ISSN 0326-646X





Sumario Vol. 42 - Nº 2 Abril - Junio 2013

Cardiorenal Syndrome

Lilia Luz Lobo Márquez, Fernando De La Serna

Dpto. de Insuficiencia Cardiaca e Hipertensión Pulmonar.
Instituto de Cardiología de Tucumán.
Av. Mitre 750 (4000) San Miguel de Tucumán.
Fax +54-381-423 0368.
Correo electrónico

The authors declare not having a conflict of interest.

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Heart failure generates the activation of compensating mechanisms among which the kidney plays a central role, since it regulates homeostasis and hydroelectrolytic circulating volume. The sodium and water renal retention increases by action of the sympathetic nervous system and the renin-angiotensin system, but can adversely affect heart function by increasing the preload and afterload, resulting in a vicious circle that may provoke heart and renal failure, regarded as Cardiorenal Syndrome. The harmful interactions of the heart and renal pathologies rise with the age of patients. A new cardiorenal interactions classification and several laboratory procedures has been proposed for clinical evaluation.

Key words: Cardiorenal syndrome. Cystatin C. N-GAL
Rev Fed Arg Cardiol. 2013; 42(2): 88-95



Heart failure (HF) generates the activation of compensating mechanisms among which, kidneys play a central role, since they regulate hydroelectrolytic homeostasis and thus, the circulating volume. The increase in renal retention of sodium and water (by the action of the Sympathetic Nervous System [SNS] and the Renin Angiotensin System [RAS]) may affect negatively the cardiac function by increase of pre-load and the post-load, thus leading to a vicious circle that will progressively cause a greater cardiac and renal dysfunction. If this is considered along with the fact that both HF and renal failure (RF) are predominantly observed in the elderly population (older than 65 years of age), to the structural and physiologic modifications we should add those proper of old age. The renal and cardiac functions are closely related, since they actively participate in the control, regulation and proper distribution of blood and fluids and electrolytes in the intravascular, extracellular and cellular compartments, and clean the organism from harmful substances. The cardiac-renal interaction is established through different ways: perfusion pressure linked to minute volume (MV), renal venous pressure, activity of the Sympathetic Nervous System (SNS), the Renin Angiotensin Aldosterone System (RAAS), Vasopressin, of Natriuretic Peptides (NP) and endothelial activity [1].

This fact should be taken into account when the therapeutic strategy is planned: any degree of renal dysfunction, even mild, may increase the cardiovascular risk and associate to a greater mortality independently from other risk factors [2].

In USA 1 every 3 adults suffers cardiovascular disease (CVD) [3], while the prevalence in USA of Chronic Kidney Disease (CKD) is 13% [4,5], which represents approximately 30 million adults. CVD is the cause of more than 50% of the deaths of the patients with HF [5]. The presence of renal involvement is common in patients with HF, and it is in them an independent risk factor of greater morbidity and mortality. In the patients that have to undergo dialysis, approximately 30% present HF [6].

Renal failure (RF) is the consequence of Chronic Kidney Disease (CKD) and is defined by a decrease in the rate of FGL, according to the National Kidney Foundation - Kidney Disease Outcomes Quality Initiative (KDOQI). It is quantified by determining creatinine clearance, estimated using the Cockcroft-Gault equations, or the MDRD (Modification of Diet in Renal Disease) [7], and the more recent use of CKD-EP [8,9]. CKD-EP would be the most accurate one, but the differences in the values of the different equations, when FGL is <60 ml/min/1.73 m2, are of little distinctive value. Serum creatinine (SCr) is not a sensitive marker for glomerular filtration.

KDOQI has established 5 stages of CKD (Table I). The presence of albuminuria is important for diagnosis, which exists when the ratio between urine albumin and SCr is 30 mg/g or more (≥3.5 mg/mmol), while a ratio of 30 to 299 mg/g (which is equivalent to 3.5-35 mg/mmol) indicates microalbuminuria, and a 300 mg/g ratio (≥35 mg/mmol) indicates macroalbuminuria [10]. A rate of FGL below 60 ml/min/1.73 m2 suggests CKD, even in the absence of albuminuria. The decrease of FGL should be present during at least three months to be able to diagnose CKD [7]. In patients with type 2 diabetes mellitus (DM-2), different factors may lead to RF without causing albuminuria [11]; approximately 30% of type 2 diabetic patients do not present microalbuminuria. This form of RFpredominates in elderly people, in the female gender and in hypercholesterolemia. Those with DM with RF and no albuminuria have a greater risk of metabolic syndrome and cardiovascular disease, but the presence of microalbuminuria in diabetic patients is an early sign of glomerular damage. Both in DM-1 and in DM-2, the risk of cardiovascular disease is greater when there is evidence of diabetic renal disease, even in the first stage of microalbuminuria [12]. Albuminuria should be considered clinically as a different entity. In hypertensive patients without DM, the presence of microalbuminuria predicts renal and cardiac complications [13].

