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on a cohort of patients hospitalized for acute heart failure show that elevations in creatinine levels greater than 20&#37; during hospitalization or greater than 10&#37; in the clinically stable phase increase mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">The conclusion to monitor renal function with creatinine levels in heart failure seems to be well-established according to the clinical practice guidelines &#40;HF recommendations&#41;&#46; However&#44; we must take into account that renal function does not always deteriorate in heart failure and that this worsening is accompanied by a poor prognosis&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">There are basically two clinical situations in which we must differentiate established deterioration of renal function from pseudo-deterioration of renal function&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">When high-dose diuretic therapy is given in acute heart failure&#44; a &#8220;pseudo-deterioration of renal function&#8221; can occur&#44; which improves patients&#8217; dyspnea and decreases their probability of readmission&#46; In the DOSE-AHF trial&#44; even though their glomerular filtration rate decreased&#44; individuals who received high doses of furosemide had a better prognosis than subjects who received low doses&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">5</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Another clinical situation that can produce &#8220;pseudo-worsening&#8221; of renal function is when neurohormonal therapy is optimized in patients with heart failure with reduced EF&#46; The use of ACE inhibitors&#44; ARBs&#44; sacubitril-valsartan&#44; antialdosteronic agents&#44; or even some SGLT2 inhibitors can decrease glomerular filtration rates without worsening disease prognosis&#44; as has been shown in published clinical trials&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">6</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Both situations must be differentiated from chronic kidney failure with established damage&#46; This may occur because patients present with decreased glomerular filtration over time that is accompanied by diuretic resistance&#44; a tendency towards congestion&#44; poor diuretic response&#44; albuminuria&#44; and presence of kidney damage on imaging tests&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">In this sense&#44; it seems important from a clinical point of view to evaluate the diuretic response via parameters such as urinary sodium excretion and diuresis volume in the first 4&#8211;6<span class="elsevierStyleHsp" style=""></span>h in subjects admitted for decompensated heart failure&#46; Subjects with urinary sodium excretion greater than 50&#8211;70<span class="elsevierStyleHsp" style=""></span>meq&#47;L after 2<span class="elsevierStyleHsp" style=""></span>h of furosemide administration tend to have a good diuretic response&#44; as do those who present with more than 3&#8211;4<span class="elsevierStyleHsp" style=""></span>L of diuresis in the first 24<span class="elsevierStyleHsp" style=""></span>h&#46; If there is little diuresis and associated renal function deterioration&#44; it is fundamental to reassess the degree of clinical congestion&#46; This can be carried out in a multidimensional manner by using validated congestion scales&#44; such as the EVEREST scale or analyses such as NT-proBNP and CA-125 biomarkers&#44; and additional imaging tests&#44; such as clinical ultrasounds&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">7</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The detection of a high number of B-lines in various lung areas and the detection of pleural effusion or vena cava dilation without collapsibility via multiorgan ultrasound are indicators that can help us establish that the patient is congestive and we must optimize the dose of diuretics&#46; In these cases&#44; renal function deterioration can be attributed to renal venous congestion&#46; On the contrary&#44; if we find parameters indicating a lack of congestion &#40;A-lines&#44; filiform vena cava&#41; and a tendency towards hypotension and oliguria&#44; renal function deterioration may be due to excessive diuretic therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">8</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">All of these clinical management recommendations are described in the Acute Heart Failure Protocol of the Spanish Society of Internal Medicine&#39;s Heart Failure and Atrial Fibrillation Working Group&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">9</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">In light of this published work&#44; we must highlight the important value of monitoring renal function in heart failure during hospitalization and early follow-up&#46; Nevertheless&#44; it also seems essential for renal function deterioration to be interpreted from a clinical and multidimensional point of view in order to make adjustments to optimal treatment that improve heart failure prognosis from the point of view of readmissions&#44; survival&#44; and quality of life&#46;</p></span>"
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DOI: 10.1016/j.rceng.2020.02.006
Monitoring renal damage in acute heart failure. Do we need a more global and comprehensive approach?
Monitorización del daño renal en insuficiencia cardiaca aguda. ¿Necesitamos un abordaje más global e integral?
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M. Méndez-Bailóna,
Corresponding author
manuel.mendez@salud.madrid.org

Corresponding author.
, M. Camafort-Babkwoskib
a Hospital Clínico San Carlos, Departamento de Medicina, Universidad Complutense de Madrid, Madrid, Spain
b Hospital Clinic Barcelona, Universidad de Barcelona, Barcelona, Spain
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