Proton-pump inhibitors (PPIs) Linked to Increased Risk of Death

MedicalResearch.com Interview with:

Ziyad Al-Aly, MD, FASNAssistant Professor of MedicineDirector of the Clinical Epidemiology CenterChief of Research and EducationDepartment of Veterans Affairs Health Care SystemSaint Louis

Dr. Ziyad Al-Aly

Ziyad Al-Aly, MD, FASN
Assistant Professor of Medicine
Director of the Clinical Epidemiology Center
Chief of Research and Education
Department of Veterans Affairs Health Care System
Saint Louis 

MedicalResearch.com: What is the background for this study?  

Response: In 2017, we published a paper showing increased risk of death associated with Proton-pump inhibitors (PPI) use. Following the publication of that 2017 paper, several key stakeholders including patients, doctors, research scientists, medical media folks, mainstream media folks, and others asked us: what do these people die from? Did you study causes of death attributable to PPI use? In the study published today, we developed a causal inference framework to answer this question.

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Gene Transfer Improved Cardiac Function in Diabetic Mouse Model

MedicalResearch.com Interview with:

H. Kirk Hammond, MDProfessor of Medicine at University of California, San DiegoBasic research scientist and cardiologistSan Diego Veterans' Affairs Healthcare System

Dr. Hammond

H. Kirk Hammond, MD
Professor of Medicine at University of California
San Diego
Basic research scientist and cardiologist
San Diego Veterans’ Affairs Healthcare System

Dr. Hammond is winner of the 2017 William S. Middleton Award – the highest research honor in the U.S. Department of Veterans Affairs 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Worldwide, 9% of adults have diabetes, predominantly due to insulin resistance, known as Type 2 diabetes. It is associated with obesity and diets high in fat and carbohydrates. In this gene transfer study we showed that a single injection of a vector encoding a natural hormone (urocortin 2, Ucn2) increased glucose disposal and improved heart function in a model of diet-induced Type 2 diabetes in mice. 

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Biomarkers Suggest Intensive Blood Pressure Treatment Does Not Cause True Kidney Damage in CKD Patients

MedicalResearch.com Interview with:

Michael G. Shlipak, MD, MPH Scientific Director , Kidney Health Research Collaborative (khrc.ucsf.edu/) Professor of Medicine, Epidemiology & Biostatistics University of California, San Francisco Associate Chief of Medicine for Research Development San Francisco VA Medical Center

Dr. Shlipak

Michael G. Shlipak, MD, MPH
Scientific Director , Kidney Health Research Collaborative (khrc.ucsf.edu)
Professor of Medicine, Epidemiology & Biostatistics
University of California, San Francisco
Associate Chief of Medicine for Research Development
San Francisco VA Medical Center

MedicalResearch.com: What is the background for this study?

  • Our study represents major advancements in our understanding of whether kidney tissue damage accompanies the diagnosis of chronic kidney disease during hypertension therapy.
  • The Systolic Blood Pressure Intervention Trial (SPRINT) was a landmark clinical trial that demonstrated that more intensive systolic blood pressure management (target <120 mmHg) reduced rates of major cardiovascular events and mortality compared with standard therapy (<140 mmHg). A recent announcement indicated that the lower systolic blood pressure target also slowed the rate of cognitive decline and dementia incidence.
  • The major concern with intensive blood pressure lowering in SPRINT is the 3-fold incidence of chronic kidney disease, as defined using the clinical standard of serum creatinine levels. This detrimental impact on the kidney was surprising because hypertension is a predominant risk factor for kidney disease, and hypertension therapy should reduce CKD risk.
  • Given the lower blood pressure targets in the recently-updated national hypertension guidelines, there has been substantial concern that guideline implementation of blood pressure targets could cause an epidemic of CKD and the attendant suffering from its downstream consequences of cardiovascular disease, heart failure, and kidney failure.
  • In our study, we compared SPRINT participants who developed CKD with matched controls, using a panel of validated urinary biomarkers of kidney damage. These urine tests can measure actual kidney damage, rather than relying on the creatinine which is an indirect reflection of the kidney’s filtering function.
  • In the group undergoing intensive blood pressure lowering in SPRINT, we found that the new cases of CKD had an overall lowering of the kidney damage biomarkers compared with the controls, contrary to what would have been expected if they were developing “real” CKD.
  • In contrast, the new CKD cases that developed in the standard treatment group did have overall elevations in the urinary biomarkers of kidney damage; 5 of the 9 biomarkers significantly increased relative to the CKD cases in the intensive treatment group. 

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