; RBP4 protein, human ; Retinol-Binding Proteins, Plasma ; Creatinine (AYI8EX34EU)
Language	English
Publishing date	2016-01-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep19667
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Article ; Online: Urinary TCP1-eta: A Cortical Damage Marker for the Pathophysiological Diagnosis and Prognosis of Acute Kidney Injury.

Sancho-Martínez, Sandra M / Sánchez-Juanes, Fernando / Blanco-Gozalo, Víctor / Fontecha-Barriuso, Miguel / Prieto-García, Laura / Fuentes-Calvo, Isabel / González-Buitrago, José M / Morales, Ana I / Martínez-Salgado, Carlos / Ramos-Barron, María A / Gómez-Alamillo, Carlos / Arias, Manuel / López-Novoa, José M / López-Hernández, Francisco J

Toxicological sciences : an official journal of the Society of Toxicology

2019 Volume 174, Issue 1, Page(s) 3–15

Abstract: Acute kidney injury (AKI) is a serious syndrome with increasing incidence and health consequences, and high mortality rate among critically ill patients. Acute kidney injury lacks a unified definition, has ambiguous semantic boundaries, and relies on ... ...

Abstract	Acute kidney injury (AKI) is a serious syndrome with increasing incidence and health consequences, and high mortality rate among critically ill patients. Acute kidney injury lacks a unified definition, has ambiguous semantic boundaries, and relies on defective diagnosis. This, in part, is due to the absence of biomarkers substratifying AKI patients into pathophysiological categories based on which prognosis can be assigned and clinical treatment differentiated. For instance, AKI involving acute tubular necrosis (ATN) is expected to have a worse prognosis than prerenal, purely hemodynamic AKI. However, no biomarker has been unambiguously associated with tubular cell death or is able to provide etiological distinction. We used a cell-based system to identify TCP1-eta in the culture medium as a noninvasive marker of damaged renal tubular cells. In rat models of AKI, TCP1-eta was increased in the urine co-relating with renal cortical tubule damage. When kidneys from ATN rats were perfused in situ with Krebs-dextran solution, a portion of the urinary TCP1-eta protein content excreted into urine disappeared, and another portion remained within the urine. These results indicated that TCP1-eta was secreted by tubule cells and was not fully reabsorbed by the damaged tubules, both effects contributing to the increased urinary excretion. Urinary TCP1-eta is found in many etiologically heterogeneous AKI patients, and is statistically higher in patients partially recovered from severe AKI. In conclusion, urinary TCP1-eta poses a potential, substratifying biomarker of renal cortical damage associated with bad prognosis.
MeSH term(s)	Acute Kidney Injury/chemically induced ; Acute Kidney Injury/pathology ; Acute Kidney Injury/physiopathology ; Acute Kidney Injury/urine ; Animals ; Apoptosis ; Biomarkers/urine ; Case-Control Studies ; Cell Line ; Chaperonin Containing TCP-1/urine ; Disease Models, Animal ; Early Diagnosis ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Kidney Tubules/physiopathology ; Male ; Predictive Value of Tests ; Prognosis ; Rats, Wistar ; Renal Elimination ; Urinalysis
Chemical Substances	Biomarkers ; CCT7 protein, human ; Cct7 protein, mouse ; Chaperonin Containing TCP-1 (EC 3.6.1.-)
Language	English
Publishing date	2019-12-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfz242
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Article ; Online: Clinical characteristics of resistant hypertension in renal transplant patients.

Arias, Manuel / Fernández-Fresnedo, Gema / Gago, Maria / Rodrigo, Emilio / Gómez-Alamillo, Carlos / Toyos, Carmen / Allende, Natalia

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2012 Volume 27 Suppl 4, Page(s) iv36–8

Abstract: Hypertension is a prevalent complication that occurs in 80-85% of all kidney transplant recipients. The pathogenesis of post-transplant hypertension is multifactorial and includes pre-transplant hypertension, donor hypertension, renin secretion from the ... ...

Abstract	Hypertension is a prevalent complication that occurs in 80-85% of all kidney transplant recipients. The pathogenesis of post-transplant hypertension is multifactorial and includes pre-transplant hypertension, donor hypertension, renin secretion from the native kidney, graft dysfunction, recurrent disease and immunosuppressive treatment. Hypertension negatively affects transplant and patient survival outcomes; cardiovascular disease (CVD) is the leading cause of morbidity and mortality in patients with chronic renal disease and after successful renal transplantation. Hypertension is a well-known risk factor for CVD and it is frequently associated with other CVD risk factors. Despite increased awareness of the adverse effects of hypertension in both graft and patient survival, long-term studies have shown that arterial hypertension in the transplant population has not been adequately controlled. Resistant hypertension (RH) is defined as office blood pressure (oBP) that remains above goal (oBP ≥ 140/90 or 130/80 mmHg) in patients with diabetes or chronic kidney disease despite the concurrent use of three antihypertensive agents, at full doses, one of them being a diuretic. Despite studies in the general population and the high prevalence of hypertension in renal transplant patients, data about RH are very scarce and the prevalence of RH in renal transplant patients is unknown and could be associated with a worse prognosis.
MeSH term(s)	Antihypertensive Agents/therapeutic use ; Drug Resistance ; Humans ; Hypertension/diagnosis ; Hypertension/drug therapy ; Hypertension/etiology ; Kidney Transplantation/adverse effects
Chemical Substances	Antihypertensive Agents
Language	English
Publishing date	2012-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfs481
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