Table 1. Stages of CKD according to FGL in patients with renal impairment (K / DOQI)


The differences in the methods to detect CKD are manifest in the results of the investigations of the Acute Decompensated Heart Failure National Registry (ADHERE) [14] from USA, published in years 2004 and 2007. In the first one, with 30,000 patients admitted and included by Acute Heart Failure Syndromes (AHFS), CKD was found in 31% of the cases (defined as creatininemia >2.0 mg/dl), while in the second [15], when there already were 153,000 patients, it was communicated that in the investigation of renal function (in 118,465 members of the population), by determining the rate of FGL and using the methods of Cockcroft-Gault and MDRD, renal dysfunction was detected in 64% of the cases, from whom 44% corresponded to stage 3, 13% to stage 4, and 7% to stage 5 of the CKD classification from the KDOQI [7,16].

HF displays as its most usual causes ischemic heart disease (IHD) and hypertension (HTN), which happen in an anatomical, histologic and physiologic substrate, linked to aging, since 80% of the patients with HF have 65 or more years. In the ADHERE, the average age of the patients was ~73 years and most of those included in the registry suffered some type of intercurrent disease, such as DM, anemia, CKD, rheumatoid arthritis, depression, cognitive disorders, etc. The prevalence of CKD is <5% of the 20-39 years old age group, <10% in that of 40-59 years, >20% in that of 60-69 years, and close to 50% for those of 70 years or older [17]. Then, age is an important risk factor of HF and CKD and thus, the prevalence of CKD is greater in patients with HF than in the general population. It has been also been suggested that renal failure (RF) indicates the severity of other risk markers, particularly widespread cardiovascular disease [18]. According to this, it is considered that the patients with HF and IHD have a high incidence of renovascular disease [19], although it has been seen that patients with HF by idiopathic dilated cardiomyopathy have the same degree of association with kidney disease [20]. The significance of the age was manifest in a study in Australia, where an overall prevalence of 11% of CKD was found, as defined by FGL <60 ml/min/1.73 m2 (Cockcroft-Gault), which was increasing with age, going from 2.5% in adults of 45 to 64 years old, to 55% at 65 years or more [21].

Metabolic syndrome (HTN, obesity, DM-2, hypertriglyceridemia) is linked to insulin resistance (IR) and it is a risk factor of CKD, regardless of the presence of DM [22-25]. CKD is associated per se with IR such as is evident by a greater incidence of DM in its most advanced stages. The mechanisms that underlie the association of CKD and IR are multifactorial and include anemia, metabolic acidosis, vitamin D deficiency, and increase in the parathyroid hormone (PTH). The presence of IR has been described in mild to moderate CKD; and anemia, metabolic acidosis and vitamin D deficiency are generally not severe. The elevation of PTH may contribute to IR. Metabolic syndrome predicts the development of CKD in patients with DM-2 [24]. The prevalence of HTN in patients with HF of the ADHERE Registry is 68%, 70%, 73%, 77% and 85%, respectively, for patients in stages 1 to 5 of KDOQI [16], while DM is 38% and 37% in stages 1 and 2, 45% in stage 3 and 54% in stages 4 and 5; in the case of CAD, the prevalence found was 41%, 51%, 61% and 67% in stages 1 to 4 and 56% in stage 5.

