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Prof. Marco Metra
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The Guidelines describe renal dysfunction as “common” in HF, with prevalence increasing with HF severity and the presence of other co-morbidities (such as hypertension and diabetes). It has been widely shown that 30-40% of patients admitted for acute HF have impaired (ie, <50% normal) renal function, and a similar proportion may develop worsening function, defined as an increase in serum creatinine of more than 0.03 mg/dL from baseline. Both conditions, kidney dysfunction and worsening renal function, are associated with a poor prognosis and often found as risk factors independent of other variables related to HF severity.
Among the Guidelines’ “gaps in evidence” is whether the specific treatment of renal dysfunction (and anaemia) in HF patients reduces their levels of morbidity and mortality. This morning Professor Marco Metra from Brescia, Italy, will present further data on the prevalence, clinical significance, mechanisms and prognosis of renal dysfunction and worsening renal function in patients with HF. Despite the strength of the association between renal dysfunction and prognosis, he proposes that – as in the case of anaemia – we are still at the hypothesis-generating stage.
In fact, an active role of kidney dysfunction in the pathogenesis of HF and its poor prognosis still needs final demonstration. Says Metra: “We still need to demonstrate that an intervention which improves renal dysfunction also improves prognosis in heart failure. Thus, we still need more data showing that new drugs first improve renal function or protect against deterioration, and second, that these renal protective effects are associated with improvement in outcome.”
Similarly lacking is any consistent data on anaemia, whose prevalence also increases with HF severity, advanced age, female gender, renal disease, and other co-morbidities. Anaemia was defined as a therapeutic target in HF in a review by Felker et al in 2004, who noted a prevalence ranging from 4% to 55% depending on the population studied. They identified “multiple potential mechanisms of interaction . . . between anemia and the clinical syndrome of HF, including hemodilution, inflammatory activation, renal insufficiency, and malnutrition”.
Their argument – as has also been postulated with renal dysfunction – is that, if a “ceiling of benefit” has been reached in the medical blockade of neurohormonal activation, is anaemia itself a relevant treatment target?
Emerging therapies for the management of the cardio-renal syndrome, Sunday 30 August 08:30-10:00, FPN 228)
Heart failure and anaemia: where are we in 2009, Sunday 30 August 16:30-18.00, Athens – Zone 4, FPN 1091-1094