Diabetes and Hypertension

Boston, MA, United States

Diabetes and Hypertension

Boston, MA, United States

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Shari M. Ling, MD has been selected to receive the first-ever Public Service Award from NKF, established to honor those who have dedicated their careers to public service and who have helped to shape public policies or government programs that improve outcomes for kidney patients.  Dr. Ling currently serves as the Deputy Chief Medical Officer for the Centers for Medicare and Medicaid Services (CMS) and Medical Officer in the Center for Clinical Standards and Quality (CCSQ).  In her role at CMS, she assists the CMS Chief Medical Officer in the agency's pursuit of better health care, healthier populations and smarter spending. Dr. Ling's committed focus is on the achievement of meaningful health outcomes for patients and families through the delivery of high quality, person-centered care, across all care settings. Her clinical focus and scientific interest is in the care of persons with dementia, multiple chronic conditions and functional limitations. Derek Forfang, a kidney patient and long-time kidney disease advocate, has been selected to receive the first-ever Celeste Castillo Lee Patient Engagement Award, established in honor of Celeste Castillo Lee, a longtime advocate for patient-centered care and empowerment. It is the highest honor given by NKF to a distinguished kidney patient who exemplifies NKF's mission and Celeste's legacy of putting patients at the center of all aspects of healthcare through their involvement with NKF and community partners.  Mr. Forfang, of San Pablo, California, has been an end-stage renal disease (ESRD) patient since 1999.  He received a kidney transplant and has also been on peritoneal dialysis and hemodialysis.  A regional leader of NKF's Kidney Advocacy Committee and a member of the Public Policy Committee, Derek has worked tirelessly to protect and improve care for the kidney community. Merck been selected to receive the 2017 Corporate Innovator Award which recognizes industry partners that advance the field of nephrology by addressing an unmet medical need, or improving upon an existing practice, therapeutic or technology.  Merck's innovative new treatment for hepatitis C, ZEPATIER, is the only direct anti-viral agent specifically tested and approved for use in patients with chronic kidney disease stages four and five. Paul Palevsky, MD has been selected to receive the Dr. J. Michael Lazarus Distinguished Award established to honor Dr. Lazarus for his major contributions to the clinical science and care of dialysis patients, and to recognize individuals whose research has yielded novel insights related to renal replacement therapy.  Dr. Palevsky is Professor of Medicine and Clinical and Translational Science in the Renal-Electrolyte Division at the University of Pittsburgh School of Medicine; and serves as Chief of the Renal Section at the VA Pittsburgh Healthcare System.  Dr. Palevsky's research has primarily focused on acute kidney injury and critical care nephrology. He will be presenting the Lazarus lecture on "We Don't Have to Fail at Acute Renal Failure: A Multidisciplinary Approach to Quality Improvement" on Friday, April 21st at 8:45 a.m. at the NKF Spring Clinical Meetings. Susanne Nicholas, MD, MPH, PhD has been selected to receive the Medical Advisory Board Distinguished Service Award established to recognize an individual for their educational activities and community service in promoting the mission of NKF on a local level.  Dr. Nicholas is a tenured Associate Professor of Medicine at UCLA in the Division of Nephrology where she maintains her clinical responsibilities, and the Division of Endocrinology, Diabetes and Hypertension, where she conducts research.  She is also a Clinical Hypertension Specialist.   Dr. Nicholas' research interests include understanding and identifying key factors that promote the pathogenesis of diabetic kidney disease (DKD); uncovering and validating novel biomarkers that may predict DKD progression; and quantifying renal structural changes associated with DKD in response to novel therapeutics, using stereology principles. Her research over the past 15 years has led to the identification of a novel biomarker of DKD, which is currently being validated in clinical studies. Katherine R. Tuttle, MD, FASN, FACP, FNKF, has been selected to receive the prestigious Garabed Eknoyan Award, created to recognize an individual who has promoted the mission of NKF in Making Lives Better for people with kidney disease through the exceptional contributions to key initiatives of NKF such as the Kidney Disease Outcomes Quality Initiative (KDOQI) or clinical research in the field of kidney disease.  Dr. Tuttle is the Executive Director for Research at Providence Health Care in Spokane, and serves as Co-Principal Investigator of the Institute of Translational Health Sciences, Investigator at Kidney Research Institute, and Clinical Professor of Medicine for the University of Washington.  