Worsening renal function during the early phase of hospitalization is related to adverse outcomes in acute heart failure (AHF). This study aimed to clarify whether added low-dose dopamine (DA) is clinically beneficial for AHF patients with diuretic resistance to human atrial natriuretic peptide (hANP). Twenty-four AHF patients, who did not have adequate diuresis by 4 hours after administration of hANP, were randomized to a low dose of DA (1-3 μg·kg·min, n = 12) or a low dose of furosemide (10-30 mg injection, n = 12). The significant increase in mean hourly urine volume from baseline (265% ± 204% with hANP + DA; 187% ± 118% with hANP + furosemide) and improvement of dyspnea were similarly observed in both groups. Significant decreases in serum creatinine levels were observed by -14.0% ± 14.2% in the hANP + DA group compared with the hANP + furosemide group (4.5% ± 9.6%, P = 0.0011) without increases in the renotubular and myocardial markers. The incidence of worsening renal function defined as a rise in serum creatinine of >0.3 mg/dL was not observed within 3 days of admission in both groups. Added low-dose DA might not have a harmful effect on renal function and effects of diuresis and symptom relief without a significant increase in troponin-T in AHF patients with diuretic resistance to hANP.

Fluid homeostasis, blood pressure and redox balance in the kidney are regulated by an intricate interaction between local and systemic anti-natriuretic and natriuretic systems. Intrarenal dopamine plays a central role on this interactive network. By activating specific receptors, dopamine promotes sodium excretion and stimulates anti-oxidant and anti-inflammatory pathways. Different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome, hypertension and renal inflammation, can be associated with impaired action of renal dopamine including alteration in biosynthesis, dopamine receptor expression and signal transduction. Given its properties on the regulation of renal blood flow and sodium excretion, exogenous dopamine has been postulated as a potential therapeutic strategy to prevent renal failure in critically ill patients. The aim of this review is to update and discuss on the most recent findings about renal dopaminergic system and its role in several diseases involving the kidneys and the potential use of dopamine as a nephroprotective agent.

Acute kidney injury complicates decompensated heart failure in ∼33% of cases and is associated with morbidity and mortality; thus, we sought to systematically review this topic in order to summarize novel diagnostic and therapeutic approaches.

Structured PubMed searches on these topics were conducted in February 2014 and relevant literature was identified. The PubMed search identified a total of 192 articles that were individually screened for inclusion in this analysis, and 58 were included.

Acute kidney injury, defined by substantial increases in serum creatinine, is associated consistently with prolonged length of stay, rehospitalization, and mortality. Biomarker studies suggested that natriuretic peptides are prognostic for shorter- and longer-term mortality. Novel proteins indicating kidney damage and albumin in the urine are associated with acute kidney injury. The most promising acute pharmacologic treatment appears to be serelaxin, which has been shown to improve acute heart failure symptoms, hemodynamic parameters, and renal function.

The presence of acute kidney injury results in worse clinical outcomes for patients with acute heart failure. Novel biomarkers and therapies hold the promise of improving both cardiac and renal outcomes in these patients.

Sodium metabolism by the kidney is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Renal dopamine plays a central role in this interactive network. The natriuretic hormones, such as the atrial natriuretic peptide, mediate some of their effects by affecting the renal dopaminergic system. Renal dopaminergic tonus can be modulated at different steps of dopamine metabolism (synthesis, uptake, release, catabolism, and receptor sensitization) which can be regulated by the atrial natriuretic peptide. At tubular level, dopamine and atrial natriuretic peptide act together in a concerted manner to promote sodium excretion, especially through the overinhibition of Na+, K+-ATPase activity. In this way, different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome or hypertension, are associated with impaired action of renal dopamine and/or atrial natriuretic peptide, or as a result of impaired interaction between these two natriuretic systems. The aim of this review is to update and comment on the most recent evidences demonstrating how the renal dopaminergic system interacts with atrial natriuretic peptide to control renal physiology and blood pressure through different regulatory pathways.