Early Impairment of Renal Hemodynamic Reserve in Patients With Asymptomatic Heart Failure Is Restored by Angiotensin II Antagonism

Magri, Paola; Rao, Maria Assunta Elena; Cangianiello, Sara; Bellizzi, Vincenzo; Russo, Rosaria; Mele, Alessandro F.; Andreucci, Michele; Memoli, Bruno; Nicola, Luca De; Volpe, Massimo

doi:10.1161/01.cir.98.25.2849

Cited by 64 publications

(64 citation statements)

References 39 publications

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“…In fact, only one group, the OOX group, failed to increase GFR; all of the other groups demonstrated normal renal functional reserve. Therefore, we suggest that in our study the glomerular response to glycine was dissociated from the tubular response, as also observed in some other studies (38,39,46,47). The lack of renal functional reserve observed in the OOX group may be attributable to a decreased NO/AngII ratio at the local level, as suggested above.…”

Section: Effects Of Glycine On Proximal Reabsorptionsupporting

confidence: 87%

Decreases in Renal Functional Reserve and Proximal Tubular Fluid Output in Conscious Oophorectomized Rats

Nielsen¹,

Flyvbjerg²,

Bruun³

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Age-dependent glomerulosclerosis with reduced GFR develops earlier among men than among women. Therefore, whether female sex hormones could prevent the agedependent decrease in GFR was investigated. The kidney function in oophorectomized rats treated with placebo (OOX group), estrogen (OOXϩE 2 group), or estrogen plus progesterone (OOXϩE 2 ϩP group) for 5 mo and in sham-operated rats (sham group) was examined. The rats were 13 mo of age at the time of the investigation. They were conscious and chronically instrumented. The results demonstrated that estrogen, alone or in combination with progesterone, was without effect on the baseline GFR and effective renal plasma flow but prevented severe decreases in the renal functional reserve and fractional proximal tubular fluid output (lithium clearance technique, fractional lithium excretion), which were observed in the OOX group. The renal functional reserve (estimated by stimulation with glycine) was Ϫ223 Ϯ 151, 483 Ϯ 129, 675 Ϯ 76, and 208 Ϯ 140 l/min in the OOX, OOXϩE 2 , OOXϩE 2 ϩP, and sham groups, respectively. Fractional lithium excretion was 12.4 Ϯ 3.1, 26.8 Ϯ 2.0, 31.8 Ϯ 2.5, and 23.6 Ϯ 3.3% in the OOX, OOXϩE 2 , OOXϩE 2 ϩP, and sham groups, respectively. In conclusion, oophorectomy at the age of 8 mo did not produce a decrease in baseline GFR in female rats within a period of 5 mo. However, oophorectomy led to severe decreases in the renal functional reserve and fractional proximal tubular fluid output. Both effects were prevented with administration of estrogen. Sham-operated rats demonstrated values for renal functional reserve and fractional lithium excretion that were between those observed for the OOX group and the groups treated with sex hormones.

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Section: Effects Of Glycine On Proximal Reabsorptionsupporting

confidence: 87%

Decreases in Renal Functional Reserve and Proximal Tubular Fluid Output in Conscious Oophorectomized Rats

Nielsen¹,

Flyvbjerg²,

Bruun³

et al. 2003

Journal of the American Society of Nephrology

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“…Even in the early stages of heart failure, renal vasoconstriction and reduced renal perfusion, together with stimulation of the adrenergic system and the renin-angiotensin-aldosterone system, result in increased sodium and water retention and promote left ventricular remodeling and deterioration of cardiac function. 23 Progressive renal dysfunction occurs as a result of the progressive drop in cardiac output and renal perfusion and the increase in renal vasoconstriction mediated by the neurohormonal and autonomic activation.…”

Section: Mechanisms Of Renal Dysfunction In Achdmentioning

confidence: 99%

Prevalence, Predictors, and Prognostic Value of Renal Dysfunction in Adults With Congenital Heart Disease