The presence of CKD in patients with HF entails a poor prognosis. It has been said that the risk of death in HF is more strongly associated with a fall of FGL than with a decrease in Ejection Fraction (EF) [25]. Khan et al [26], studying the population of the SOLVD study (Studies of Left Ventricular Dysfunction) found that mortality is not greater in patients with FGL between 60 and 90 ml/min/1.73 m2, but that significantly increases once it falls below 60 ml/min/1.73 m2, and in regard to progression, when FGL drops more than 10 ml/min/1.73 m2, it indicates greater mortality. The group of patients in high risk of rapid progression includes some with basal FGL of 90 ml/min/1.73 m2, i.e. that apparent normalcy does not indicate protection from functional worsening in individuals with systolic dysfunction [26, 27]. Weiner et al [28] studied a population of 18,000 patients constituted by the combination of ARIC (Atherosclerosis Risk in Communities) and CHS (Cardiovascular Health Study) cohorts and draw the conclusion that the greatest risk of a poor evolution is for those with FGL <60 ml/min/1.73 m2, and that even in those that in evolution experienced an upward increase of this figure (biochemical improvement), a greater morbidity appears. In the CHARM (Candesartan in Heart Failure Assessment of Reduction of Mortality and Morbidty) study [29] it was shown that the level of renal dysfunction is a powerful predictor of death or readmittance by HF. In the DIG study (Digitalis Investigation Group) there were 757 deaths in the group without CKD and 882 in the group with CKD (p<0.001).

Curiously, the mortality associated to CKD was greater in the patients with diastolic HF (p=0.001) than in those with systolic dysfunction [30,31]. In a meta-analysis of studies about HF, Smith et al [32] found a mortality rate of 51% in those with moderate to severe RF, while it was only 24% for those with normal renal function. Moreover in patients with HF, the presence of CKD is associated with an increase in admittances, as was proven by Campbell et al [33] who state that the worse evolution is not due to the association with usual risk factors of HF (ischemic heart disease, HTN, DM, medication, etc.) but RFproper; moreover, they consider that if we take FGL <60 ml/min/1.73 m2 as a cut-off point for the diagnosis of RF, a heterogeneous group is taken that almost reaches normalcy. For this reason, they proposed a lower threshold (<46 ml/min/1.73 m2).

Gottdiener et al, in the Cardiovascular Health Study (CHS) [34] consider that in elderly patients, the increase in the levels of creatininemia is associated to a greater risk of HF incidence. For Shlipak et al [35], the decline of renal function, diagnosed early for the rapid decrease of cystatin C, is associated with a greater risk of HF, myocardial infarction (MI) and peripheral vascular disease. Dhingra et al [36], just as Smith et al (see previous paragraph) consider that moderate RF, even in the absence of DM or HTN, indicates a high risk of appearance of HF and death.

In the COACH study (Coordinating Study Evaluating Outcome of Advising and Counseling in Heart Failure) [37], it was shown that persistent RF after hospital discharge is associated to an increase in the risk of death after 1 year (Hazard Ratio=1.5) (although the prognosis would not be so bad when RF is solved before discharge) [38].

Anemia is a frequent pathology in chronic diseases and is associated to CRS [39], thus being part of a kind of pathological trifecta, which has come to be called “cardiorenal-anemia syndrome”[40]; it is a significant independent risk factor for cardiovascular complications [39,41]. In patients with CKD, the prevalence of anemia is >50% and in those with HF of 51%.

Cardiorenal syndrome (CRS) is defined as the coexistence of HF with RI. For Liang [42], CRS is a stage of advanced cardiorenal dysregulation that presents in patients that suffer HF. Boerrigter and Burnett [43], consider that in CRS both organs, heart and kidneys, fail mutually in their performance compensating each other’s functional alteration, thus constituting a vicious circle that ultimately leads to the decompensation of the whole circulatory system. In a more restricted sense, they define CRS as the worsening of renal function (WRF) or acute kidney injury (AKI) in patients admitted by HF.

The name acute renal failure (ARF) has been replaced by that of acute kidney injury (AKI) since a rapid drop of FGL occurs in patients, frequently fatal, precipitated by a significant tubular or glomerularinjury, which causes from SCr and plasma urea increases, to oliguria and anuria [44].

Cruz and Bagshaw [5] describe in detail the epidemiological and clinical aspects of the different types of CRS, which make up the Ronco et al [45] classification, adopted by the consensus Acute Dialysis Quality Initiative group (ADQI) [46], where the following stand out: Type 1 – acute Cardiorenal Syndrome: in which acute HF (cardiogenic shock or Acute Heart Failure Syndrome [AHFS] is the cause of AKI); Type 2 – chronic Cardiorenal Syndrome; in which chronic HF causes progressive CKD; Type 3 – renocardial: AKI (acute renal ischemia, glomerulonephritis) is the cause of cardiac dysfunction (HF, ischemia, arrhythmia); Type 4 – renocardial: CKD state that contributes to a decrease in cardiac function, cardiac hypertrophy and greater risk of adverse cardiac events; Type 5 – Secondary cardiorenal syndromes: systemic processes (e.g., septicemia) that cause cardiac and renal dysfunction at the same time2.

