Pathophysiology of low renin syndromes: Sites of renal renin secretory impairment and prorenin overexpression

Lush, David; King, Jean A.; Fray, J. C. S.

doi:10.1038/ki.1993.140

Cited by 49 publications

(23 citation statements)

References 116 publications

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“…It has been postulated that those with diabetes are more likely to have relative aldosterone insensitivity and therefore are predisposed to the development of acidosis and hyperkalemia (31). In addition, inadequate insulin secretion may lead to extracellular potassium shifts (32).…”

Section: Discussionmentioning

confidence: 99%

Serum Potassium and Outcomes in CKD

Korgaonkar¹,

Tilea²,

Gillespie³

et al. 2010

Clinical Journal of the American Society of Nephrology

201

159

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Background and objectives:The relationship between serum potassium (S K ) and mortality in chronic kidney disease (CKD) has not been systematically investigated.Design, setting, participants, & measurements: We examined the predictors and mortality association of S K in the Renal Research Institute CKD Study cohort, wherein 820 patients with CKD were prospectively followed at four US centers for an average of 2.6 years. Predictors of S K were investigated using linear and repeated measures regression models. Associations between S K and mortality, the outcomes of ESRD, and cardiovascular events in time-dependent Cox models were examined.Results: The mean age was 60.5 years, 80% were white, 90% had hypertension, 36% had diabetes, the average estimated GFR was 25.4 ml/min per 1.73 m 2 , and mean baseline S K was 4.6 mmol/L. Higher S K was associated with male gender, lower estimated GFR and serum bicarbonate, absence of diuretic and calcium channel blocker use, diabetes, and use of angiotensinconverting enzyme inhibitors and/or statins. A U-shaped relationship between S K and mortality was observed, with mortality risk significantly greater at S K <4.0 mmol/L compared with 4.0 to 5.5 mmol/L. Risk for ESRD was elevated at S K <4 mmol/L in S K categorical models. Only the composite of cardiovascular events or death as an outcome was associated with higher S K (>5.5).Conclusions: Although clinical practice usually emphasizes greater attention to elevated S K in the setting of CKD, our results suggest that patients who have CKD and low or even low-normal S K are at higher risk for dying than those with mild to moderate hyperkalemia.

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Section: Discussionmentioning

confidence: 99%

Serum Potassium and Outcomes in CKD

Korgaonkar¹,

Tilea²,

Gillespie³

et al. 2010

Clinical Journal of the American Society of Nephrology

201

159

View full text Add to dashboard Cite

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“…This can be due to diabetes mellitus or acute or chronic interstitial nephritis and may be exacerbated by long-standing hypertension. Patients with diabetes who have low plasma renin activity have a defect in conversion of prorenin to active renin (202). In addition, expanded plasma volume leads to enhanced atrial natriuretic peptide which in turn, can lead to suppression of renin and aldosterone (53).…”

Section: Acquired Hypoaldosteronismmentioning

confidence: 99%

Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

Magill

2014

Comprehensive Physiology

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The renin-angiotensin-aldosterone system (RAAS) is a major regulator of blood pressure control, fluid, and electrolyte balance in humans. Chronic activation of mineralocorticoid production leads to dysregulation of the cardiovascular system and to hypertension. The key mineralocorticoid is aldosterone. Hyperaldosteronism causes sodium and fluid retention in the kidney. Combined with the actions of angiotensin II, chronic elevation in aldosterone leads to detrimental effects in the vasculature, heart, and brain. The adverse effects of excess aldosterone are heavily dependent on increased dietary salt intake as has been demonstrated in animal models and in humans. Hypertension develops due to complex genetic influences combined with environmental factors. In the last two decades, primary aldosteronism has been found to occur in 5% to 13% of subjects with hypertension. In addition, patients with hyperaldosteronism have more end organ manifestations such as left ventricular hypertrophy and have significant cardiovascular complications including higher rates of heart failure and atrial fibrillation compared to similarly matched patients with essential hypertension. The pathophysiology, diagnosis, and treatment of primary aldosteronism will be extensively reviewed. There are many pitfalls in the diagnosis and confirmation of the disorder that will be discussed. Other rare forms of hyper- and hypo-aldosteronism and unusual disorders of hypertension will also be reviewed in this article.

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“…Angiotensin II also increases Animal models suggest that both ACE and chymase/ chymase-like pathways contribute to angiotensin II synthe cellular expression of fibronectin [59]. However, in 415 Renin-Angiotensin-Aldosterone-Kinin System and CVD in DM tissue angiotensin II levels has previously been reported, [63][64][65][66] both in types I and II diabetes mellitus [68,69].…”

Section: Anatomicmentioning

confidence: 99%

“…However, circulating renin activity falls progressively with key role in the impairment of endothelial function. This observation is directly relevant to the RAAK system given increasing duration of diabetes [66,67]. Suppressed total renin activity also correlates with poor glycemic control that pharmacological blockade of the ACE/kinninase II enzyme with an ACE inhibitor reverses endothelial dysand with the presence of late diabetic complications of nephropathy and retinopathy [63,65].…”

Section: Overview Of the Raak System In Diabetes Mellitusmentioning

confidence: 99%

Renin-Angiotensin-Aldosterone-Kinin System Influences on Diabetic Vascular Disease and Cardiomyopathy

Flack

Hamaty

Staffileno

1998

Mineral Electrolyte Metab

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Diabetes mellitus is associated with an inordinately high risk of virtually all manifestations of cardiovascular-renal disease including atherosclerotic coronary and peripheral vascular disease, congestive heart failure, stroke, nephropathy, and cardiomyopathy unassociated with coronary heart disease. Abnormalities in the renin-angiotensin-aldosterone-kinin (RAAK) cascade have been implicated in the pathogenesis and clinical expression of these cardiovascular-renal sequelae. Thus, pharmacological modulation of the RAAK system is an attractive therapeutic target in diabetes mellitus. Indeed, emerging data from human clinical studies appear to confirm this thesis.

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Pathophysiology of low renin syndromes: Sites of renal renin secretory impairment and prorenin overexpression

Cited by 49 publications

References 116 publications

Serum Potassium and Outcomes in CKD

Serum Potassium and Outcomes in CKD

Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

Renin-Angiotensin-Aldosterone-Kinin System Influences on Diabetic Vascular Disease and Cardiomyopathy

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