Dr. Tuttle's major research interests include diabetic kidney disease, hypertension, renal vascular disease, nutrition in chronic kidney disease, and transitional care.  She has chaired numerous workgroups focused on diabetes and kidney disease including NKF's KDOQI Workgroup for Diabetes and Chronic Kidney Disease. Jonathan Himmelfarb, MD has been selected to receive the Donald W. Seldin Award, established to recognize excellence in clinical nephrology in the tradition of one of the foremost teachers and researchers in the field, Dr. Donald W. Seldin.  Dr. Himmelfarb is a Professor of Medicine, Director of the Kidney Research Institute, and holds the Joseph W. Eschbach, M.D. Endowed Chair in Kidney Research at the University of Washington School of Medicine.   He is the author of more than 200 peer-reviewed publications, has served on numerous grant review committees and scientific advisory boards and has held leadership positions in many national and international nephrology societies.  Dr. Himmelfarb has served on expert panels for the U.S. Food and Drug Administration, Veterans Health Administration, and Centers for Medicare & Medicaid Services. He is also a nephrologist who cares for patients with kidney disease, and an internationally recognized educator about kidney disease. Raymond R. Townsend, MD has been selected to receive the Shaul G. Massry Distinguished Lecture Award, established to honor Dr. Massry for his scientific achievements and contribution to the kidney health care community and to NKF.  Dr. Townsend is Professor of Medicine and an Associate Director of the Center for Human Phenomic Studies at the University of Pennsylvania.  He is currently a Principal Investigator evaluating the role of demographic, phenotypic, humoral and genetic factors in the progression of kidney disease and the development and progression of cardiovascular disease in patients with chronic kidney disease.  He was also the Principal Investigator of a multicenter effort evaluating the specific role of pulse wave velocity in the renal and cardiovascular consequences of chronic kidney disease.   Dr. Townsend led the work group that wrote the KDOQI Commentary on the 2012 KDIGO Guideline on this subject, and most recently co-chaired the NKF workshop on Potassium Homeostasis in Disease and Health, the report on which will soon be published in the American Journal of Kidney Disease and Journal of the American Society of Hypertension. Tilakavati Karupaiah, PhD, APD, AN has been selected to receive the Joel D. Kopple Award, an annual award honoring an individual who has made significant contributions to the field of renal nutrition.  Dr. Karupaiah is an Accredited Practicing Dietitian with Dietitian's Association of Australia, a Professor and Head of the Dietetics Program at the National University of Malaysia; and also Adjunct Associate Professor at Wayne State University, Detroit.    Dr. Karupaiah's involvement in renal nutrition began because of a lack of dietitians in this field in Malaysia, and dialysis patients needed patient-friendly information about local diets. At the National University of Malaysia, she encouraged early exposure of dietetic students to renal patient care through community engagement, outpatient counseling and practical skills on patient diet planning. Dr. Karupaiah is now targeting capacity building mentorship for developing renal dietitians in Malaysia through nutrition research. For the past 26 years, nephrology healthcare professionals from across the country have come to NKF's Spring Clinical Meetings to learn about the newest developments related to all aspects of nephrology practice, network with colleagues, and present their research findings. The NKF Spring Clinical Meetings are designed for meaningful change in the multidisciplinary healthcare teams' skills, performance, and patient health outcomes.  It is the only conference of its kind that focuses on translating science into practice for the entire healthcare team. 1 in 3 American adults is at risk for kidney disease.  26 million American adults have kidney disease—and most aren't aware of it.  Risk factors for kidney disease include diabetes, high blood pressure, family history, and age 60+.  People of African American; Hispanic; Native American; Asian; or Pacific Islander descent are at increased risk for developing the disease.  African Americans are 3 ½ times more likely, and Hispanics 1 ½ times more likely, to experience kidney failure. The National Kidney Foundation (NKF) is the largest, most comprehensive and longstanding organization dedicated to the awareness, prevention and treatment of kidney disease.  For more information about NKF visit www.kidney.org. :  Full press releases on each award recipient, including quotes for attribution, are hyperlinked by recipient's name and can also be found in the Newsroom at www.kidney.org. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/national-kidney-foundation-honors-leading-researchers-clinicians-patient-advocates-and-more-at-its-26th-annual-spring-clinical-meetings-300442333.html


