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Article ; Online: Metabolism as Disease Tolerance: Implications for Sepsis-Associated Acute Kidney Injury.

Huen, Sarah C

2021 Volume 146, Issue 3, Page(s) 291–294

Abstract: Sepsis is a significant cause for mortality among critically ill patients. Metabolic derangements that develop in sepsis are often considered to be pathologic, contributing to sepsis morbidity and mortality. However, alterations in metabolism during ... ...

Abstract	Sepsis is a significant cause for mortality among critically ill patients. Metabolic derangements that develop in sepsis are often considered to be pathologic, contributing to sepsis morbidity and mortality. However, alterations in metabolism during sepsis are multifaceted and are incompletely understood. Acute anorexia during infection is an evolutionarily conserved response, suggesting a potential protective role of anorexia in the host response to infection. In animal models of bacterial inflammation, fasting metabolic programs associated with acute anorexia such as those regulated by fibroblast growth factor 21 and ketogenesis are associated with improved survival. Other fasting metabolic pathways such as fatty acid oxidation and autophagy are also implicated in preventing acute kidney injury (AKI). Global metabolic changes during sepsis and current clinical interventions can potentially affect disease tolerance mechanisms and modify the risk of AKI.
MeSH term(s)	Acute Kidney Injury/complications ; Animals ; Anorexia/complications ; Critical Illness ; Female ; Humans ; Inflammation/complications ; Male ; Sepsis/pathology
Language	English
Publishing date	2021-06-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000516877
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Article ; Online: Metabolism and Nutrition in Sepsis: In Need of a Paradigm Shift.

Collins, Kristina / Huen, Sarah C

Nephron

2023 Volume 147, Issue 12, Page(s) 733–736

Abstract: Background: Sepsis continues to cause significant morbidity and mortality despite technological advancements in medical management. While sepsis is defined as organ dysfunction owing to the dysregulated host response to infection, our understanding of ... ...

Abstract	Background: Sepsis continues to cause significant morbidity and mortality despite technological advancements in medical management. While sepsis is defined as organ dysfunction owing to the dysregulated host response to infection, our understanding of the dysregulation of the host response remains incomplete. Summary: Many metabolic derangements that occur during sepsis, including those associated with anorexia, hyperglycemia, and proteolysis, have largely been considered maladaptive. Supportive medical and nutritional interventions targeted at correcting these metabolic derangements have not led to improved outcomes, suggesting a reappraisal of our approach to metabolism and nutrition in critically ill septic patients is needed. Key messages: Explanations of the lack of efficacy of these clinical interventions may include targeting the wrong metric or patient population, or the possibility that some of these metabolic changes could be protective. In this mini-review, we propose a paradigm shift that is needed in metabolism and nutrition management in sepsis.
MeSH term(s)	Humans ; Sepsis/therapy ; Sepsis/metabolism ; Nutritional Status ; Critical Illness
Language	English
Publishing date	2023-09-13
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000534074
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Article ; Online: Targeting protein translation to prevent septic kidney injury.

Huen, Sarah C

The Journal of clinical investigation

2018 Volume 129, Issue 1, Page(s) 60–62

Abstract: The development of acute kidney injury (AKI) in patients with sepsis causes significant morbidity and mortality. The pathogenesis of AKI in sepsis is incompletely understood. In this issue of the JCI, Hato et al. investigate the renal translatome during ... ...

Abstract	The development of acute kidney injury (AKI) in patients with sepsis causes significant morbidity and mortality. The pathogenesis of AKI in sepsis is incompletely understood. In this issue of the JCI, Hato et al. investigate the renal translatome during bacterial sepsis and identify the global shutdown of renal protein translation mediated by the eukaryotic translation initiation factor 2-α kinase 2/eukaryotic translation initiation factor 2α (EIF2AK2/eIF2α) axis as a major pathway in mediating septic AKI. The results of this study suggest that inhibiting this pathway could be a potential therapeutic strategy for preventing septic AKI.
MeSH term(s)	Acute Kidney Injury ; Antiviral Agents ; Humans ; Kidney ; Sepsis
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2018-12-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI125432
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Article ; Online: When a calorie isn't just a calorie: a revised look at nutrition in critically ill patients with sepsis and acute kidney injury.

