Epidemiology, pathophysiology and diagnosis:
HF is defined by the 2016 European Society of Cardiology guidelines and divided into subgroups: HF with preserved ejection fraction ≥ 50% (HFp), HF with reduced ejection fraction <40% (HFr) and HF with moderate deterioration or in an intermediate range between 40 and 49% (CI-FEm). (2)
CKD is defined by a persistent decrease in glomerular filtration rate (eGFR) <60ml / min / 1.73m2. It is divided into stages: Normal (eGFR ≥60ml / min / 1.73m2); Stage 2 (eGFR 45 to 59 ml / min / 1.73m2); Stage 3 (eGFR 30 to 44ml / min / 1.73m2), Stage 4 (eGFR 15 to 29ml / min / 1.73m2); Stage 5 (eGFR <15ml / min / 1.73m2). (3)
The incidence of de novo HF in known CKD varies between 17% and 21% (4) and its appearance changes according to the stage of CKD and the type of renal replacement therapy, including renal transplantation (RTxR) (Figure 1). The reduction in eGFR is associated with a higher risk of all-cause mortality, cardiovascular mortality, and hospitalization in patients with HFpEF or HFrEF. (5,6) Considering that as the severity of CKD increases, so does it According to the prevalence of HF, it is estimated that 44% of hemodialysis (HD) patients have HF (10% with HFp-HF, 13% with rHF-HF, and 21% with mHF-HF). (7) The pathophysiology it is complex and in an integrated way, it is shown in figure 2. 20 to 57% of patients with chronic HF (CHF) have CKD; of hospitalized HF patients, 25% to 33% have acute renal failure, eGFR is a predictor of mortality in HF patients, and 20% to 30% of HF patients are resistant to diuretic treatment. (8, 10)
TREATMENT
The recommendations for the management of patients with HF and concomitant CKD do not differ, in general, from those of patients with normal eGFR. (2) It should be considered that patients with severe CKD (eGFR <30 ml / min / 1.73 m2), have been excluded from most clinical trials, however, in the few available studies, the benefit observed in most of these studies was similar, and even greater, than in patients with eGFR between 30-60 ml / min / 1.73 m2. (9)
Patients with CKD and HF benefit from hygienic-dietary measures, such as: reduction in salt intake, control of arterial hypertension (HTN) and glycemia, treatment of dyslipidemia and exercise according to their capacity.
APPROACH TO TREATMENT ACCORDING TO THE SYSTOLIC FUNCTION OF THE LEFT VENTRICLE (LVEF)
Patients with CKD and HFrF: Medications that can reduce adverse outcomes include angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor antagonists II (AIIRAs), angiotensin receptor antagonists and neprilysin inhibitors (RNAI), beta-blockers (BB) and mineralocorticoid receptor antagonists (MRA), (11,12) to which they have been added in recent years, gliflozins: empagliflozin (13) and dapagliflozin (14) both with a primary end point of significant decrease in the combination of cardiovascular death or hospitalization due to worsening of HF. The DAPA-HF study included patients with an eGFR> 30ml / min / 1.73m2 and a compound with a reduction of ≥50% in eGFR for at least 28 days, end-stage renal disease was defined as worsening of renal function or death from kidney causes. End-stage renal disease was defined as: eGFR <15 ml / min / 1.73 m2 (≥28 days), long-term dialysis (≥28 days) TxR. Serious adverse events of acute kidney injury were reported in 23 patients (1.0%) in the dapagliflozin group and in 46 (1.9%) in the placebo group (P = 0.007) (12) and in the EMPEROR study. which includes patients with eGFR <30ml / min / 1.73m2 on replacement therapy with chronic dialysis or TxR or even eGFR <15ml / min / 1.73m2; the rate of decrease in eGFR during the double-blind treatment period was slower in the empagliflozin group than in the placebo group (–0.55 ml / min / 1.73 m2 per year versus –2.28 ml / min / 1.73 m2 per year, respectively), for a difference between groups of 1.73 ml / min / 1.73 m2 per year (95% CI, 1.10 to 2.37; P <0.001), which that gives us security for the use of these medications in these patients. (13) We should not forget loop diuretics as part of the treatment, if diuresis is preserved
In patients with CKD and HFpEF: currently we do not have studies that show us the impact on survival and treatment is focused on treating the causes of HF, such as hypertension, diabetes mellitus (DM), obesity, arrhythmias, to improve lifestyle, in addition to regular monitoring.
