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Article ; Online: Urate-Lowering Therapy and Chronic Kidney Disease Progression.

Feig, Daniel I

2020 Volume 382, Issue 26, Page(s) 2567–2568

MeSH term(s)	Allopurinol ; Diabetes Mellitus, Type 1 ; Disease Progression ; Gout Suppressants ; Humans ; Renal Insufficiency, Chronic ; Uric Acid
Chemical Substances	Gout Suppressants ; Uric Acid (268B43MJ25) ; Allopurinol (63CZ7GJN5I)
Language	English
Publishing date	2020-09-14
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMe2015886
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Article ; Online: Allopurinol and Chronic Kidney Disease. Reply.

Feig, Daniel I

The New England journal of medicine

2020 Volume 383, Issue 17, Page(s) 1692

MeSH term(s)	Allopurinol/therapeutic use ; Gout Suppressants/therapeutic use ; Humans ; Renal Insufficiency, Chronic/drug therapy
Chemical Substances	Gout Suppressants ; Allopurinol (63CZ7GJN5I)
Language	English
Publishing date	2020-10-21
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMc2026125
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Article ; Online: Hyperuricemia and abnormal nocturnal dipping impact glomerular filtration rate in patients with sickle cell anemia.

Lebensburger, Jeffrey D / Aban, Inmaculada / Hilliard, Lee M / Feig, Daniel I

American journal of hematology

2021 Volume 96, Issue 5, Page(s) E143–E146

MeSH term(s)	Adolescent ; Age Factors ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/physiopathology ; Blood Pressure/physiology ; Blood Pressure Monitoring, Ambulatory ; Child ; Circadian Rhythm ; Disease Progression ; Female ; Glomerular Filtration Rate ; Humans ; Hypertension/complications ; Hypertension/physiopathology ; Hyperuricemia/blood ; Hyperuricemia/etiology ; Kidney/physiopathology ; Male ; Prospective Studies ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/physiopathology ; Sickle Cell Trait/complications ; Sickle Cell Trait/physiopathology ; Young Adult ; beta-Thalassemia/complications ; beta-Thalassemia/physiopathology
Language	English
Publishing date	2021-02-18
Publishing country	United States
Document type	Comparative Study ; Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.26115
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Zs.A 1251: Show issues

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Article ; Online: Serum uric acid and the risk of hypertension and chronic kidney disease.

Feig, Daniel I

Current opinion in rheumatology

2014 Volume 26, Issue 2, Page(s) 176–185

Abstract: Purpose of review: To discuss the evolving data regarding uric acid as a potential cause of hypertension and progressive renal dysfunction and its clinical and research implications.: Recent findings: The potential mechanisms by which uric acid could ...

Abstract	Purpose of review: To discuss the evolving data regarding uric acid as a potential cause of hypertension and progressive renal dysfunction and its clinical and research implications. Recent findings: The potential mechanisms by which uric acid could cause vasoconstriction and a progressive ateriolopathy were established in animal models between 1999 and 2004. Since then, there has been a growing interest in the topic and numerous retrospective and prospective observational studies. The preponderance of data support the hypothesis that serum uric acid is a cause or exacerbating factor of hypertension and progressive kidney disease. Over the last couple of years clinical intervention trials, including randomized controlled trials in the young have supported this mechanistic role. Summary: Current evidence supports the role of uric acid as marker and mediator of risk for both hypertension and progressive decline in renal function. Data on the impact of xanthine oxidase inhibitors or uricosurics on clinical hypertension and chronic kidney disease are suggestive but inconclusive. Considerably, more data will be required to determine if uric acid lowering therapy will become a mainstay of management in diseases other than gout and tumor lysis syndrome.
MeSH term(s)	Animals ; Biomarkers/blood ; Clinical Trials as Topic ; Enzyme Inhibitors/therapeutic use ; Humans ; Hypertension/blood ; Hypertension/drug therapy ; Hypertension/etiology ; Hyperuricemia/blood ; Hyperuricemia/complications ; Hyperuricemia/drug therapy ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/etiology ; Risk Factors ; Uric Acid/blood ; Uricosuric Agents/therapeutic use ; Xanthine Oxidase/antagonists & inhibitors
Chemical Substances	Biomarkers ; Enzyme Inhibitors ; Uricosuric Agents ; Uric Acid (268B43MJ25) ; Xanthine Oxidase (EC 1.17.3.2)
Language	English
Publishing date	2014-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1045317-9
ISSN	1531-6963 ; 1040-8711
ISSN (online)	1531-6963
ISSN	1040-8711
DOI	10.1097/BOR.0000000000000033
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Zs.A 3028: Show issues

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Article ; Online: Kidney implications of SARS-CoV2 infection in children.