et al. 2008

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Background-Renal insufficiency in patients with ischemic heart disease and acquired heart failure is associated with higher mortality and morbidity. We studied the prevalence of renal dysfunction in adult patients with congenital heart disease (ACHD) and its relation to outcome. Methods and Results-A total of 1102 adult patients with congenital heart disease (age 36.0Ϯ14.2 years) attending our institution between 1999 and 2006 had creatinine concentration measured. Glomerular filtration rate (GFR) was calculated with the Modification of Diet in Renal Disease equation. Patients were divided into groups of normal GFR (Ն90 mL · min Ϫ1 · 1.73 m Ϫ2 ), mildly impaired GFR (60 to 89 mL · min Ϫ1 · 1.73 m Ϫ2), and moderately/severely impaired GFR (Ͻ60 mL · min Ϫ1 · 1.73 m Ϫ2). Survival was compared between GFR groups by Cox regression. Median follow-up was 4.1 years, during which 103 patients died. Renal dysfunction was mild in 41% of patients and moderate or severe in 9%. A decrease in GFR was more common among patients with Eisenmenger physiology, of whom 72% had reduced GFR (Ͻ90 mL · min Ϫ1 · 1.73 m Ϫ2 , PϽ0.0001 compared with the remainder), and in 18%, this was moderate or severe (Pϭ0.007). Renal dysfunction had a substantial impact on mortality (propensity score-weighted hazard ratio 3.25, 95% CI 1.54 to 6.86, Pϭ0.002 for moderately or severely impaired versus normal GFR). Conclusions-Deranged physiology in adult patients with congenital heart disease is not limited to the heart but also affects the kidney. Mortality is 3-fold higher than normal in the 1 in 11 patients who have moderate or severe GFR reduction. (Circulation. 2008;117:2320-2328.)Key Words: heart defects, congenital Ⅲ kidney Ⅲ renal function Ⅲ prognosis A s the number of patients with congenital heart disease reaching adulthood (ACHD) continues to increase, it is becoming clear that pathophysiological derangement occurs not only in the heart but in other organs as well. Renal dysfunction has been reported in ACHD patients, but its prevalence and relation to outcome in this population remain unknown. [1][2][3][4][5][6][7][8] In acquired heart disease, renal dysfunction is an ominous sign. 9 -14 We sought to assess the prevalence of renal dysfunction across the spectrum of ACHD and its predictors and impact on survival. Editorial p 2311 Clinical Perspective p 2328 MethodsAll ACHD patients attending our institution from 1999 to June 2006 and in whom serum creatinine concentration was measured were entered into the study. Only the first measurement was used if there were several. For each subject, an estimated glomerular filtration rate (GFR) was calculated from serum creatinine levels by the Modification of Diet in Renal Disease equation, which adjusts for age, gender, and race. 15 Patients were categorized into groups according to the cutoff values suggested by the National Kidney Foundation practice guidelines: GFR Ͼ90 mL · min Ϫ1 · 1.73 m Ϫ2 was considered normal, 60 to 89 mL · min Ϫ1 · 1.73 m Ϫ2 was considered mildly decreased, and Ͻ60 mL · min Ϫ1 ...

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“…In another interesting study, Magri et al (10) infused amino acid into normal and mild asymptomatic CHF patients. Normally, an amino acid infusion will reduce renal vascular resistance and increase GFR.…”

Section: Altered Glomerular Hemodynamicsmentioning

confidence: 99%

The cardiorenal syndrome

Klug¹

2017

SAHJ

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blockers has meant that more patients survive into the later stages of the disease. The clinical challenge ironically then retrogresses to one that involves optimal fl uid balance while preserving renal function. What we may not realise is that the underlying pathophysiology of this "terminal phase" of CHF is poorly understood. The management thereof can be an emotionally and cognitively demanding saga and ultimately there is no consensus amongst the "experts" as to its appropriate care. The cardiorenal syndrome in CHF results from major aberrations in the mutually benefi cial interaction between heart and kidney. It can be seen as a complex interaction between the heart, kidney and vasculature. DEFINITIONThe cardiorenal syndrome is defi ned as "worsening renal function that The defi nition of worsening renal function remains controversial, with suggestions including a 26.5 umol/l increase in serum creatinine (SCr) above baseline, a rise in SCr above a threshold (221umol/l), a percentage increase from baseline (>25%), or a combination of these factors. (1,2) Whatever the defi nition, clinically this syndrome is not diffi cult to recognise -the challenge is to fi nd effective therapies and management strategies. Seventy percent of patients admitted for acute deteriorating heart failure have decreased renal function and 20-45% will experience an increase in SCr in excess of 26.5 umol/l while in hospital.

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Early Impairment of Renal Hemodynamic Reserve in Patients With Asymptomatic Heart Failure Is Restored by Angiotensin II Antagonism

Cited by 64 publications

References 39 publications

Decreases in Renal Functional Reserve and Proximal Tubular Fluid Output in Conscious Oophorectomized Rats

Decreases in Renal Functional Reserve and Proximal Tubular Fluid Output in Conscious Oophorectomized Rats

Prevalence, Predictors, and Prognostic Value of Renal Dysfunction in Adults With Congenital Heart Disease

The cardiorenal syndrome

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