Elderly patients are prone to develop hyper- or hypokalemia, since they are susceptible to drugs or diets that affect the urinary or fecal potassium (K+) excretion. In aging mouse kidneys, in addition to glomerulosclerosis, proximal tubular atrophy, and atherosclerosis in renal arterioles, there was diffuse tubulointerstitial fibrosis with a number of inflammatory leukocytes infiltrating into the cortical interstitium. Since these pathological features greatly influence renal K+ handling, slowing the progression of kidney aging would fundamentally reduce the risk of developing hyper- or hypokalemia. Immunohistochemistry demonstrated the overexpression of K+ channels (Kv1.3) in leukocytes within the cortical interstitium, which was strongly associated with “chronic inflammation” in aging kidneys and the subsequent progression of renal fibrosis. In our basic studies, antihypertensive drugs (benidipine, nifedipine, verapamil, diltiazem) and anticholesterol drugs (lovastatin, simvastatin, pravastatin) strongly suppressed the leukocyte Kv1.3 channels and thus exerted anti-inflammatory effects. Given such pharmacological properties of these drugs, they may also be useful in slowing the progression of tubulointerstitial fibrosis in aging kidneys and reducing the risk of hyper- or hypokalemia in elderly patients.

Elderly patients are prone to develop hyper- or hypokalemia, since they are susceptible to drugs or diets that affect the urinary or fecal potassium (K+) excretion. In aging mouse kidneys, in addition to glomerulosclerosis, proximal tubular atrophy, and atherosclerosis in renal arterioles, there was diffuse tubulointerstitial fibrosis with a number of inflammatory leukocytes infiltrating into the cortical interstitium. Since these pathological features greatly influence renal K+ handling, slowing the progression of kidney aging would fundamentally reduce the risk of developing hyper- or hypokalemia. Immunohistochemistry demonstrated the overexpression of K+ channels (Kv1.3) in leukocytes within the cortical interstitium, which was strongly associated with “chronic inflammation” in aging kidneys and the subsequent progression of renal fibrosis. In our basic studies, antihypertensive drugs (benidipine, nifedipine, verapamil, diltiazem) and anticholesterol drugs (lovastatin, simvastatin, pravastatin) strongly suppressed the leukocyte Kv1.3 channels and thus exerted anti-inflammatory effects. Given such pharmacological properties of these drugs, they may also be useful in slowing the progression of tubulointerstitial fibrosis in aging kidneys and reducing the risk of hyper- or hypokalemia in elderly patients.

Elderly patients are prone to develop hyper- or hypokalemia, since they are susceptible to drugs or diets that affect the urinary or fecal potassium (K+) excretion. In aging mouse kidneys, in addition to glomerulosclerosis, proximal tubular atrophy, and atherosclerosis in renal arterioles, there was diffuse tubulointerstitial fibrosis with a number of inflammatory leukocytes infiltrating into the cortical interstitium. Since these pathological features greatly influence renal K+ handling, slowing the progression of kidney aging would fundamentally reduce the risk of developing hyper- or hypokalemia. Immunohistochemistry demonstrated the overexpression of K+ channels (Kv1.3) in leukocytes within the cortical interstitium, which was strongly associated with “chronic inflammation” in aging kidneys and the subsequent progression of renal fibrosis. In our basic studies, antihypertensive drugs (benidipine, nifedipine, verapamil, diltiazem) and anticholesterol drugs (lovastatin, simvastatin, pravastatin) strongly suppressed the leukocyte Kv1.3 channels and thus exerted anti-inflammatory effects. Given such pharmacological properties of these drugs, they may also be useful in slowing the progression of tubulointerstitial fibrosis in aging kidneys and reducing the risk of hyper- or hypokalemia in elderly patients.

Elderly patients are prone to develop hyper- or hypokalemia, since they are susceptible to drugs or diets that affect the urinary or fecal potassium (K+) excretion. In aging mouse kidneys, in addition to glomerulosclerosis, proximal tubular atrophy, and atherosclerosis in renal arterioles, there was diffuse tubulointerstitial fibrosis with a number of inflammatory leukocytes infiltrating into the cortical interstitium. Since these pathological features greatly influence renal K+ handling, slowing the progression of kidney aging would fundamentally reduce the risk of developing hyper- or hypokalemia. Immunohistochemistry demonstrated the overexpression of K+ channels (Kv1.3) in leukocytes within the cortical interstitium, which was strongly associated with “chronic inflammation” in aging kidneys and the subsequent progression of renal fibrosis. In our basic studies, antihypertensive drugs (benidipine, nifedipine, verapamil, diltiazem) and anticholesterol drugs (lovastatin, simvastatin, pravastatin) strongly suppressed the leukocyte Kv1.3 channels and thus exerted anti-inflammatory effects. Given such pharmacological properties of these drugs, they may also be useful in slowing the progression of tubulointerstitial fibrosis in aging kidneys and reducing the risk of hyper- or hypokalemia in elderly patients.