Type 1 (acute CRS): is observed when an acute decompensation of cardiac function causes acute renal failure (ARF) consecutive to AKI. The patients hospitalized by HF with preexisting RF frequently experience worsening of renal function (WRF), which is defined as acute or subacute changes of the renal function that appear in ~1/3 of the cases of AHFS, or in cases of Acute Coronary Syndrome (ACS), manifest for most investigators, as an increase of SCr ≥26.5 mmol/l (0.3 mg/dl). Others consider that there is WRF when the increase of SCr is ≥44.2 umol/l (0.5 mg/dl) or there is ≥25% of increase of serum level at the time of admittance, combined with an increase of 0.3 mg/dl [5]. Aronson [47] diagnosed WRF when there is increase of plasma urea above 50% of the values at the patient’s admittance.

The incidence of WRF associated to HF decompensation goes from 24% to 45% [5]. From the patients admitted by HF in ~70%, some increase of SCr will be observed, and among them in 20-30% an increase >0.3 mg/dl of SCr will be verified [43,48]. The patients that present WRF in the presence of AHFS and persistent congestion are those with long standing HF that decompensate acutely in the treatment with high doses of diuretics [43]. The predictive risk factors of acute CRS, the CKD base, DM, prior HF and initial presentation with HTN [49]. The mechanisms that lead to WRF in patients with AHFS are numerous, although the drop of MV is predominant, to which systemic hemodynamic disturbances are added that alter renal perfusion [50-52]; the patients that evolve with hemodynamic complications in their hospital stay have a greater mortality. The use of high doses of loop diuretics, in an attempt to correct the circulating congestion existing in HF, is associated with a higher risk of RF [53]; in the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) study [54], the high doses of diuretics produced an increase 5 times greater of the WRF rates.

The following are independent predictors of WRF: history of CKD, NYHA Functional Class and EF [55]. There are different mechanisms responsible for WRF, among which neurohormonal activation, decrease of renal perfusion, and increase of endothelin and adenosine levels stand out [45]. WRF may present in AHFS, in ACS, in cardiogenic shock, and in the post-surgical low minute volume syndrome [56], is generally observed in the first days of admittance [56], suggesting that cardiorenal impairment is related to acute hemodynamic changes from decompensation. Krumholz et al [55] and Cowie et al [57] consider that 70-90% of the cases, WRF appears during the first week of admittance. Renal decompensation may be caused by the medication for HF, as the administration of exaggerated doses of furosemide or the excessive use of NSAI or the unregulated use of ACEI or ARB and other drugs [42]. It could also be that a greater use of loop diuretics is due to the existence of more advanced degrees of HF with significant venous circulation congestion, more frequent when there is renal dysfunction. For Butler et al [53], the data about the use of high doses of diuretics and development of CRS suggest the presence of resistance to diuretics. These investigators did not find an association between the use of ACEI and CRS. DM and HTN, history of HF, sinus tachycardia and female gender are factors strongly associated to the tendency to  CRS development. In type 1 CRS, there is a greater risk of evolution to more advanced stages of CKD (stages 4-5 of KDOQI classification).

A special circumstance is represented by type 1 CRS that originates in revascularization procedures. In ~15-30% of the patients AKI occurs, consecutive to the use of angiographic contrast or extracorporeal circulation substances [50]. At times it is difficult to differentiate between Type 1 (cardiorenal) and Type 3 (renocardial) of CRS, since it may not be known exactly what was the initial process: heart failure or renal failure? Thus for example, McCullough [50] considers that AKI induced by contrast substance is included in group 1, while Cruz and Bagshaw [5] describe Type 3. For McCullough, cardiac surgery (with extracorporeal circulation) could be the cause of Type 1, while the ADQI consensus [46] and Cruz and Bagshaw consider it the cause of Type 3.

