arteriolosclerosis/potasyòm

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Morphologic aspects of low-potassium and low-sodium nephropathy.

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Renal biopsies from 40 patients with hypokalemia and hyponatremia of an average of 10 years' duration due to abuse of laxatives or diuretics, anorexia nervosa, or chronic vomiting were examined with morphometric methods. Light microscopy revealed the following alterations in the renal cortex as

Cause of residual hypertension after adrenalectomy in patients with primary aldosteronism.

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The cause of residual hypertension after adrenalectomy for primary aldosteronism (PA) is unknown. The purpose of this study is to investigate the characteristic pathological kidney features associated with PA. Between 1977 and 1999 at our hospital, 26 patients with PA caused by a unilateral adrenal

Primary hyperaldosteronism without suppressed renin due to secondary hypertensive kidney damage.

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Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. Renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory

ABCC9/SUR2 in the brain: Implications for hippocampal sclerosis of aging and a potential therapeutic target.

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The ABCC9 gene and its polypeptide product, SUR2, are increasingly implicated in human neurologic disease, including prevalent diseases of the aged brain. SUR2 proteins are a component of the ATP-sensitive potassium ("KATP") channel, a metabolic sensor for stress and/or hypoxia that has been shown

Pharmacological inhibition of fatty acid-binding protein 4 alleviated kidney inflammation and fibrosis in hyperuricemic nephropathy

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Hyperuricemia is an independent risk factor for chronic kidney disease (CKD). Excessive uric acid (UA) level in the blood leads to hyperuricemic nephropathy (HN), which is characterized by glomerular hypertension, arteriolosclerosis and tubulointerstitial fibrosis. Fatty acid binding protein 4

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