Navarro V.M.,Diabetes and Hypertension | Bosch M.A.,Oregon Health And Science University | Leon S.,University of Cordoba, Spain | Leon S.,Institute Salud Carlos III | And 14 more authors.
Endocrinology | Year: 2015

Tachykinins are comprised of the family of related peptides, substance P (SP), neurokinin A (NKA), and neurokinin B (NKB). NKB has emerged as regulator of kisspeptin release in the arcuate nucleus (ARC), whereas the roles of SP and NKA in reproduction remain unknown. This work explores the roles of SP and NKA in the central regulation of GnRH release. First, central infusion of specific agonists for the receptors of SP (neurokinin receptor 1, NK1R), NKA (NK2R) and NKB (NK3R) each induced gonadotropin release in adult male and ovariectomized, estradiol-replaced female mice, which was absent in Kiss1r-/- mice, indicating a kisspeptin-dependent action. The NK2R agonist, however, decreasedLHrelease in ovariectomized-sham replaced females, as documented forNK3R agonists but in contrast to the NK1R agonist, which further increased LH release. Second, Tac1 (encoding SP and NKA) expression in the ARC and ventromedial nucleus was inhibited by circulating estradiol but did not colocalize with Kiss1 mRNA. Third, about half of isolated ARC Kiss1 neurons expressed Tacr1 (NK1R) and 100% Tacr3 (NK3R); for anteroventral-periventricular Kiss1 neurons andGnRHneurons, approximately one-fourth expressed Tacr1 and one-tenth Tacr3; Tacr2 (NK2R) expression was absent in all cases. Overall, these results identify a potent regulation of gonadotropin release by the SP/NK1R and NKA/NK2R systems in the presence of kisspeptin-Kiss1r signaling, indicating that they may, along with NKB/NK3R, control GnRH release, at least in part through actions on Kiss1 neurons. Copyright © 2015 by the Endocrine Society.


Pham P.-T.T.,University of California at Los Angeles | Edling K.L.,Diabetes and Hypertension | Chakkera H.A.,Mayo Clinic Hospital | Pham P.-C.T.,View Medical
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy | Year: 2012

New-onset diabetes mellitus after transplantation (NODAT) is a serious and common complication following solid organ transplantation. NODAT has been reported in 2% to 53% of all solid organ transplants. Kidney transplant recipients who develop NODAT have variably been reported to be at increased risk of fatal and nonfatal cardiovascular events and other adverse outcomes including infection, reduced patient survival, graft rejection, and accelerated graft loss compared with those who do not develop diabetes. Limited clinical studies in liver, heart, and lung transplants similarly suggested that NODAT has an adverse impact on patient and graft outcomes. Early detection and management of NODAT must, therefore, be integrated into the treatment of transplant recipients. Studies investigating the best screening or predictive tool for identifying patients at risk for developing NODAT early after transplantation, however, are lacking. We review the clinical predictive values of fasting plasma glucose, oral glucose tolerance test, and A1C in assessing the risk for NODAT development and as a screening tool. Simple diabetes prediction models that incorporate clinical and/or metabolic risk factors (such as age, body mass index, hyper triglyceridemia, or metabolic syndrome) are also presented. © 2012 Pham et al, publisher and licensee Dove Medical Press Ltd.


Lee C.,University of Southern California | Zeng J.,University of Southern California | Drew B.G.,Diabetes and Hypertension | Sallam T.,University of California at Los Angeles | And 7 more authors.
Cell Metabolism | Year: 2015

Mitochondria are known to be functional organelles, but their role as a signaling unit is increasingly being appreciated. The identification of a short open reading frame (sORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additional sORFs in the mtDNA. Here we report a sORF within the mitochondrial 12S rRNA encoding a 16-amino-acid peptide named MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) that regulates insulin sensitivity and metabolic homeostasis. Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity. These results suggest that mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome. © 2015 Elsevier Inc.


Beaven S.W.,Howard Hughes Medical Institute | Matveyenko A.,Diabetes and Hypertension | Matveyenko A.,University of California at Los Angeles | Wroblewski K.,Howard Hughes Medical Institute | And 8 more authors.
Cell Metabolism | Year: 2013

Liver X receptors (LXRs) regulate lipogenesis and inflammation, but their contribution to the metabolic syndrome is unclear. We show that LXRs modulate key aspects of the metabolic syndrome in mice. LXRαβ-deficient-ob/ob (LOKO) mice remain obese but show reduced hepatic steatosis and improved insulin sensitivity compared to ob/ob mice. Impaired hepatic lipogenesis in LOKO mice is accompanied by reciprocal increases in adipose lipid storage, reflecting tissue-selective effects on the SREBP, PPARγ, and ChREBP lipogenic pathways. LXRs are essential for obesity-driven SREBP-1c and ChREBP activity in liver, but not fat. Furthermore, loss of LXRs in obesity promotes adipose PPARγ and ChREBP-β activity, leading to improved insulin sensitivity. LOKO mice also exhibit defects in β cell mass and proliferation despite improved insulin sensitivity. Our data suggest that sterol sensing by LXRs in obesity is critically linked with lipid and glucose homeostasis and provide insight into the complex relationships between LXR and insulin signaling. © 2013 Elsevier Inc.


