Optimal haemoglobin during treatment with recombinant human erythropoietin

Ritz, Eberhard; Amann, Kerstin

doi:10.1093/ndt/13.suppl_2.16

Cited by 22 publications

(6 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Noting the continued controversy regarding optimal target hemoglobin (hematocrit) levels, Stevens et al [39], Muirhead [40], and Ritz and Amann [41] reviewed both clinical data and physiologic concepts underlying the treatment of anemia. They recommend individualized hemoglobin targets for specific patient populations.…”

Section: Discussionmentioning

confidence: 99%

Hematocrit was not validated as a surrogate end point for survival among epoetin-treated hemodialysis patients

Cotter

Stefanik

Zhang

et al. 2004

Journal of Clinical Epidemiology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Hematocrit was not validated as a surrogate end point for survival among epoetin-treated hemodialysis patients

Cotter

Stefanik

Zhang

et al. 2004

Journal of Clinical Epidemiology

View full text Add to dashboard Cite

“…On the other hand, partial reversal of anemia through administration of recombinant human erythropoeitin (rHuEPO) reduced left ventricular mass (LVM), but failed to normalize it (11, 22, 23). Because Hb was not normalized, it is uncertain whether complete normalization of Hb may cause a further decrease of LVM; this issue is currently the object of several controlled studies (24). By multivariate analysis, London (21) further identified increased cardiac output as an important contributor of LVH.…”

Section: Pathomechanisms Of Left Ventricular Hypertrophy In Renal Faimentioning

confidence: 99%

Left Ventricular Hypertrophy in Renal Failure

Amann¹,

Rychlík

Miltenberger-Miltény

et al. 1999

Seminars in Dialysis

View full text Add to dashboard Cite

“…On the other hand, partial reversal of anemia through administration of recombinant human erythropoeitin (rHuEPO) reduced left ventricular mass (LVM), but failed to normalize it (11,22,23). Because Hb was not normalized, it is uncertain whether complete normalization of Hb may cause a further decrease of LVM; this issue is currently the object of several controlled studies (24). By multivariate analysis, London (21) further identified increased cardiac output as an important contributor of LVH.…”

Section: Pathomechanisms Of Left Ventricular Hypertrophy In Renal Faimentioning

confidence: 99%

Left ventricular hypertrophy in renal failure

Amann

Rychlík

Miltenberger-Miltény

et al. 1998

Kidney International

View full text Add to dashboard Cite

Left ventricular hypertrophy (LVH) is one of the major cardiovascular complications of end stage renal failure. There is consensus that echocardiography is the gold standard for diagnosing LVH. A number of recent studies (1-4) document the high frequency of this condition in patients entering renal replacement therapy, i.e. between 60% (2) and 80% (3). Left ventricular mass increases progressively with duration of dialysis treatment even in normotensive patients (5). Particularly in patients with incipient LVH, asymmetric septal hypertrophy (ASH) may be encountered (6). One usually encounters a mixture of concentric and eccentric hypertrophy, reflecting the variable contributions of increased preload and afterload (4).Increased LVH persists even after renal transplantation (7), and a relationship between blood pressure and LVH is found even in normotensive recipients of renal grafts. Is renal disease-related LVH unique to end stage renal failure? As shown in Table 1, increased septal thickness (mostly within the normal range) is found even in the earliest stages of glomerular disease, i.e. in patients with IgA glomerulonephritis, non-nephrotic proteinuria and normal inulin clearance, who have blood pressures within the range of normotension according to World Health Organization criteria (8). Even at this early stage of glomerulonephritis, cardiac remodeling is accompanied by impaired diastolic LV function as reflected by the ratio between early diastolic/late diastolic (atrial contraction) inflow velocity across the mitral valve. Clinical Significance of Left Ventricular HypertrophyIn patients with essential hypertension, it has been well established that LVH, independent of blood pressure, is predictive of ventricular arrhythmia (9) and cardiac death (10). The same is true for uremic patients on maintenance hemodialysis. Silberberg et al. (11) noted that actuarial 5 year survival is significantly higher (56% vs 22%) in patients with normal LV mass. (<125 g/1.73 m 2 ) than with increased LV mass. By multivariate analysis, LV mass emerged as a predictor which was independent of blood pressure.LVH has a number of important clinical sequelae: 1) impaired LV compliance; 2) increased coronary resistance; and 3) arrhythmogenesis (12). Impaired LV ComplianceLVH reduces compliance of the LV. As a consequence, cardiac filling is more sensitive to changes in LV filling pressure. On the one hand, hypervolemia will more readily cause an increase in left atrial pressure and thus predispose the patient to pulmonary edema. On the other hand, a decrease of LV filling pressure (e.g. during ultrafiltration) will predispose the patient to abrupt LV underfilling, reduced ejection volume, tachycardia and hypotension. If LV underfilling activates the Bezold Jarisch reflex, then vagovasal syncopy and bradycardia will result. Ruffmann et al. (13) found a very significant relation between disturbed LV compliance, as assessed by transmitral inflow velocity (E/A ratio) and propensity to intradialytic hypotension. This point is important b...

show abstract

Optimal haemoglobin during treatment with recombinant human erythropoietin

Cited by 22 publications

References 15 publications

Hematocrit was not validated as a surrogate end point for survival among epoetin-treated hemodialysis patients

Hematocrit was not validated as a surrogate end point for survival among epoetin-treated hemodialysis patients

Left Ventricular Hypertrophy in Renal Failure

Left ventricular hypertrophy in renal failure

Contact Info

Product

Resources

About