A decrease in cardiac output such as what has been observed in heart failure causes a progressive deterioration of the glomerular filtration rate. Therefore, an inadequate renal blood flow or a decrease in the renal perfusion pressure lead to a release of tensin by the juxtaglomerular cells, with the resulting activation of the RAAS, which leads to the retention of sodium and water, the contraction of the renal afferent arterioles (thus causing a decrease in glomerular perfusion) and an increase in cardiac, vascular and renal fibrosis [2].

Cardiac output depends on the existence of a sufficiently large pressure gradient through the capillary bed. In patients with heart failure, the increase in central venous pressure reduces the pressure gradient in the glomerular capillary network, which limits the renal blood flow and leads to a deterioration of the renal function.

When there is an increase of the intra-abdominal pressure, there is an increase in the pressure of renal veins, which leads to a phenomenon similar to the increase of the central venous pressure, which in turn results in the deterioration of the renal function [3,4].

An increase in the systolic dysfunction of the left ventricle leads to a decrease in the renal blood flow and the renal perfusion pressure, which causes an activation of the renal sympathetic nerves and the release of catecholamines, which result in a decrease of glomerular filtration.

Neurohormones trigger and mediate an oxidative damage cascade that leads to endothelial dysfunction, inflammation and cell death in cardiorenal syndrome.

The treatment of patients with type 1 or type 2 cardiorenal syndrome is extremely complicated, because the most important objectives are an improvement of cardiac function and the relief of the symptoms derived from the volume overload. This can be tried with the use of loop diuretics. However, diuretics are not always effective, because the decrease in renal perfusion prevents it from reaching its working site in the nephron, thus reducing its pharmacological action. This leads to a worsening of the heart failure and further reduces cardiac output, which means that this resistance to diuretics can lead to death. This happens when the ejection fraction drops below 35% [2].

This is the reason why other therapies need to be implemented, such as extracorporeal ultrafiltration or peritoneal dialysis which improve the clinical state and reduce the hospitalization rate, although they cannot reduce the mortality rates for this entity [5].

Extracorporeal ultrafiltration, either by itself or combined with hemodialysis, is an optimal treatment to treat short- term volume overload. This technique can improve the heart function by reducing the preload and eliminating neurohormonal substances. However, this technique pre- sents the disadvantage that a fast and intermittent elimination of fluid is associated with hypotension, coronary ischemia and arrhythmias, which leads to a worsening of cardiovascular function [4]. Therefore, a more gradual elimination of the extracellular fluid is preferred, and in this case peritoneal dialysis can play a much more important role in acute cases and in long-term treatments.

This technique represents an optimal treatment to combat decompensate cardiac failure as a long-term therapy in patients with refractory heart failure with or without advanced chronic kidney disease; and also as a temporary support therapy until a heart transplant is performed (the only definitive treatment for type 1 and 2 cardiorenal syndrome).

Peritoneal dialysis can reduce the weight of the patient, volume overload and edema, which means that the heart function improves, and also the symptoms of hydric overload, hyponatremia and renal function, thus reducing the resistance to diuretics.

Therefore, the admission time is reduced [6,7], and so is the number of drugs used, while the quality of life significantly improves.

This technique provides considerable advantages compared with extracorporeal ultrafiltration of the dialysis, such as the fact that the fluid elimination is gradual and takes place over long periods of time, there is no need for anticoagulation and there is a possibility of an ambulatory treatment [8,9].

When the technique is implemented in a situation of acute heart decompensation, low volumes must be used (750 to 1000 mL), and the dialysis must be changed often (approximately every 1 - 2 hours), with dialysis solutions based on icodextrin (a glucose polymer with a high ultrafiltration potential) or hypertonic glucose, in order to prevent complications, such as the pericatheter leakage of peritoneal fluid [10,11].

In long-term treatments, both intermittent peritoneal dialysis and continuous ambulatory peritoneal dialysis may be used [11]. However, this last technique offers more advantages to the patients, because it provides hemodynamic stability and the slow and gradual control of nitrogen products [12].

The dialysis scheme must be adapted to the needs of each patient and it must take into account the peritoneal transport, the residual renal function, the degree of heart deterioration, the need of control of nitrogen products, the frequency of admissions caused by heart decompensation and the response to ultrafiltration [13].

It is recommended to start with continuous ambulatory peritoneal dialysis with solutions of hypertonic glucose with short cycles and, once that the behavior of the peritoneal membrane has been assessed, this technique can be maintained or, if the patients present residual renal function or they do not need to eliminate nitrogen products, it can be replaced by automatic peritoneal dialysis with hypertonic glucose-based solutions or a night cycle of icodextrin two or three times per week [14].

In patients who do not present residual renal function and who, therefore, also need to eliminate nitrogen products, the most adequate option would be ambulatory continuous dialysis, with a night cycle of icodextrin or an automatic dialysis and the use of icodextrin in a cycle during the day [14].

The use of peritoneal dialysis in the treatment of cardiorenal syndrome is not without its complications. The amount and speed of the elimination of volume overload is less predictable than with extracorporeal ultrafiltration. Other complications are related to the insertion of a Tenckhoff catheter, pericatheter leakage, wall hematomas, surface or deep hemorrhage or peritonitis [12].