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Article ; Online: Genetic Markers Regulating Blood Pressure in Extreme Discordant Sib Pairs.

Yasmin / O'Shaughnessy, Kevin M

2023 Volume 14, Issue 10

Abstract: Genome-wide scans performed in affected sib pairs have revealed small and often inconsistent clues to the loci responsible for the inherited components of hypertension. Since blood pressure is a quantitative trait regulated by many loci, two siblings at ... ...

Abstract	Genome-wide scans performed in affected sib pairs have revealed small and often inconsistent clues to the loci responsible for the inherited components of hypertension. Since blood pressure is a quantitative trait regulated by many loci, two siblings at opposite extremes of the blood pressure distribution are more likely to have inherited different alleles at any given locus. Hence, we investigated an extreme discordant sib pair strategy to analyse markers from two previous loci of interest: (1) the Gordons syndrome locus that includes the WNK4 gene and (2) the ROMK locus identified in our first genome-wide scan. For this study, 24 sib pairs with strong family histories of essential hypertension were selected from the top and bottom 10% of the blood pressure distribution and genotyped for highly polymorphic microsatellite markers on chromosomes 11 and 17. The mean age of the population was 39.8 ± 7.8 years. A significant inverse correlation was found between the squared difference in pulse pressure and the number of alleles shared by IBD between the siblings for the DS11925 marker (r = -0.44,
MeSH term(s)	Humans ; Adult ; Middle Aged ; Genetic Markers/genetics ; Blood Pressure/genetics ; Genotype ; Phenotype ; Hypertension/genetics
Chemical Substances	Genetic Markers
Language	English
Publishing date	2023-09-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14101862
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Article ; Online: Modified HEK cells simulate DCT cells in their sensitivity and response to changes in extracellular K.

Murthy, Meena / O'Shaughnessy, Kevin M

Physiological reports

2019 Volume 7, Issue 22, Page(s) e14280

Abstract: A potassium ( ... ...

Abstract	A potassium (K
MeSH term(s)	Animals ; Dose-Response Relationship, Drug ; Extracellular Fluid/drug effects ; Extracellular Fluid/metabolism ; HEK293 Cells ; Humans ; Kidney Tubules, Distal/cytology ; Kidney Tubules, Distal/drug effects ; Kidney Tubules, Distal/metabolism ; Membrane Potentials/drug effects ; Membrane Potentials/physiology ; Mice ; Potassium Chloride/metabolism ; Potassium Chloride/pharmacology
Chemical Substances	Potassium Chloride (660YQ98I10)
Language	English
Publishing date	2019-11-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.14280
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Article ; Online: β1-Adrenoreceptor Polymorphisms and Blood Pressure: 49S Variant Increases Plasma Renin But Not Blood Pressure in Hypertensive Patients.

Sandilands, Alastair J / O'Shaughnessy, Kevin M

American journal of hypertension

2019 Volume 32, Issue 5, Page(s) 447–451

Abstract: Background: Activation of beta-1 adrenoreceptor (β1-AR) in the kidney releases renin that plays a major role in the maintenance of blood pressure. Genetic variation in β1-AR could therefore alter the physiological and clinical effects of this hormone. ... ...

Abstract	Background: Activation of beta-1 adrenoreceptor (β1-AR) in the kidney releases renin that plays a major role in the maintenance of blood pressure. Genetic variation in β1-AR could therefore alter the physiological and clinical effects of this hormone. We tested this hypothesis in patients from a primary care cohort being screened for primary hyperaldosteronism (n = 467). Methods: Demographic and hemodynamic data were measured and plasma renin was determined by a standard immunoassay. Subjects were genotyped for the 2 common single-nucleotide polymorphisms Arg389Gly (rs1801253) and Ser49Gly (rs1801252), and thus the 4 possible haplotypes in β1-AR gene. Results: In patients being screened for hyperaldosteronism, plasma renin was significantly elevated in Ser49 homozygotes (49SS) compared with Gly49 (49G) allele carriers (0.307 ± 0.03 vs. 0.164 ± 0.05; P = 0.01). However, this did not translate into differences in either blood pressure or heart rate. On the other hand, the Arg389Gly polymorphism did not affect either plasma renin or blood pressure in this group. There was also no evidence that the 2 loci were linked in this group of patients. Conclusion: These data suggest that in this cohort the Ser49 variant of the Ser49Gly β1-AR gene polymorphism associates with higher renin levels. However, these common β1-AR gene polymorphisms do not affect blood pressure in the same cohort.
MeSH term(s)	Alleles ; Biomarkers/blood ; Blood Pressure/physiology ; DNA/genetics ; Genotype ; Haplotypes ; Humans ; Hyperaldosteronism/blood ; Hyperaldosteronism/complications ; Hyperaldosteronism/genetics ; Hypertension/etiology ; Hypertension/genetics ; Hypertension/metabolism ; Polymorphism, Single Nucleotide ; Receptors, Adrenergic, beta-1/genetics ; Receptors, Adrenergic, beta-1/metabolism ; Renin/blood
Chemical Substances	Biomarkers ; Receptors, Adrenergic, beta-1 ; DNA (9007-49-2) ; Renin (EC 3.4.23.15)
Language	English
Publishing date	2019-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639383-4
ISSN	1941-7225 ; 1879-1905 ; 0895-7061
ISSN (online)	1941-7225 ; 1879-1905
ISSN	0895-7061
DOI	10.1093/ajh/hpz019
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Article ; Online: Gordon Syndrome: a continuing story.