As a guide for the diagnosis and characterization of AKI, the Acute Dialysis Outcome Initiative (ADQI) group [58] has proposed the RIFLE (Risk, Injury, Failure, Loss, End stage) classification [59] of AKI, where 3 degrees of severityare established: Class R (Risk) or Class 1, Class I or Class 2, Class F or Class 3; and 2 developmental classes: Class L or Class 4, and Class E or Class 5 (Table II). This way of classifying uses separate criteria on creatininemia and FGL and urine output. In a study in 500 patients on the evaluation of the impact on the long-term prognosis of AKI in patients with AHFS, Shirakabe et al [60], using RIFLE found that classes I (Class 2)and F (Class 3) are independently associated to a greater all-cause mortality, and class F with HF events. The prognosis was significantly worse in class I than in class R, and than in cases without AKI, and significantly worse in class F than in case of no AKI or in case of class R or class I.

Table 2. Classification of acute RF: RIFLE (Risk, Injury, Failure, Loss, End stage)


It has been proposed to modify the RIFLE classification by the AKIN (Acute Kidney Injury Network) [61] (Table III)

Table 3. AKIN Classification (Acute Kidney Injury Network) modifying RIFLE

The RIFLE classification has been deservedly accepted, since it allows an earlier diagnosis: the process of AKI starts much earlier than what it can be detected by determining SCr, that although it is a reliable marker of renal function, for its slow production [62] it is late in AKI, so the early diagnosis allows for a rapid and more favorable treatment.

In HF, elderly people prevail, who tend to present acute changes in FGL during decompensation episodes, so the estimations based on creatinine may not be the optimal method of evaluating renal function in them. In this situation, it has been seen that increases in plasma urea are associated to a greater mortality in the short and mid term [63-65]. Some studies suggest that plasma urea may be a marker indicating evolution.

Faced with the need of a more accurate and early diagnosis, numerous biological markers of AKI have been proposed [44,65], that are present in urine or in plasma, or in both. Among them, cystatin C has shown a greater sensibility than SCr to detect early decreases for renal function [65-68]; its increase plus microalbuminuria are independently associated to stage 3 CKD. Different studies indicate that cystatin C is safer than SCr to estimate FGL, especially in adult patients, especially in adult patients with FGL estimated ≥60 ml/min/1.73 m2. Stevens et al [67] using three equations in which cystatine C intervenes, found that they estimate FGL with a greater security than the MDRD equation. Cystatin C may detect an association between mild renal disease and unfavorable cardiovascular evolution, with greater mortality [68].

Currently, neutrophil gelatinase-associated lipocalin (N-GAL) stands out as biomarker for renal failure [65,69-72]. N-GAL is a small protein secreted in low amounts by the lung, kidney, stomach and colon, and it is a strong predictor of the evolution of HF at 30 days, stronger than BNP and considerably better than conventional determination of renal function such as creatinine and FGL, estimated by MDRD. It is then a risk predictor of renal failure but mainly, a strong predictor of risks for cardiac events. In the RCT GALLANT (The NGAL Evaluation Alog with B-type Natriuretic peptide in acutely decompensated heart failure trial) it is indicated that 41% of patients with the diagnosis of AKI would have gone undetected if only SCr had been determined [72]. The specificity of NGAL is low in chronic RF, while it is high in the case of acute RF, so it would be advisable using it in the last case [65].

N-acetyl-beta-D-glucosamindase (NAG) is a lysosomal enzyme that is removed by urine in the case of proximal tubule impairment when there is KD, but also after surgery with assisted circulation and diabetic nephropathy. It is prominent predictor of AKI or WRF [73]. High levels of NAG are associated to a poor evolution in patients with HF, regardless from FGL [65]. It would present the problem of a low specificity when appearing in urine infections.

KIM-1 (Kidney Injury Molecule-1) [65] may be detected in urine in normal individuals, but is excreted in large amounts after hypoxic AKI (proximal tubule damage, especially in areas of early fibrosis). Urine levels of KIM-1 have been found strongly elevated in patients with stable chronic HF, accompanied only by mild FGL alteration [65,74]. Its usefulness is limited, given its low specificity.

Type 2 (chronic CRS): manifests when chronic cardiovascular anomalies – as chronic HF, atrial fibrillation, cardiomyopathies or chronic ischemic heart disease – cause a progressive renal dysfunction. A third of patients with cardiovascular diseases have concomitant CKD, and when both processes are combined, a progression of the causing diseases is generated. HF is accompanied by neurohormonal compensating reactions and hemodynamic alterations, with involvement of renal circulation, which lead to renal lesions. Atherosclerosis, DM, HTN and smoking are associated with the presence of CKD. The clinical investigations establish that cardiac disease and chronic kidney disease coexist frequently, but it is usual that it is not possible to determine the primary or secondary process [5,75].