Nadamuni, Mridula / Venable, Andrea H / Huen, Sarah C

Current opinion in nephrology and hypertension

2022 Volume 31, Issue 4, Page(s) 358–366

Abstract: Purpose of review: To discuss how nutritional management could be optimized to promote protective metabolism in sepsis and associated acute kidney injury.: Recent findings: Recent evidence suggests that sepsis is a metabolically distinct critical ... ...

Abstract	Purpose of review: To discuss how nutritional management could be optimized to promote protective metabolism in sepsis and associated acute kidney injury. Recent findings: Recent evidence suggests that sepsis is a metabolically distinct critical illness and that certain metabolic alterations, such as activation of fasting metabolism, may be protective in bacterial sepsis. These findings may explain the lack of survival benefit in recent randomized controlled trials of nutrition therapy for critical illness. These trials are limited by cohort heterogeneity, combining both septic and nonseptic critical illness, and the use of inaccurate caloric estimates to determine energy requirements. These energy estimates are also unable to provide information on specific substrate preferences or the capacity for substrate utilization. As a result, high protein feeding beyond the capacity for protein synthesis could cause harm in septic patients. Excess glucose and insulin exposures suppress fatty acid oxidation, ketogenesis and autophagy, of which emerging evidence suggest are protective against sepsis associated organ damage such as acute kidney injury. Summary: Distinguishing pathogenic and protective sepsis-related metabolic changes are critical to enhancing and individualizing nutrition management for critically ill patients.
MeSH term(s)	Acute Kidney Injury/therapy ; Critical Illness/therapy ; Energy Intake ; Humans ; Nutritional Support ; Sepsis/therapy
Language	English
Publishing date	2022-06-10
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000801
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Zs.A 3686: Show issues

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Article ; Online: Fasting-induced HMGCS2 expression in the kidney does not contribute to circulating ketones.

Venable, Andrea H / Lee, Lauren E / Feola, Kyle / Santoyo, John / Broomfield, Tatyana / Huen, Sarah C

American journal of physiology. Renal physiology

2022 Volume 322, Issue 4, Page(s) F460–F467

Abstract: Mitochondrial hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) is the rate-limiting enzyme in ketogenesis. The liver expresses high levels of HMGCS2 constitutively as the main ketogenic organ. It has been suggested that the kidney could be ketogenic as ... ...

Abstract	Mitochondrial hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) is the rate-limiting enzyme in ketogenesis. The liver expresses high levels of HMGCS2 constitutively as the main ketogenic organ. It has been suggested that the kidney could be ketogenic as HMGCS2 is expressed in the kidney during fasting and diabetic conditions. However, definitive proof of the capacity for the kidney to produce ketones is lacking. We demonstrated that during fasting, HMGCS2 expression is induced in the proximal tubule of the kidney and is peroxisome proliferator activated receptor-α dependent. Mice with kidney-specific
MeSH term(s)	Animals ; Fasting ; Hydroxymethylglutaryl-CoA Synthase/genetics ; Hydroxymethylglutaryl-CoA Synthase/metabolism ; Ketone Bodies/metabolism ; Ketones ; Ketosis/metabolism ; Kidney/metabolism ; Mice
Chemical Substances	Ketone Bodies ; Ketones ; HMGCS2 protein, mouse (EC 2.3.3.10) ; Hydroxymethylglutaryl-CoA Synthase (EC 2.3.3.10)
Language	English
Publishing date	2022-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00447.2021
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Uc I Zs.89: Show issues

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Article ; Online: Macrophages in Renal Injury and Repair.

Huen, Sarah C / Cantley, Lloyd G

Annual review of physiology

2017 Volume 79, Page(s) 449–469

Abstract: Acute kidney injury (AKI) is a growing global health concern, yet no treatment is currently available to prevent it or to promote kidney repair after injury. Animal models demonstrate that the macrophage is a major contributor to the inflammatory ... ...