Bjornstad, Erica C / Seifert, Michael E / Sanderson, Keia / Feig, Daniel I

Pediatric nephrology (Berlin, Germany)

2021 Volume 37, Issue 7, Page(s) 1453–1467

Abstract: Research indicates that severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection can impact every organ, and the effects can range from asymptomatic to severe disease. Since it was first discovered in December 2019, our understanding has ... ...

Abstract	Research indicates that severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection can impact every organ, and the effects can range from asymptomatic to severe disease. Since it was first discovered in December 2019, our understanding has grown about its impact on kidney disease. In general, children have less severe disease than adults, and this tendency appears to extend to special pediatric kidney populations (e.g., chronic kidney disease and immunosuppressed patients with solid organ transplants or nephrotic syndrome). However, in a fraction of infected children, SARS-CoV2 causes an array of kidney manifestations, ranging from acute kidney injury to thrombotic microangiopathy, with potential implications for increased risk of morbidity and mortality. Additional considerations surround the propensity for clotting extracorporeal circuits in children with SARS-CoV2 infection that are receiving kidney replacement therapy. This review provides an update on our current understanding of SARS-CoV2 for pediatric nephrologists and highlights knowledge gaps to be addressed by future research during this ongoing pandemic, particularly the social disparities magnified during this period.
MeSH term(s)	Acute Kidney Injury/epidemiology ; Acute Kidney Injury/etiology ; Acute Kidney Injury/therapy ; Adult ; COVID-19/complications ; Child ; Humans ; Kidney ; RNA, Viral ; SARS-CoV-2
Chemical Substances	RNA, Viral
Language	English
Publishing date	2021-08-28
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-021-05249-8
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Zs.A 2196: Show issues

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Article ; Online: Adverse childhood experiences are associated with vascular changes in adolescents that are risk factors for future cardiovascular disease.

Kellum, Cailin E / Kemp, Keri M / Mrug, Sylvie / Pollock, Jennifer S / Seifert, Michael E / Feig, Daniel I

Pediatric nephrology (Berlin, Germany)

2023 Volume 38, Issue 7, Page(s) 2155–2163

Abstract: Background: Adverse childhood experiences (ACEs), such as abuse, neglect, and household dysfunction, are associated with a higher risk of cardiovascular disease (CVD) and indicators of future CVD risk in adulthood, such as greater vascular stiffness. ... ...

Abstract	Background: Adverse childhood experiences (ACEs), such as abuse, neglect, and household dysfunction, are associated with a higher risk of cardiovascular disease (CVD) and indicators of future CVD risk in adulthood, such as greater vascular stiffness. The impact of ACEs in adolescence is unclear, and understanding how ACEs relate to blood pressure (BP) and vascular function during early life is key for the development of prevention strategies to reduce CVD risk. We hypothesized that exposure to ACEs would be associated with changes in central hemodynamics such as increased vascular stiffness and higher BP during adolescence. Methods: This pilot study enrolled 86 adolescents recruited from the Children's of Alabama. A validated ACE questionnaire was employed, and ACEs were modeled both as a continuous variable and a categorical variable (ACE ≥ 1 vs. ACE = 0). The primary outcomes used are considered to be indicators of future cardio-renal disease risk: aortic augmentation index normalized to 75 bpm (Alx75, a surrogate for vascular stiffness), carotid-femoral PWV (m/s), and ambulatory BP patterns. Results: Adolescents with ACE ≥ 1 had significantly higher Alx75 (ACE: 5.2% ± 2.2 compared to no ACE: - 1.4% ± 3.0; p = 0.043). PWV only reflected this trend when adjustments were made for the body mass index. Adolescents with ACEs showed no differences in ambulatory BP patterns during the 24-h, wake, or sleep periods compared to adolescents with no ACEs. Conclusions: ACEs were associated with higher AIx75 in adolescence, which is a risk factor for future CVD. Adolescence could present an opportunity for early detections/interventions to mitigate adverse cardiovascular outcomes in adulthood. A higher resolution version of the Graphical abstract is available as Supplementary information.
MeSH term(s)	Humans ; Adolescent ; Child ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; Adverse Childhood Experiences ; Pilot Projects ; Risk Factors ; Child Abuse
Language	English
Publishing date	2023-01-09
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-022-05853-2
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Article ; Online: Hyperuricemia and hypertension.