O'Shaughnessy, Kevin M

Pediatric nephrology (Berlin, Germany)

2014 Volume 30, Issue 11, Page(s) 1903–1908

Abstract: Gordon Syndrome (GS) is a rare familial hypertension syndrome with a characteristic hyperkalaemia which distinguishes it from other syndromic forms of hypertension that typically cause hypokalaemia. Patients with GS respond to aggressive salt-restriction ...

Abstract	Gordon Syndrome (GS) is a rare familial hypertension syndrome with a characteristic hyperkalaemia which distinguishes it from other syndromic forms of hypertension that typically cause hypokalaemia. Patients with GS respond to aggressive salt-restriction or relatively small doses of thiazide diuretics, which suggests that activation of the thiazide-sensitive Na/Cl cotransporter (NCC) in the distal nephron is to blame. However, the mechanism has proved to be complex. In 2001, mutations in genes encoding two serine/threonine kinases, WNK1 and WNK4, were identified as causing GS. However, it took several years to appreciate that these kinases operated in a cascade with downstream serine/threonine kinases (SPAK and OSR1) actually phosphorylating and activating NCC and the closely related cotransporters NKCC1 and NKCC2. The hyperkalaemia in GS arises from an independent action of WNK1/WNK4 to reduce cell-surface expression of ROMK, the secretory K-channel in the collecting ducts. However, mutations in WNK1/4 are present in a small minority of GS families, and further genes have emerged (CUL3 and KLHL3) that code for Cullin-3 (a scaffold protein in an ubiquitin-E3 ligase) and an adaptor protein, Kelch3, respectively. These new players regulate the ubiquitination and proteasomal degradation of WNK kinases, thereby adding to the complex picture we now have of NCC regulation in the distal nephron.
MeSH term(s)	Humans ; Pseudohypoaldosteronism/genetics ; Pseudohypoaldosteronism/physiopathology
Language	English
Publishing date	2014-12-11
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/s00467-014-2956-7
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Article ; Online: Nonadherence to antihypertensive medications amongst patients with uncontrolled hypertension: A retrospective study.

Kulkarni, Spoorthy / Rao, Raunak / Goodman, James Delman Harry / Connolly, Kathleen / O'Shaughnessy, Kevin M

Medicine

2021 Volume 100, Issue 14, Page(s) e24654

Abstract: Abstract: Medication nonadherence represents a modifiable risk factor for patients with hypertension. Identification of nonadherent patients could have significant clinical and economic implications in the management of uncontrolled hypertension.We ... ...