Abstract	Acute kidney injury (AKI) is a growing global health concern, yet no treatment is currently available to prevent it or to promote kidney repair after injury. Animal models demonstrate that the macrophage is a major contributor to the inflammatory response to AKI. Emerging data from human biopsies also corroborate the presence of macrophages in AKI and their persistence in progressive chronic kidney disease. Macrophages are phagocytic innate immune cells that are important mediators of tissue homeostasis and host defense. In response to tissue injury, macrophages become activated based on specific signals from the damaged microenvironment. The activation and functional state of the macrophage depends on the stage of tissue injury and repair, reflecting a dynamic and diverse spectrum of macrophage phenotypes. In this review, we highlight our current understanding of the mechanisms by which macrophages contribute to injury and repair after AKI.
MeSH term(s)	Acute Kidney Injury/physiopathology ; Animals ; Cellular Microenvironment/physiology ; Disease Models, Animal ; Humans ; Immunity, Innate/physiology ; Inflammation/pathology ; Kidney/physiopathology ; Macrophages/physiology
Language	English
Publishing date	2017-02-12
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	207933-1
ISSN	1545-1585 ; 0066-4278
ISSN (online)	1545-1585
ISSN	0066-4278
DOI	10.1146/annurev-physiol-022516-034219
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Uc I Zs.226: Show issues

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Article ; Online: Molecular phenotyping of clinical AKI with novel urinary biomarkers.

Huen, Sarah C / Parikh, Chirag R

American journal of physiology. Renal physiology

2015 Volume 309, Issue 5, Page(s) F406–13

Abstract: Acute kidney injury (AKI) is a common hospital complication. There are no effective treatments to minimize kidney injury or limit associated morbidity and mortality. Currently, serum creatinine and urine output remain the gold standard used clinically in ...

Abstract	Acute kidney injury (AKI) is a common hospital complication. There are no effective treatments to minimize kidney injury or limit associated morbidity and mortality. Currently, serum creatinine and urine output remain the gold standard used clinically in the diagnosis of AKI. Several novel biomarkers can diagnose AKI earlier than elevations of serum creatinine and changes in urine output. Recent long-term observational studies have elucidated a subgroup of patients who have positive biomarkers of AKI but do not meet criteria for AKI by serum creatinine or urine output, termed subclinical AKI. These patients with subclinical AKI have increased risk of both short- and long-term mortality. In this review, we will highlight the implications of what these patients may represent and the need for better phenotyping of AKI by etiology, severity of injury, and ability to recover. We will discuss two AKI biomarkers, neutrophil gelatinase-associated lipocalin (NGAL) and breast regression protein-39 (BRP-39)/YKL-40, that exemplify the need to characterize the complexity of the biological meaning behind the biomarker, beyond elevated levels reporting on tissue injury. Ultimately, careful phenotyping of AKI will lead to identification of therapeutic targets and appropriate patient populations for clinical trials.
MeSH term(s)	Acute Kidney Injury/blood ; Acute Kidney Injury/diagnosis ; Acute Kidney Injury/urine ; Acute-Phase Proteins/urine ; Biomarkers/blood ; Biomarkers/urine ; Creatinine/blood ; Glycoproteins/urine ; Humans ; Lipocalin-2 ; Lipocalins/urine ; Phenotype ; Proto-Oncogene Proteins/urine
Chemical Substances	Acute-Phase Proteins ; Biomarkers ; Glycoproteins ; LCN2 protein, human ; Lipocalin-2 ; Lipocalins ; Proto-Oncogene Proteins ; Creatinine (AYI8EX34EU)
Language	English
Publishing date	2015-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00682.2014
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Article ; Online: The double-face onlay-tube-onlay transverse preputial flap: An advantageous alternative to the two-stage hypospadias repair?

Huen, Kathy H / Macaraeg, Amanda / Davis-Dao, Carol A / Williamson, Sarah H / Boswell, Timothy C / Suhale, Zayn / Chamberlin, Joshua D / Chuang, Kai-Wen / Stephany, Heidi A / Wehbi, Elias J / Khoury, Antoine E

Journal of pediatric urology

2023 Volume 19, Issue 6, Page(s) 701.e1–701.e8

Abstract: Objective: To compare the surgical outcomes and complications of boys who underwent double-face onlay-tube-onlay transverse preputial island flap (DFOTO) one-stage repair vs. two-stage repair for proximal hypospadias.: Study design: Males with ... ...