Feig, Daniel I

Advances in chronic kidney disease

2012 Volume 19, Issue 6, Page(s) 377–385

Abstract: Over the past century, uric acid has been considered a possible risk factor for hypertension and cardiovascular disease. However, only in the past decade, animal models and clinical trials have supported a more mechanistic link. Results from animal ... ...

Abstract	Over the past century, uric acid has been considered a possible risk factor for hypertension and cardiovascular disease. However, only in the past decade, animal models and clinical trials have supported a more mechanistic link. Results from animal models suggest a 2-phase mechanism for the development of hyperuricemic hypertension in which uric acid induces acute vasoconstriction by activation of renin-angiotensin system, followed by uric acid uptake into vascular smooth muscle cells leading to cellular proliferation and secondary arteriolosclerosis that impairs pressure natriuresis. This acute hypertension remains uric acid dependent and sodium independent, whereas the chronic hypertension becomes uric acid independent and sodium dependent. Small clinical trials, performed in adolescents with newly diagnosed essential hypertension, demonstrate that reduction of serum uric acid can reduce blood pressure. Although more research is clearly necessary, the available data suggest that uric acid is likely causative in some cases of early onset hypertension.
MeSH term(s)	Adolescent ; Animals ; Disease Models, Animal ; Humans ; Hypertension/complications ; Hypertension/drug therapy ; Hypertension/etiology ; Hyperuricemia/blood ; Hyperuricemia/complications ; Rats ; Risk Factors ; Uric Acid/blood ; Uric Acid/metabolism
Chemical Substances	Uric Acid (268B43MJ25)
Language	English
Publishing date	2012-11
Publishing country	United States
Document type	Journal Article
ISSN	1548-5609 ; 1548-5595
ISSN (online)	1548-5609
ISSN	1548-5595
DOI	10.1053/j.ackd.2012.05.009
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Article ; Online: The role of uric acid in the pathogenesis of hypertension in the young.

Feig, Daniel I

Journal of clinical hypertension (Greenwich, Conn.)

2012 Volume 14, Issue 6, Page(s) 346–352

Abstract: Uric acid has been suspected to be a risk factor for hypertension since the 1870s. Numerous epidemiological studies demonstrate an association between uric acid and both incident and prevalent hypertension in diverse populations. Studies in elderly ... ...

Abstract	Uric acid has been suspected to be a risk factor for hypertension since the 1870s. Numerous epidemiological studies demonstrate an association between uric acid and both incident and prevalent hypertension in diverse populations. Studies in elderly patients have had more variable results, raising the possibility that uric acid may be more significant to hypertension in the young. Animal models support a two-phase mechanism for the development of hyperuricemic hypertension. Initially, uric acid induces vasoconstriction by activation of the renin-angiotensin system and reduction of circulating nitric oxide, which can be reversed by lowering uric acid. Over time, uric acid uptake into vascular smooth muscle cells causes cellular proliferation and secondary arteriolosclerosis that impairs pressure natriuresis, causing sodium-sensitive hypertension. Consistent with the animal model data, small clinical trials performed in adolescents with newly diagnosed essential hypertension demonstrate that at least in certain young patients, reduction of serum uric acid can mitigate blood pressure elevation. While more research is clearly necessary, the available data suggest that uric acid is likely causative in some cases of early-onset hypertension.
MeSH term(s)	Age Factors ; Animals ; Child ; Child Welfare ; Disease Models, Animal ; Humans ; Hypertension/epidemiology ; Hypertension/pathology ; Hyperuricemia ; Risk Factors ; United States/epidemiology ; Uric Acid/blood ; Uric Acid/metabolism
Chemical Substances	Uric Acid (268B43MJ25)
Language	English
Publishing date	2012-05-21
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2077222-1
ISSN	1751-7176 ; 1524-6175
ISSN (online)	1751-7176
ISSN	1524-6175
DOI	10.1111/j.1751-7176.2012.00662.x
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Article ; Online: Uric acid and hypertension.

