Global Policy Barriers and Enablers to Exercise and Physical Activity in Kidney Care

Objective: Impairment in physical function and physical performance leads to decreased independence and health-related quality of life in people living with chronic kidney disease and end-stage kidney disease. Physical activity and exercise in kidney care are not priorities in policy development. We aimed to identify global policy-related enablers, barriers, and strategies to increase exercise participation and physical activity behavior for people living with kidney disease. Design and Methods: Guided by the Behavior Change Wheel theoretical framework, 50 global renal exercise experts developed policy barriers and enablers to exercise program implementation and physical activity promotion in kidney care. The consensus process consisted of developing themes from renal experts from North America, South America, Continental Europe, United Kingdom, Asia, and Oceania. Strategies to address enablers and barriers were identified by the group, and consensus was achieved. Results: We found that policies addressing funding, service provision, legislation, regulations, guidelines, the environment, communication, and marketing are required to support people with kidney disease to be physically active, participate in exercise, and improve health-related quality of life. We provide a global perspective and highlight Japanese, Canadian, and other regional examples where policies have been developed to increase renal physical activity and rehabilitation. We present recommendations targeting multiple stakeholders including nephrologists, nurses, allied health clinicians, organizations providing renal care and education, and renal program funders. Conclusions: We strongly recommend the nephrology community and people living with kidney disease take action to change policy now, rather than idly waiting for indisputable clinical trial evidence that increasing physical activity, strength, fitness, and function improves the lives of people living with kidney disease

Inhibition of angiotensin converting enzyme (ACE) in plasma and tissues: studies ex vivo after administration of ACE inhibitors

Two methods of radio-inhibitor binding to tissue membrane homogenates and in vitro autoradiography have been used for ex vivo studies on the inhibition of tissue angiotensin converting enzyme (ACE) following acute and chronic administration of ACE inhibitors. Tissue ACE is differentially inhibited in time and degree in different tissues of the rat. Plasma and kidney ACE are inhibited completely at low doses whereas lung and aorta are only inhibited by 60-70%, even after very high does of ACE inhibitors. In the brain only those structures outside the blood-brain barrier are inhibited at low doses but at high doses perindopril appears able to cross the blood-brain barrier. Similarly, testicular ACE is not inhibited and appears to be protected by a blood-testis barrier. Preliminary results suggest that after chronic administration there is also a variable pattern of induction and inhibition of ACE in different tissues. By relating the degree of tissue inhibition to physiological responses it may be possible to determine the role of local renin-angiotensin systems in regional haemodynamics and in the hypotensive action of ACE inhibitors. Further, the techniques of radioligand inhibitor binding and in vitro autoradiography can be extended to other important cardiovascular enzymes (renin and kallikrein) when suitable high affinity specific inhibitors become available

Interaction between atrial natriuretic peptide and the renin angiotensin aldosterone system. Endogenous antagonists

The biologic actions of the cardiac peptide hormone atrial natriuretic peptide (ANP) of vasorelaxation, diuresis and natriuresis, suppression of aldosterone, vasopressin release, and thirst are the opposite of those of the renin angiotensin system. This close relationship is further strengthened by the complementary localization of their receptors in the brain, adrenal gland, vasculature, and kidney. In many physiologic situations including postural changes, volume expansion, water immersion, high altitude, and lower body negative pressure, the plasma levels of ANP and angiotensin II change inversely. In congestive heart failure, renin and aldosterone levels may initially be suppressed by high levels of ANP. Similarly the low renin levels associated with increasing age and with elderly hypertensive patients, may be the result of the elevation of plasma ANP that occurs with aging. ANP may thus be the endogenous antagonist of the renin angiotensin aldosterone system. These two opposing systems allow fine-tuning of volume and pressure by the body