Abstract	Objective: To compare the surgical outcomes and complications of boys who underwent double-face onlay-tube-onlay transverse preputial island flap (DFOTO) one-stage repair vs. two-stage repair for proximal hypospadias. Study design: Males with proximal hypospadias who underwent DFOTO or two-stage repair at a single institution from 2008 to 2021 were identified. Patients who had prior hypospadias surgery were excluded. Outcomes were surgical complications, number of surgical procedures, operative time, and post-operative uroflowmetry results. Results: Fifty-three males who underwent DFOTO and 39 who underwent two-stage repair were included. Median age at surgery was 1.1 years (IQR 0.83-1.6) and median follow-up was 3.0 years (IQR 1.2-6.8). Although not statistically significant, the DFOTO group had higher rates of urethrocutaneous fistula (30% vs. 15%, p = 0.10), urethral stricture (15% vs. 3%, p = 0.07) and urethral diverticulum (8% vs. 3%, p = 0.39). Although the unplanned re-operation rate was higher in DFOTO (58% vs. 33%, p = 0.02), the mean number of procedures and median total surgical time were lower in DFOTO (1.8 ± 0.9 vs. 2.4 ± 0.8, p = 0.0004; 337 min [IQR 278-460] vs. 468 min [IQR 400-563], p = 0.008). There were no significant differences between groups for mean peak flow rates and post void residuals. Conclusions: In males who underwent DFOTO, 42% achieved completion of their proximal hypospadias repair with one operation, while the remainder had largely minor complications. Accounting for reoperation rates, the mean number of procedures per patient was lower in the DFOTO group. Comparable results can be achieved with both techniques; the risks of higher unplanned operation rates in the DFOTO group should be considered with the benefit of fewer total procedures.
MeSH term(s)	Male ; Humans ; Infant ; Hypospadias/surgery ; Urethra/surgery ; Surgical Flaps ; Plastic Surgery Procedures ; Urethral Stricture/surgery ; Urologic Surgical Procedures, Male/methods ; Retrospective Studies
Language	English
Publishing date	2023-08-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2237683-5
ISSN	1873-4898 ; 1477-5131
ISSN (online)	1873-4898
ISSN	1477-5131
DOI	10.1016/j.jpurol.2023.08.007
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Zs.A 6387: Show issues

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Article ; Online: Macrophage-mediated injury and repair after ischemic kidney injury.

Huen, Sarah C / Cantley, Lloyd G

Pediatric nephrology (Berlin, Germany)

2014 Volume 30, Issue 2, Page(s) 199–209

Abstract: Acute ischemic kidney injury is a common complication in hospitalized patients. No treatment is yet available for augmenting kidney repair or preventing progressive kidney fibrosis. Animal models of acute kidney injury demonstrate that activation of the ... ...

Abstract	Acute ischemic kidney injury is a common complication in hospitalized patients. No treatment is yet available for augmenting kidney repair or preventing progressive kidney fibrosis. Animal models of acute kidney injury demonstrate that activation of the innate immune system plays a major role in the systemic response to ischemia/reperfusion injury. Macrophage depletion studies suggest that macrophages, key participants in the innate immune response, augment the initial injury after reperfusion but also promote tubular repair and contribute to long-term kidney fibrosis after ischemic injury. The distinct functional outcomes seen following macrophage depletion at different time points after ischemia/reperfusion injury suggest heterogeneity in macrophage activation states. Identifying the pathways that regulate the transitions of macrophage activation is thus critical for understanding the mechanisms that govern both macrophage-mediated injury and repair in the postischemic kidney. This review examines our understanding of the complex and intricately controlled pathways that determine monocyte recruitment, macrophage activation, and macrophage effector functions after renal ischemia/reperfusion injury. Careful delineation of repair and resolution pathways could provide therapeutic targets for the development of effective treatments to offer patients with acute kidney injury.
MeSH term(s)	Acute Kidney Injury/immunology ; Animals ; Humans ; Macrophages/immunology ; Reperfusion Injury/immunology
Language	English
Publishing date	2014-01-19
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-013-2726-y
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Article ; Online: Survey of Current Practices of Outpatient Hemodialysis for AKI Patients.

Ortiz-Soriano, Victor / Butler, Catherine R / Levy, Marla / Huen, Sarah C / Castaneda, Jorge L / Sakhuja, Ankit / Basu, Rajit K / Liu, Kathleen D / Cerda, Jorge / Neyra, Javier A

Kidney international reports

2021 Volume 6, Issue 4, Page(s) 1156–1160

Language	English
Publishing date	2021-01-28
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2021.01.002
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