TREATMENT ACCORDING TO KIDNEY FUNCTION:
Medical therapy in patients with CKD, according to eGFR:
According to the degree of CKD and the evidence of each of the drugs, the treatment proposal is shown in Figure 3. (10)
In Figure 3, it is necessary to add the RNAI, empaglifozin and dapaglifozin, which should be adapted in the recommendations according to their level of evidence, especially in patients with eGFR <30 ml / min / 1.73m2. Iron deficiency and anemia. Erythropoiesis-stimulating agents have no effect on the prevention or treatment of HF in patients with CKD. (15, 16) However, for patients with chronic HF and iron deficiency with or without anemia, treatment with intravenous iron carboxymaltose improves symptoms, functional capacity, and quality of life. (17)
Considering renal replacement therapies:
To talk about them, first you have to refer to the cardiorenal syndrome (CRS), which is divided into:
Type I - acute HF, leading to acute kidney disease (ARD).
Type II - CHF causes progressive deterioration of kidney function leading to CKD.
Type III - ARD or exacerbated CKD leads to acute HF.
Type IV - Advanced CKD causes CHF.
These last two types of SCR will be addressed in this document.
Type III CRS, in this group of patients dialysis to perform ultrafiltration (UF) is indicated, because acute HF can lead to deterioration of eGFR through exacerbated neurohormonal activity (that is, low forward flow) or overload fluid and renal venous congestion (ie, high back pressure). UF could counteract these maladaptive interactions primarily through congestion correction. Figure 4. (18)
We must consider that those who most need UF are hemodynamically unstable patients with IC-FEr <40%. Their worse tolerance to this treatment is due to the fact that they show low cardiac output, high neurohormonal activity, increased activity of the renin angiotensin aldosterone system, decreased tissue perfusion and an inflammatory process secondary to the systemic inflammatory response, which generates a vicious circle that leads to deterioration of the eGFR, worsening of the HF and congestion, which can be stopped by the UF.
Those patients with HFpEF generally have a good tolerance to this treatment.
SCR Type IV. In this group, UF is also indicated and we must consider that the patients who most need UF are those with HF-FEr, but they are the ones with the worst tolerance to this treatment, so we must take the necessary measures to avoid complications, by On the contrary, patients with HFpEF, in general, have a good tolerance to this treatment.
In these 2 types of CRS, it must be considered that, if the patient still has a diuretic response, there is the possibility of treatment with loop diuretics, especially in those centers where the necessary experience to perform UF is not available or not it can be done as quickly as necessary.
In patients with CKD and HF-EF, there is the possibility of peritoneal dialysis (PD) as an alternative to hemodialysis (HD), which is less aggressive, more physiological and can be performed at home.
Increasing the frequency of dialysis sessions, such as short daily HD, reduces LV mass, the risk of cardiovascular death, and hospitalizations. Patients on home dialysis, HD and / or PD, have a lower risk of hospitalization for HF and cardiovascular mortality (less risk of HF, fluid overload and cardiomyopathy). (19) To date, there are no studies that demonstrate superiority of PD over HD. Strategies to maintain residual renal function, when possible, are desirable as this can mitigate some of the significant fluid and hemodynamic changes that occur with volume depletion during dialysis. (9) KIDNEY TRANSPLANTATION In patients undergoing TxR, HF has been identified more frequently in clinical databases and less frequently in studies such as echocardiography. Data on the prevalence and prognosis of HF before HTx are scarce, but the prevalence of LVAD in patients on the waiting list for HTx can reach 25%. TxR is associated with an increased risk of mortality, cardiovascular events, and graft failure. Based on Medicare billing data, the incidence of de novo HF after TxR is 18% at 3 years. (9) Diagnosis and screening for HF in kidney transplant recipients There is little evidence as to whether an echocardiogram should be performed to evaluate LVEF in all candidates for HRT, however, it is reasonable to obtain an echocardiogram if there are symptoms of HF, history cardiovascular disease, patients with DM or hemodynamic instability on dialysis. The de novo approach to HF in TxR recipients is the same as in the general population, including evaluation of the disease. (9) Treatment of HF in kidney transplant recipients TxR recipients with HF should be treated similarly to the general population. Definitive intervention studies of ACEI or ARB II, MRA, BB, calcium channel blockers, nitrates, vasodilators, or RNAI have not been performed in the treatment of HF in TxR recipients. In a small study of LV hypertrophy TxR recipients, lisinopril reduced the LV mass index compared to placebo (20). There are no reports evaluating interventions that could prevent or delay the development of de novo HF in patients with TxR, nor are there any trials in patients with TxR that have included HF as an endpoint. (9) Clinical reversal and improvement in LV systolic function have been described after TxR, supporting the idea of a probable reversible uremic cardiomyopathy. (less likely reversal in dialysis patients), therefore we should not exclude candidates for TxR based on their LVEF. (21,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,38) In those patients with CKD on HD with HFrF, observed greater survival in those patients who underwent a heart-kidney transplant vs those who received a heart transplant (75% vs 51%). (39)
CONCLUSIONS
SCIENTIFIC REFERENCES
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