The plot thickens: hemoconcentration, renal function, and survival in heart failure.

Acute worsening of renal function is common in hospitalized patients with acute decompensated heart failure and is associated with increased risk of hospital readmission and both in-hospital and postdischarge mortality.1 The pathogenesis of worsening of renal function in hospitalized heart failure patients is thought to be attributable to 2 interdependent multifactorial mechanisms: (1) a short-term and in most cases reversible decrease in glomerular filtration due to decreased renal blood flow, pharmacological inhibition of angiotensin-II signaling, sympathetic activation, and tubuloglomerular feedback mechanisms and (2) a longer-term and in some cases irreversible ischemic renal tubular injury triggered by decreased renal oxygen supply (due to decreased arterial perfusion pressure, increased renal vein pressure, and anemia) and/or increased renal oxygen demand (caused by increased tubular sodium and water reabsorption mediated by activation of vasoconstrictor hormones and tubuloglomerular feedback mechanisms).2,3 Clinical observation of the time course for return to preadmission serum creatinine levels is most often used to retrospectively determine the principal underlying mechanism in individual patients. Because there is no definitive diagnostic test to uncover the mechanism of worsening renal function, it is uncertain how these underlying causes relate to increased risk of in-hospital and postdischarge adverse outcomes.