Renal Vasoactive Hormones in Scleroderma (Progressive Systemic Sclerosis)

Oliver, Juan A.; Vinci, Joseph M.; Bowden, Robert E.; Weinberger, Andrew B.; Baer, Leslie; Keiser, Harry R.; Cannon, Paul J.

doi:10.1159/000182325

Nephron

1981

DOI: 10.1159/000182325

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Renal Vasoactive Hormones in Scleroderma (Progressive Systemic Sclerosis)

Juan A. Oliver¹,

Joseph M. Vinci²,

Robert E. Bowden³

et al.

Abstract: Plasma renin activity and the urinary excretions of kallikrein, kinin, immunoreactive PGE (iPGE) and aldosterone were determined in 23 patients with progressive systemic sclerosis (PSS) on a fixed sodium and potassium intake who had no clinically apparent renal disease. Urinary excretions of kallikrein and kinin in the PSS patients were not significantly different from those of a group of sex and race-matched normal controls. In the female PSS patients urinary excretion of iPGE was also found to be normal. Upr… Show more

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1986

2023

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Cited by 3 publications

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Angiotensin-Converting Enzyme Inhibition and Renal Protection

Hollenberg

Raij²

1993

Arch Intern Med

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The role of hypertension in the pathogenesis of renal damage is a subject of both historical interest and current investigation. Because of the difficulty associated with studying the pathophysiologic role of glomerular injury in systemic hypertension, experimental models have provided much of the data in this field. The mechanisms leading to glomerular injury are complex and not fully elucidated. Mesangial and endothelial cell injury are thought to be important pathophysiologic mechanisms in the renal injury associated with hypertension. One hypothesis suggests that glomerular hypertension (ie, a hemodynamic event) is the primary pathogenetic mechanism, but another supports the notion that glomerular hypertrophy (ie, abnormal growth-related events) contributes to injury. The intrarenal renin-angiotensin system may play an important pathogenetic role in end-stage renal disease. Angiotensin-converting enzyme (ACE) inhibition has been shown to arrest the progression of renal injury in animal models. Although the clinical database is incomplete, the findings of anecdotal reports and short-term studies suggest that ACE inhibition may preserve renal function in patients with scleroderma renal crisis, reduce proteinuria in patients with diabetic nephropathy, and normalize renal hemodynamics in patients with a variety of renal diseases. The beneficial effects of ACE inhibition may be due to both hemodynamic (eg, reduction in glomerular capillary and intraglomerular pressures) and nonhemodynamic (eg, potassium-sparing and reduction in mesangial proliferation) mechanisms. The precise role of ACE inhibitors in the prevention of renal damage awaits the results of ongoing long-term, double-blind clinical studies. Nevertheless, ACE inhibition may be an appropriate therapeutic alternative in the hypertensive patient whose renal injury is progressing despite aggressive antihypertensive therapy.

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Angiotensin-Converting Enzyme Inhibition and Renal Protection

Hollenberg

Raij²

1993

Arch Intern Med

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The cardiovascular manifestations of systemic sclerosis (scleroderma)

Follansbee¹

1986

Current Problems in Cardiology

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Steroid hormones in systemic sclerosis: associations with disease characteristics and modifications during scleroderma renal crisis

Collet,

Sanges,

Ghulam

et al. 2023

Rheumatology

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Objective The renin-angiotensin-aldosterone system (RAAS) and glucocorticoids (GCs) are involved in vascular remodeling and fibrosis, but have not been extensively studied in systemic sclerosis (SSc). Our aim was to investigate the RAAS and GC hormones in SSc patients. Methods Serum levels of renin (dosage and activity), aldosterone and its precursors (DOC, B, 18-OH-DOC, 18-OH-B), and GCs (cortisol, cortisone, 11-deoxycortisol, 18-OH-F) were assessed in 122 SSc patients and 52 healthy controls. After applying stringent inclusion criteria aimed at ensuring accurate hormone assessments (exclusion of interfering drugs, strict sampling conditions), we analyzed RAAS hormones in 61 patients, and GCs in 96 patients. Hormone levels were compared between patients and controls; and associations with disease characteristics were assessed in patients. Results Regarding RAAS hormones, SSc patients displayed significantly lower aldosterone levels (although within normal range), similar renin levels, and higher B levels than controls. Abnormal RAAS hormone levels were associated with a more severe SSc phenotype (lung and skin fibrosis, heart and pulmonary vascular involvements, inflammation). Regarding GC hormones, SSc patients had higher levels of cortisol, 11-desoxycortisol (precursor) and 18-OH-F (metabolite) but lower levels of cortisone (inactive counterpart) than controls. RAAS hormone levels were assessed in 5 SSc patients before and during scleroderma renal crisis (SRC): concentrations varied considerably between patients, but consistently included normal/increased aldosterone levels and elevated renin levels. Conclusion RAAS and GC hormones are abnormally produced in SSc patients, especially in patients with severe SSc and during SRC. This could suggest a participation of these hormonal systems in SSc pathogenesis.

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Renal Vasoactive Hormones in Scleroderma (Progressive Systemic Sclerosis)

Cited by 3 publications

References 14 publications

Angiotensin-Converting Enzyme Inhibition and Renal Protection

Angiotensin-Converting Enzyme Inhibition and Renal Protection

The cardiovascular manifestations of systemic sclerosis (scleroderma)

Steroid hormones in systemic sclerosis: associations with disease characteristics and modifications during scleroderma renal crisis

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