Type 3 (acute renocardiac syndrome [RCS]): defined by the presence of AKI that contributes to the appearance of significant cardiac alterations, such as myocardial infarction, HF, or arrhythmias [5]. Ischemia is the most common cause of acute AKI. As Legrand et al [76] point out, kidneys are particularly susceptible to injuries that may accompany circumstances such as heart transplantation, treatment of suprarenal aneurysms, renal artery reconstruction, nephropathy by contrast agent, major (noncardiac) surgery, cardiac arrest and cardiogenic shock. From the patients that suffer acute RF and survive, 2-10% will require chronic dialysis. Hypoxia becomes more manifest when the demand linked to the increase of the solutes and the high rate of aerobic glycolysis exchange grows. The pathophysiology of AKI by ischemia that includes reperfusion associated to oxidative stress, cell dysfunction and signaling alteration, is complex. According to the yearly report of the US Renal Data System 2007, 2/3 of the patients in dialysis develop HF within 3 years [77]. Foley [78] points out that ~40% of the patients with CKD have HF in their initial presentation and the next year another 31% develop it: the coexistence of HF and CKD is explained because they share similar risk factors. Renal failure is responsible for HTN, anemia and volume overload, as well as phosphorus and calcium metabolism disorder (secondary hyperparathyroidism) [12,19,50,51,79,80]. The alterations in mineral metabolism are evident by disorders in calcium, phosphorus, 1,25-dihydroxyvitamin D, parathyroid hormone and FGF (Fibroblast Growth Factor) concentrations, with hyperphosphatemia appearing, and increase in the parathyroid hormone and vitamin D decrease (these alterations are called CKD plus mineral and bone disorder [CKD-MBD]), and are accompanied by vascular and valvular calcifications. An association of hypovitaminosis D and coronary calcification have also been noticed [81-84]. In a significant study, in a cohort of 51,037 patients in chronic hemodialysis, Teng et al [85] found that the group that received vitamin D had a significant greater survival than those that did not receive it.

The risk of death in HF is strongly associated to WRF [53]; mortality by cardiovascular disease is 10 times greater in patients in dialysis in comparison to a non-uremic population. In patients with WRF in stages 2-3, there is a greater chance of death by cardiovascular disease than by development of terminal RF [57]. Another possible cause of Type 3 is AKI associated to cardiac surgery [50] (although it could also be considered a form of type 1 CRS).

Type 4 (chronic RCS): the cardiac consequences of CKD are ventricular hypertrophy and remodeling, and fostering of presentation of cardiovascular events such as myocardial infarction, HF or stroke [5]. Just as it happens in Type 2, it is very difficult to establish clearly which dysfunction is primary; cardiac or renal. In the case of terminal RF, 80% of patients have cardiac disease at admittance. It has been pointed out that chronic hemodialysis induces repetitive myocardial injury [86].

Type 5 (secondary CRS): it is the coexistence of heart failure with renal injury induced by a wide variety of systemic, acute and chronic diseases. Within the acute ones, there is septic and hemorrhagic shock, or by multiple trauma or burns, infections such as AIDS and hepatitis C, intoxications, connective tissue diseases, vasculitis, leucosis and chronic systemic diseases [5]. The paradigm is sepsis, since between 11 and 64% of the patients present renal injury [5,87,88], and in ~50% sepsis is a main factor in the development of AKI.


2. With all due respect to the positive qualities of the classification by Ronco, we consider that it would be more appropriate to say: 1) Cardiorenal Syndrome, a consequence of heart failure: a) acute and b) chronic; 2) Cardiorenal Syndrome, a consequence of renal injury: a) acute and b) chronic; and 3) Cardiorenal Syndrome secondary to systemic process, with mixed cardiorenal failure. If “renocardiac” is used, it indicates that it is not cardiorenal, and it can hardly then be as a form of CRS, although the intention of the authors may have been to denote where the syndrome originates. However, we will continue using the mentioned classification, since it is accepted virtually in all recent publications.



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Publication: June 2013

Editorial Electrónica
de FAC

8vo. Congreso Virtual de Cardiología

1º Setiembre al
30 Noviembre, 2013

XXXI Congreso Nacional de Cardiología

30-31 Mayo,
1º Junio, 2013
Organiza: Región Patagónica

Revista de FAC


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