Fluid overload in peritoneal dialysis (PD) patients can manifest as generalized edema, pulmonary edema, and hypertension. It contributes to left ventricular hypertrophy and is a major contributor to cardiovascular disease, the leading cause of death in all dialysis patients. It is also associated with hypoalbuminemia, malnutrition, inflammation, and atherosclerosis (Demirci, 2011); and it is a significant cause of technique failure, especially in long-term PD patients (Woodrow, 2011).

I. ASSESSMENT OF FLUID STATUS. This is based primarily on clinical examination, which gives at best a crude estimation. The target body weight or “dry weight” for PD is that weight which gives a well-tolerated normotensive, edema-free state, and, just as in hemodialysis, it is determined by trial and error. Since PD patients tend to be seen less frequently than those on hemodialysis, there is a risk that this process will be more protracted and less well done. It requires frequent clinical reassessment of patients.

Alternative methods of assessing volume status include bioimpedance, serum levels of brain natriuretic peptide (BNP), and ultrasound of the inferior cava or of the lungs. Bioimpedance analysis can be done with relatively simple devices and involves attachment of electrodes and application of low-voltage currents. This allows extracellular and intracellular fluid volumes to be estimated. It is being used clinically in some centers but without high-grade evidence to justify it (John, 2010). Serum BNP levels are in clinical use and are predictive of patient outcomes, but do not reliably distinguish fluid overload from cardiac injury (Granja, 2007; Wang, 2007).

II. MECHANISMS OF FLUID OVERLOAD. Fluid overload in a PD patient may reflect any combination of inappropriate prescription, noncompliance, loss of residual renal function, mechanical problems, and peritoneal membrane dysfunction. Awareness that any one factor alone may not explain an individual PD patient’s volume overload is important and one should avoid thoughtlessly attributing all fluid overload to membrane-related ultrafiltration failure (UFF).

III. DIAGNOSIS OF PERITONEAL MEMBRANE DYSFUNCTION AND ULTRAFILTRATION FAILURE. UFF is defined as fluid overload in association with an ultrafiltration volume <400 mL in a modified peritoneal equilibration test (PET) (Ho-dac-Pannakeet, 1997). The modified PET uses a 4.25% dialysate dwell instead of the usual 2.5% bag used in the standard PET (described in Chapter 21). UFF should not be diagnosed if the ultrafiltration volume exceeds 400 mL or if there is no clinical evidence of significant volume overload. UFF should not be diagnosed until catheter malfunction and leaks have been excluded. An ultrafiltration volume >400 mL in the modified PET implies normal peritoneal membrane function, and if fluid overload is present, closer attention needs to be paid to nonmembrane causes as listed in Table 26.1.

If UFF is diagnosed, the next step is to review the solute transport characteristics of the patient using the results of the modified 4.25% PET (or the standard PET as the results are very similar).

A. High transporter with UFF (type I). In this situation, the dialysate dextrose concentration falls quickly after infusion because of rapid absorption, resulting in loss of the concentration gradient that drives fluid removal. This is the most common cause and is often called type I UFF. It typically develops after 3 or more years on PD. It is believed to reflect an increase in the effective peritoneal surface area consequent to the increased membrane vascularity that occurs with time on PD. This occurs to a greater extent in some patients than in others. The contribution of interstitial fibrosis and resultant thickening of the membrane is increasingly recognized (Davies, 2005). Causes of type I UFF include cumulative exposure of the membrane to high glucose loads (Davies, 2001) and perhaps to other bioincompatible features of PD solutions, including low pH, lactate, and toxic glucose degradation products. Other causes may be related to cumulative episodes of peritonitis or to systemic inflammation seen in uremia generally. Type I UFF may also occur transiently in some patients with acute peritonitis who have a temporary increase in transport status during and after the episode owing to acute inflammation of the membrane.

B. Low transporter with UFF (type II). This group of patients has reduced small solute clearance and reduced fluid removal. This is also called type II UFF and is much less common. It reflects decreased membrane surface area and is most often due to adhesions and scarring after a severe peritonitis or other intra-abdominal complication. It is difficult to maintain these patients on PD unless they have significant residual renal function.

C. UFF with transport in the normal range (usually high-average and low-average transporters). Careful consideration once again should be made to exclude mechanical causes for poor fluid removal in this group.

1. Increased lymphatic absorption of peritoneal fluid is the cause in some patients and this is called type III UFF. Lymphatic absorption can be quantified by measuring the disappearance rate of dextran 70 from the peritoneal cavity, but this is rarely done in clinical practice, and the diagnosis tends to be one of exclusion.

2. Aquaporin deficiency. A similar pattern can be seen with the interesting but rarer condition of aquaporin deficiency. This can be diagnosed by measuring the change in dialysate sodium concentration after 30-60 minutes of a 2-L dialysis dwell with 4.25%, dextrose compared with a 2-L dwell using 1.5%, dextrose. Why does the dialysate sodium fall during the early part of a dwell? When dialysate glucose levels are high, osmotically driven UF occurs primarily via aquaporin channels, which transport water but not sodium. The result is an early lowering in the dialysate sodium concentration by 5-10 mmol/L with a 4.25% glucose dwell. This leads to a sodium gradient between blood and dialysate, and sodium diffusion brings the dialysate sodium level up again as the dwell proceeds (Fig. 21.7

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