Risk Factors For Progressive Loss Research Articles

Association of body mass index with the development of metabolic acidosis in patients with chronic kidney disease.

Higher body mass index (BMI) is associated with higher bone mass and bone serves as a buffer during the development of metabolic acidosis. The authors sought to examine the relationship between BMI and metabolic acidosis in patients with chronic kidney disease (CKD). The study utilized a large US longitudinal data repository including over 103 million patients from healthcare provider organizations to evaluate the relationship between the exposure variable (BMI) and the prevalence and incidence of metabolic acidosis among patients with estimated glomerular filtration rate <60ml/min/1.73m2. Incident metabolic acidosis was identified at the first of two consecutive post-index serum bicarbonate values, 10-365days apart, between 12 and <22 mEq/L in patients with normal index serum bicarbonate. Cox proportional hazard models were adjusted for multiple variables including demographics, comorbidities, income, education, and kidney function. 103,766 patients qualified for this study; 6472 (6.2%) had metabolic acidosis at index. An inverse association between BMI category and metabolic acidosis was observed for both baseline (prevalence) and new-onset (incidence) metabolic acidosis. Compared to BMI category of 18.5 to <25kg/m2, each category of incrementally higher BMI was associated with a decreasing risk of incident metabolic acidosis; the adjusted hazard ratios (95% confidence interval) were 0.866 (0.824-0.911), 0.770 (0.729-0.813), 0.664 (0.622-0.709), and 0.612 (0.571-0.655) for BMI 25 to <30, 30 to <35, 35 to <40, and 40+ kg/m2, respectively. Among patients with CKD, an incremental increase in BMI was inversely associated with both the prevalence and incidence of metabolic acidosis. These associations suggest that increased body weight may protect against the development of metabolic acidosis, a risk factor for progressive loss of kidney function.

Nutritional Mediators of Cellular Decline and Mitochondrial Dysfunction in Older Adults

Aging is the primary risk factor for progressive loss of function, onset of disease, and increased vulnerability to negative health-related outcomes. These clinical manifestations arise from a decline in mitochondrial and metabolic processes considered the hallmarks of aging. Collectively, these changes can be defined as age associated cellular decline (AACD) and are often associated with signs and symptoms such as fatigue, reduced strength and low physical activity. This symposium will explore mechanisms, clinical signs, and emerging nutritional interventions for AACD. Dr. Feige’s presentation will serve as an introduction by highlighting mechanisms underlying functional declines in skeletal muscle with aging. He will discuss the Multi-Ethnic Molecular determinants of Sarcopenia (MEMOSA) study, which found impaired mitochondrial bioenergetic capacity in skeletal muscle of older adults with sarcopenia compared to age-matched controls, and identified mitochondrial function as a key target for intervention. Dr. Guralnik will discuss the connection between cellular changes and clinical manifestations of AACD. He will report on an expert consensus study group which developed an initial framework to identify self-reported symptoms and observable signs of AACD in adults over50 years. Lastly, Dr. Singh will discuss the evidence for nutritional interventions to address sources of AACD, focusing on those targeting mitochondrial dysfunction. Recent research on dietary interventions with urolithin A (an activator of mitophagy) and nicotinamide riboside (an NAD+ booster) will be reviewed. Overall, this symposium will highlight key mechanisms and clinical signs of AACD, and the potential for novel nutrition interventions to support cellular function and healthy aging.

Ambulatory Blood Pressure Monitoring: Profiles in Chronic Kidney Disease Patients and Utility in Management.

Optimal control of blood pressure (BP) may reduce the risk of progression of CKD. Misclassification of hypertension (HTN) and status of control may result in suboptimal management. Clinic or home BP may overestimate or underestimate status of control compared with ambulatory BP monitoring (ABPM), which is considered the gold standard. The latter relates not only to the superiority of ABPM concerning outcome prognosis but also to its ability to accurately diagnose white coat and masked HTN, which is critical in assuring adequate BP control. However, ABPM has not gained widespread use in practice because of limited third-party reimbursement and a paucity of high quality randomized controlled intervention studies evaluating its use. Herein, we review HTN phenotypes that have been identified in patients with CKD, and the potential value of ABPM in this high-risk population.