PubMed | U.S. National Institute on Aging, Diabetes and Hypertension, University of Southern California and University of California at Los Angeles
Type: Journal Article | Journal: Cell metabolism | Year: 2015

Mitochondria are known to be functional organelles, but their role as a signaling unit is increasingly being appreciated. The identification of a short open reading frame (sORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additional sORFs in the mtDNA. Here we report a sORF within the mitochondrial 12S rRNA encoding a 16-amino-acid peptide named MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) that regulates insulin sensitivity and metabolic homeostasis. Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity. These results suggest that mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome.


Saxena A.R.,Diabetes and Hypertension | Karumanchi S.A.,Beth Israel Deaconess Medical Center | Brown N.J.,Vanderbilt University | Royle C.M.,Beth Israel Deaconess Medical Center | And 2 more authors.
Hypertension | Year: 2010

Pregnancies complicated by new-onset hypertension are associated with increased sensitivity to angiotensin II, but it is unclear whether this sensitivity persists postpartum. We studied pressor response to infused angiotensin II in 25 normotensive postpartum women in both high-and low-sodium balance. Ten women had a history of hypertensive pregnancy (5 with preeclampsia; 5 with transient hypertension of pregnancy), and 15 women had a history of uncomplicated, normotensive pregnancy. Systolic and diastolic blood pressures, aldosterone, and soluble fms-like tyrosine kinase 1 levels were measured before and after angiotensin II infusion in both dietary phases. In high sodium balance, women with a history of hypertensive pregnancy were normotensive but had significantly higher systolic and diastolic blood pressures than controls (115 versus 104 mm Hg and 73 versus 65 mm Hg, respectively; P<0.05). Women with a history of hypertensive pregnancy had a pressor response to salt loading, demonstrated by an increase in systolic blood pressure on a high-salt diet. They also had greater systolic pressor response (10 versus 2 mm Hg; P=0.03), greater increase in aldosterone (56.8 versus 30.8 ng/dL; P=0.03), and increase in soluble fms-like tyrosine kinase 1 levels (11.0 versus-18.9 pg/mL; P=0.02) after infusion of angiotensin II in low-sodium balance compared with controls. Thus, women with a history of hypertensive pregnancy demonstrated salt sensitivity of blood pressure and had increased pressor, adrenal, and soluble fms-like tyrosine kinase 1 responses to infused angiotensin II in low-sodium balance. Increased sensitivity to angiotensin II observed during pregnancy in women with hypertensive pregnancy is present postpartum; this feature may contribute to future cardiovascular risk in these women. Copyright © 2010 American Heart Association. All rights reserved.


Babwah A.V.,University of Western Ontario | Babwah A.V.,Lawson Health Research Institute | Pampillo M.,University of Western Ontario | Pampillo M.,Lawson Health Research Institute | And 5 more authors.
Endocrinology | Year: 2012

The kisspeptin receptor (KISS1R) is a Gαq/11-coupled seven-transmembrane receptor activated by a group of peptides referred to as kisspeptins (Kps). The Kp/KISS1R signaling system is a powerful regulator of GnRH secretion, and inactivating mutations in this system are associated with hypogonadotropic hypogonadism. A recent study revealed that Kp triggers prolonged signaling; not from the inability of the receptor to undergo rapid desensitization, but instead from the maintenance of a dynamic and active pool of KISS1R at the cell surface. To investigate this further, we hypothesized that if a dynamic pool of receptor is maintained at the cell surface for a protracted period, chronic Kp-10 treatment would trigger the sustained activation of Gαq/11 as evidenced through the prolonged activation of phospholipase C, protein kinase C, and prolonged mobilization of intracellular Ca2+. Through single-cell analyses, we tested our hypothesis in human embryonic kidney (HEK) 293 cells and found that was indeed the case. We subsequently determined that prolonged KISS1R signaling was not a phenomenon specific to HEK 293 cells but is likely a conserved property of KISS1R-expressing cells because evidence of sustained KISS1R signaling was also observed in the GT1-7 GnRH neuronal and Chinese hamster ovary cell lines. While exploring the regulation of prolonged KISS1R signaling, we identified a critical role for extracellular Ca2+. We found that although free intracellular Ca2+, primarily derived from intracellular stores, was sufficient to trigger the acute activation of a major KISS1R secondary effector, protein kinase C, it was insufficient to sustain chronic KISS1R signaling; instead extracellular Ca2+ was absolutely required for this. Copyright © 2012 by The Endocrine Society.


