Normotensive Hyperreninemia in Systemic Lupus erythematosus

Herrera-Acosta, Jaime; Guerrero, Jaime; Erbessd, María Luisa; Paz-Barahona, Miguel; Chessal, Francisco; Alarcón‐Segovia, Donato; Peña, José Carlos

doi:10.1159/000181433

Cited by 5 publications

(2 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…(SLE: n ϭ 7, control: n ϭ 7). secondarily to changes in renal function is not well defined (10, 14,19,49). Renin substrate is reportedly increased in both the plasma and urine in some patients with SLE and can be reduced with RAS blockade (26,52).…”

Section: Fig 4 Renal Cortical Expression Of Angiotensin Type 1 Recementioning

confidence: 99%

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

Venegas-Pont

Mathis

Iliescu

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

-Inflammation and immune system dysfunction contributes to the development of cardiovascular and renal disease. Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that carries a high risk for both renal and cardiovascular disease. While hemodynamic changes that may contribute to increased cardiovascular risk have been reported in humans and animal models of SLE, renal hemodynamics have not been widely studied. The renin-angiotensin system (RAS) plays a central role in renal hemodynamic control, and although RAS blockade is a common therapeutic strategy, the role of RAS in hemodynamic function during SLE is not clear. This study tested whether mean arterial pressure (MAP) and renal hemodynamic responses to acute infusions of ANG II in anesthetized animals were enhanced in an established female mouse model of SLE (NZBWF1). Baseline MAP was not different between anesthetized SLE and control (NZWLacJ) mice, while renal blood flow (RBF) was significantly lower in mice with SLE. SLE mice exhibited an enhanced pressor response and greater reduction in RBF after ANG II infusion. An acute infusion of the ANG II receptor blocker losartan increased RBF in control mice but not in mice with SLE. Renin and ANG II type 1 receptor expression was significantly lower, and ANG II type 2 receptor expression was increased in the renal cortex from SLE mice compared with controls. These data suggest that there are fewer ANG II receptors in the kidneys from mice with SLE but that the existing receptors exhibit an enhanced sensitivity to ANG II. inflammation; angiotensin receptor; autoimmune INFLAMMATION AND IMMUNE SYSTEM dysregulation are recognized as prominent contributors to the development and progression of cardiovascular and renal disease. Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder associated with a high risk for the development of renal and cardiovascular disease, which are major causes of mortality in these patients (43). Almost all patients with SLE have at least some evidence of renal damage on biopsy (4, 11), and measures of declining renal function, including elevated serum creatinine and blood urea nitrogen or reduced filtration fraction, are commonly reported (11,20,28).The renin-angiotensin system (RAS) is well known for its critical role in renal hemodynamic control and blood pressure regulation and is a common therapeutic target in patients with SLE. Although renal dysfunction and blockade of the RAS system are common to patients with SLE, renal hemodynamic responses to ANG II have not been previously investigated. In the present study, we tested the hypothesis that during SLE, there is an enhanced renal hemodynamic response to acute infusion of ANG II. This hypothesis was tested using an experimental mouse model of SLE.The New Zealand Black/White F1 hybrid (NZBWF1) is an established and widely used model of lupus nephritis (8). Like humans with SLE, female NZBWF1 mice exhibit declining renal function with age (5, 23, 29, 42), and we previously reporte...

show abstract

Section: Fig 4 Renal Cortical Expression Of Angiotensin Type 1 Recementioning

confidence: 99%

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

Venegas-Pont

Mathis

Iliescu

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…Lehman et al [2] also observed extraglomerular immunoglobulin deposits in 22 of 32 patients with SLE and rough correlation between their occurrence and the degree of tubulointerstitial injury. It is thought that immune deposits at the tubular and inter stitial sites may contribute to development and evolution of renal impairment in SLE, and clinically a spectrum ranging from latent tubular defect of renal acidification [3], sodium conservation [4] to severe renal failure [5][6][7] have been reported.…”

Section: Introductionmentioning

confidence: 99%

Tubular Dysfunction in Systemic Lupus erythematosus

Yeung¹,

Wong²,

Ng³

et al. 1984

Nephron

View full text Add to dashboard Cite

20 patients with systemic lupus erythematosus undergoing renal biopsies had their tubular function assessed by maximal concentrating ability, maximal urinary acidification and fractional urinary excretion of β₂-microglobulin. 80% of patients showed disturbances in one or more of the parameters tested with fractional β₂-microglobulin excretion being most frequently abnormal. No correlation was found between the histological changes and functional disturbances.

show abstract

Predictive value of clinical, laboratory, pathologic, and treatment variables in steroid/lmmunosuppressive resistant lupus nephritis

Wallace

Goldfinger

Savage

et al. 1988

J of Clinical Apheresis

View full text Add to dashboard Cite

Twenty-seven patients with lupus nephritis and nephrotic syndrome had persistent disease activity despite an adequate trial of corticosteroids and immunosuppressive drugs; 30% were Asians, compared with 7% of our overall SLE population. Two years later, seven had a very good outcome and seven a poor outcome. Thirty clinical, pathological, laboratory, and treatment variables were analyzed in a good versus poor responder subset comparison in an effort to determine which factors were associated with favorable outcome. Administration of pulse steroids (P = .069) and a low biopsy chronicity index (P = .048) were associated with the good responder subset. Serum creatinine, biopsy class, blood pressure, complement, and anti-DNA values at entry as well as the choice of immunosuppressive drug were not helpful in predicting outcome. All seven good responders were plasmapheresed (P = .026). Patients with refractory lupus nephritis who have a low biopsy chronicity index may benefit from the use of pulse steroids or plasmapheresis, and controlled studies are suggested.

show abstract

Normotensive Hyperreninemia in Systemic Lupus erythematosus

Cited by 5 publications

References 29 publications

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

Tubular Dysfunction in Systemic Lupus erythematosus

Predictive value of clinical, laboratory, pathologic, and treatment variables in steroid/lmmunosuppressive resistant lupus nephritis

Contact Info

Product

Resources

About