Feig, Daniel I

Seminars in nephrology

2011 Volume 31, Issue 5, Page(s) 441–446

Abstract: A link between serum uric acid and the development of hypertension was first hypothesized in the 1870s. Although numerous epidemiologic studies in the 1980s and 1990s suggested an association, relatively little attention was paid to it until recently. ... ...

Abstract	A link between serum uric acid and the development of hypertension was first hypothesized in the 1870s. Although numerous epidemiologic studies in the 1980s and 1990s suggested an association, relatively little attention was paid to it until recently. Animal models have suggested a two-step pathogenesis by which uric acid initially activates the renin angiotensin system and suppresses nitric oxide, leading to uric acid-dependent increase in systemic vascular resistance, followed by a uric acid-mediated vasculopathy, involving renal afferent arterioles, resulting in a late sodium-sensitive hypertension. Initial clinical trials in young patients have supported these mechanisms in young patients but do not yet support pharmacologic reduction of serum uric acid as first-line therapy for hypertension.
MeSH term(s)	Animals ; Humans ; Hypertension/etiology ; Hyperuricemia/complications ; Uric Acid/metabolism
Chemical Substances	Uric Acid (268B43MJ25)
Language	English
Publishing date	2011-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2011.08.008
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Se 784: Show issues

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Article ; Online: Sugar-sweetened beverages and hypertension.

Feig, Daniel I

Future cardiology

2010 Volume 6, Issue 6, Page(s) 773–776

Abstract: Consumption of sugar-sweetened beverages has been associated with the development and maintenance of obesity, as well as the risk for multiple obesity-related comorbidities. Some experts have hypothesized that the effect is entirely associated with ... ...

Abstract	Consumption of sugar-sweetened beverages has been associated with the development and maintenance of obesity, as well as the risk for multiple obesity-related comorbidities. Some experts have hypothesized that the effect is entirely associated with excess caloric intake, while others suggest that a component of sweeteners may have a physiologic impact on the development of hypertension, insulin resistance and nonalcoholic fatty liver disease. Chen et al. have presented the first, large-scale clinical trial, assessing the direct effect of modest changes in sweetened drink consumption on blood pressure in a racially diverse population. The study team utilized data from the PREMIER: Lifestyle Interventions for Blood Pressure Control trial, in which 810 adult subjects were randomized to three groups: advice only; comprehensive lifestyle modification aimed at weight loss, increased exercise and dietary sodium reduction; or comprehensive lifestyle modification with incorporation of the Dietary Approach to Stop Hypertension (DASH) diet. Sweetened drink intake was estimated from 24-h subject recall, assessed by unscheduled phone calls to subjects at baseline, 6 months and 18 months. Over the duration of the study, a reduction of one 12-oz serving of sugar-sweetened beverages per day was associated with an average of 1.8 mmHg reduction in systolic blood pressure and an average of 1.1 mmHg reduction in diastolic blood pressure.
MeSH term(s)	Beverages ; Blood Pressure ; Dietary Sucrose/therapeutic use ; Humans ; Hypertension/diet therapy ; Hypertension/etiology ; Hypertension/prevention & control ; Life Style ; Mental Recall ; Multivariate Analysis ; Randomized Controlled Trials as Topic ; Regression Analysis ; Statistics, Nonparametric ; United States
Chemical Substances	Dietary Sucrose
Language	English
Publishing date	2010-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2274267-0
ISSN	1744-8298 ; 1479-6678
ISSN (online)	1744-8298
ISSN	1479-6678
DOI	10.2217/fca.10.92
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