Garza A.E.,Diabetes and Hypertension | Rariy C.M.,Diabetes and Hypertension | Sun B.,Diabetes and Hypertension | Williams J.S.,Diabetes and Hypertension | And 12 more authors.
Hypertension | Year: 2015

Striatin is a novel protein that interacts with steroid receptors and modifies rapid, nongenomic activity in vitro. We tested the hypothesis that striatin would in turn affect mineralocorticoid receptor function and consequently sodium, water, and blood pressure homeostasis in an animal model. We evaluated salt sensitivity of blood pressure in novel striatin heterozygote knockout mice. Compared with wild type, striatin heterozygote exhibited a significant increase in blood pressure when sodium intake was increased from restricted (0.03%) to liberal (1.6%) sodium. Furthermore, renal expression of mineralocorticoid receptor and its genomic downstream targets serum/glucocorticoid-regulated kinase 1, and epithelial sodium channel was increased in striatin heterozygote versus wild-type mice on liberal sodium intake while the pAkt/Akt ratio, readout of mineralocorticoid receptor's rapid, nongenomic pathway, was reduced. To determine the potential clinical relevance of these findings, we tested the association between single nucleotide polymorphic variants of striatin gene and salt sensitivity of blood pressure in 366 white hypertensive subjects. HapMap-derived tagging single nucleotide polymorphisms identified an association of rs2540923 with salt sensitivity of blood pressure (odds ratio, 6.25; 95% confidence interval, 1.7-20; P=0.01). These data provide the first in vivo evidence in humans and rodents that associates striatin with markers of mineralocorticoid receptor activity. The data also support the hypothesis that the rapid, nongenomic mineralocorticoid receptor pathway (mediated via striatin) has a role in modulating the interaction between salt intake and blood pressure. © 2014 American Heart Association, Inc.


Kikic Z.,Medical University of Vienna | Regele H.,Medical University of Vienna | Nordmeyer V.,Medical University of Vienna | Wahrmann M.,Medical University of Vienna | And 3 more authors.
Transplantation | Year: 2011

Background. Although diffuse linear C4d deposition in peritubular capillaries (PTCs) is a well-established criterion of alloantibody-mediated kidney transplant rejection, the actual relevance of focal or granular C4d deposits or staining outside PTC (glomeruli and arterioles) has yet to be established. Methods. This study was designed to evaluate the diagnostic significance of such nontypical C4d staining patterns. A total of 539 early indication biopsies (329 kidney transplants) were analyzed by immunohistochemistry using a polyclonal anti-C4d antibody. Results. We found a close interrelationship between diffuse or focal linear C4d deposition in PTC, linear endothelial deposition in glomeruli, and arteriolar C4d. These specific patterns were also related to transplant glomerulitis and recipient presensitization. No such associations, however, were observed for other patterns, such as granular C4d in PTC. Detection of diffuse but not focal linear C4d in PTC was found to be associated with adverse allograft survival (5-year death-censored graft survival: 48% vs. 82%, 89%, or 84% in patients with focal, minimal, or no C4d, respectively; P<0.0001). Univariate analysis also revealed inferior graft survival in recipients with linear C4d in glomeruli (P=0.02). Applying multivariate Cox regression analysis, however, only diffuse linear PTC staining was found to be predictive of graft loss (hazard ratio 3.95 [95% confidence interval 1.62-9.60]; P=0.002). Conclusion. There might be a relationship between humoral alloimmunity and distinct less established staining patterns, such as focal linear C4d in PTC, endothelial C4d in glomeruli, or arteriolar C4d. Nevertheless, our results reemphasize the prognostic value of diffuse linear PTC staining. Copyright © 2011 by Lippincott Williams & Wilkins.

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