Abstract	Abstract: Medication nonadherence represents a modifiable risk factor for patients with hypertension. Identification of nonadherent patients could have significant clinical and economic implications in the management of uncontrolled hypertension.We analysed the results of 174 urinary adherence screens from patients referred to Addenbrooke's Hospital, Cambridge, for uncontrolled hypertension. Cases were identified for evaluation by results of liquid chromatography-tandem mass spectrometry of urine samples (males: 91; females: 83; age range: 17-87). We performed a binary logistic regression analysis for nonadherence using age, sex, and number of medications prescribed (both antihypertensives and non-antihypertensives separately) as independent predictors. Rates of nonadherence for individual antihypertensive drugs were calculated if prescribed to ≥10 patients.The overall rate of nonadherence to one or more prescribed antihypertensive medications was 40.3%. 14.4% of all patients were nonadherent to all prescribed antihypertensive medications (complete nonadherence), whereas 25.9% of all patients were nonadherent to at least 1, (but not all) prescribed antihypertensive medications (partial nonadherence). 72% of patients were prescribed ≥3 antihypertensives And for every increase in the number of antihypertensive medications prescribed, nonadherence increased with adjusted odds ratios of 2.9 (P < .001). Logistic regression showed that women were 3.3 times more likely to be nonadherent (P = .004). Polypharmacy (≥6 medications prescribed for hypertension and/or concomitant comorbidities) was prevalent in 52%. Bendroflumethiazide and chlortalidone demonstrated the highest and lowest nonadherences respectively (45.5% and 11.8%).Rate of nonadherence in patients with hypertension was significantly impacted by sex and number of antihypertensive medications prescribed. Understanding these factors is crucial in identifying and managing nonadherence.
MeSH term(s)	Adult ; Aged ; Antihypertensive Agents/therapeutic use ; Antihypertensive Agents/urine ; Female ; Humans ; Hypertension/drug therapy ; Male ; Medication Adherence/statistics & numerical data ; Middle Aged ; Polypharmacy ; Retrospective Studies ; Sex Distribution
Chemical Substances	Antihypertensive Agents
Language	English
Publishing date	2021-04-08
Publishing country	United States
Document type	Journal Article ; Observational Study
ZDB-ID	80184-7
ISSN	1536-5964 ; 0025-7974
ISSN (online)	1536-5964
ISSN	0025-7974
DOI	10.1097/MD.0000000000024654
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Article ; Online: Authors' reply to Ninan and Millar and Abou-saleh.

O'Shaughnessy, Kevin M / Kennard, Lucinda

BMJ (Clinical research ed.)

2016 Volume 353, Page(s) i2253

Language	English
Publishing date	2016--26
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	1362901-3
ISSN	1756-1833 ; 0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
ISSN (online)	1756-1833
ISSN	0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
DOI	10.1136/bmj.i2253
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Article ; Online: Treating hypertension in patients with medical comorbidities.

Kennard, Lucinda / O'Shaughnessy, Kevin M

BMJ (Clinical research ed.)

2016 Volume 352, Page(s) i101

MeSH term(s)	Antihypertensive Agents/therapeutic use ; Comorbidity ; Humans ; Hypertension/drug therapy ; Practice Guidelines as Topic ; United Kingdom
Chemical Substances	Antihypertensive Agents
Language	English
Publishing date	2016-02-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1362901-3
ISSN	1756-1833 ; 0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
ISSN (online)	1756-1833
ISSN	0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
DOI	10.1136/bmj.i101
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Article: In Vivo Activity of Metal Complexes Containing 1,10-Phenanthroline and 3,6,9-Trioxaundecanedioate Ligands against

O'Shaughnessy, Megan / Piatek, Magdalena / McCarron, Pauraic / McCann, Malachy / Devereux, Michael / Kavanagh, Kevin / Howe, Orla

Biomedicines

2022 Volume 10, Issue 2

Abstract: ... Drug- ... ...

Abstract	Drug-resistant
Language	English
Publishing date	2022-01-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10020222
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Article ; Online: Tobacco exposure in adults and children with proteinuric glomerulopathies: a NEPTUNE cohort study.

Wang, Linda / Smith-Salzberg, Bayle / Meyers, Kevin Ec / Glenn, Dorey A / Tuttle, Katherine R / Derebail, Vimal K / Brady, Tammy M / Gibson, Keisha / Smith, Abigail R / O'Shaughnessy, Michelle M / Srivastava, Tarak / Hall, Gentzon / Zee, Jarcy / Bitzer, Markus / Sethna, Christine B

BMC nephrology

2023 Volume 24, Issue 1, Page(s) 30

Abstract: Background: Tobacco exposure has been recognized as a risk factor for cardiovascular disease (CVD) and progression of kidney disease. Patients with proteinuric glomerulopathies are at increased risk for cardiovascular morbidity and mortality. Multiple ... ...

Abstract	Background: Tobacco exposure has been recognized as a risk factor for cardiovascular disease (CVD) and progression of kidney disease. Patients with proteinuric glomerulopathies are at increased risk for cardiovascular morbidity and mortality. Multiple studies have linked tobacco exposure to CVD and chronic kidney disease, but the relationships between smoking and proteinuric glomerulopathies in adults and children have not been previously explored. Methods: Data from the Nephrotic Syndrome Study Network (NEPTUNE), a multi-center prospective observational study of participants with proteinuric glomerulopathies, was analyzed. 371 adults and 192 children enrolled in NEPTUNE were included in the analysis. Self-reported tobacco exposure was classified as non-smoker, active smoker, former smoker, or exclusive passive smoker. Baseline serum cotinine levels were measured in a sub-cohort of 178 participants. Results: The prevalence of active smokers, former smokers and exclusive passive smoking among adults at baseline was 14.6%, 29.1% and 4.9%, respectively. Passive smoke exposure was 16.7% among children. Active smoking (reference non-smoking) was significantly associated with greater total cholesterol among adults (β 17.91 95% CI 0.06, 35.76, p = 0.049) while passive smoking (reference non-smoking) was significantly associated with greater proteinuria over time among children (β 1.23 95% CI 0.13, 2.33, p = 0.03). Higher cotinine levels were associated with higher baseline eGFR (r = 0.17, p = 0.03). Conclusion: Tobacco exposure is associated with greater risk for CVD and worse kidney disease outcomes in adults and children with proteinuric glomerulopathies. Preventive strategies to reduce tobacco exposure may help protect against future cardiovascular and kidney morbidity and mortality in patients with proteinuric glomerulopathies.
MeSH term(s)	Humans ; Adult ; Child ; Cohort Studies ; Cotinine ; Nicotiana ; Tobacco Smoke Pollution/adverse effects ; Neptune ; Kidney Diseases/chemically induced ; Cardiovascular Diseases
Chemical Substances	Cotinine (K5161X06LL) ; Tobacco Smoke Pollution
Language	English
Publishing date	2023-02-09
Publishing country	England
Document type	Observational Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2041348-8
ISSN	1471-2369 ; 1471-2369
ISSN (online)	1471-2369
ISSN	1471-2369
DOI	10.1186/s12882-023-03073-w
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Article ; Online: WNK signalling pathways in blood pressure regulation.

Murthy, Meena / Kurz, Thimo / O'Shaughnessy, Kevin M

Cellular and molecular life sciences : CMLS

2016 Volume 74, Issue 7, Page(s) 1261–1280

Abstract: Hypertension (high blood pressure) is a major public health problem affecting more than a billion people worldwide with complications, including stroke, heart failure and kidney failure. The regulation of blood pressure is multifactorial reflecting ... ...

Abstract	Hypertension (high blood pressure) is a major public health problem affecting more than a billion people worldwide with complications, including stroke, heart failure and kidney failure. The regulation of blood pressure is multifactorial reflecting genetic susceptibility, in utero environment and external factors such as obesity and salt intake. In keeping with Arthur Guyton's hypothesis, the kidney plays a key role in blood pressure control and data from clinical studies; physiology and genetics have shown that hypertension is driven a failure of the kidney to excrete excess salt at normal levels of blood pressure. There is a number of rare Mendelian blood pressure syndromes, which have shed light on the molecular mechanisms involved in dysregulated ion transport in the distal kidney. One in particular is Familial hyperkalemic hypertension (FHHt), an autosomal dominant monogenic form of hypertension characterised by high blood pressure, hyperkalemia, hyperchloremic metabolic acidosis, and hypercalciuria. The clinical signs of FHHt are treated by low doses of thiazide diuretic, and it mirrors Gitelman syndrome which features the inverse phenotype of hypotension, hypokalemic metabolic alkalosis, and hypocalciuria. Gitelman syndrome is caused by loss of function mutations in the thiazide-sensitive Na/Cl cotransporter (NCC); however, FHHt patients do not have mutations in the SCL12A3 locus encoding NCC. Instead, mutations have been identified in genes that have revealed a key signalling pathway that regulates NCC and several other key transporters and ion channels in the kidney that are critical for BP regulation. This is the WNK kinase signalling pathway that is the subject of this review.
MeSH term(s)	Animals ; Blood Pressure/physiology ; Cullin Proteins/metabolism ; Humans ; Hypertension/genetics ; Hypertension/metabolism ; Hypertension/pathology ; Neovascularization, Physiologic ; Protein Serine-Threonine Kinases/metabolism ; Pseudohypoaldosteronism/genetics ; Pseudohypoaldosteronism/pathology ; Receptors, Drug/chemistry ; Receptors, Drug/genetics ; Receptors, Drug/metabolism ; Signal Transduction ; Sodium Chloride Symporters/chemistry ; Sodium Chloride Symporters/genetics ; Sodium Chloride Symporters/metabolism ; Sodium-Potassium-Chloride Symporters/genetics ; Sodium-Potassium-Chloride Symporters/metabolism
Chemical Substances	Cullin Proteins ; Receptors, Drug ; Sodium Chloride Symporters ; Sodium-Potassium-Chloride Symporters ; thiazide receptor ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2016-11-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-016-2402-z
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