Correlates of potassium transport during peritoneal equilibration tests using different dialysate glucose concentrations
Análisis del transporte peritoneal de potasio mediante pruebas de equilibrio peritoneal con diferentes concentraciones de glucosa
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Gomes, A. Rodríguez-Carmona, Miguel Pérez Fontán, A. López Muñiz, N. Blanco Castro, M. da Cunha, T. García Falcón" "autores" => array:7 [ 0 => array:3 [ "Iniciales" => "A.M." "apellidos" => "Gomes" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:3 [ "Iniciales" => "A." "apellidos" => "Rodríguez-Carmona" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 2 => array:4 [ "nombre" => "Miguel" "apellidos" => "Pérez Fontán" "email" => array:1 [ 0 => "miguel.perez.fontan@sergas.es" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] ] ] 3 => array:3 [ "Iniciales" => "A." "apellidos" => "López Muñiz" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 4 => array:3 [ "Iniciales" => "N." "apellidos" => "Blanco Castro" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 5 => array:3 [ "Iniciales" => "M." "apellidos" => "da Cunha" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 6 => array:3 [ "Iniciales" => "T." "apellidos" => "García Falcón" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Servicio de Nefrología, Hospital Universitario de La Coruña, La Coruña, España, " "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] 1 => array:3 [ "entidad" => "Departamento de Medicina, Hospital Universitario de La Coruña. Facultad de Ciencias de la Salud. Universidad de La Coruña, La Coruña, España, " "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Análisis del transporte peritoneal de potasio mediante pruebas de equilibrio peritoneal con diferentes concentraciones de glucosa" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_t1_pag97.jpg" "Alto" => 382 "Ancho" => 403 "Tamanyo" => 43782 ] ] "descripcion" => array:1 [ "en" => "Study population" ] ] ] "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara">In clinical practice, the peritoneal equilibration test (PET) is the reference procedure for categorising peritoneal transport characteristics in patients undergoing peritoneal dialysis (PD). As such, it focuses on creatinine and glucose, but has also been modified to analyze the transport characteristics of other solutes.<span class="elsevierStyleSup">1</span> The standard PET is performed with 2.27% glucose-based dialysate, but there is increasing support for the use of the 3.86% solution, which is said to permit a more accurate assessment of the ultrafiltration (UF) and free water transport capacities.<span class="elsevierStyleSup">1-3</span> PET sessions based on either 1.36%, 2.27% or 3.86% glucose-based dialysate appear to yield similar results for creatinine, with some expected differences  for other  small solutes, including glucose and sodium.<span class="elsevierStyleSup">4,5</span> On the other hand, there are some gaps in our knowledge of the factors which may influence the peritoneal transport of potassium during PD. Importantly, a significant fraction of the potassium recovered from spent dialysate during a PD exchange may have a cellular origin, aside from the classic diffusive and convective pathways from the circulation.<span class="elsevierStyleSup">6,7</span> The mechanisms for cellular efflux of potassium are not clear, but local cell apoptosis, low fluid pH and cell dehydration in the presence of hypertonic dialysate may both contribute to the phenomenon.<span class="elsevierStyleSup">8</span> This situation raises the possibility that the composition of dialysate and other clinical or biochemical factors may specifically influence the peritoneal transport of potassium. The PET may represent a useful tool for approaching these questions.</p><p class="elsevierStylePara">We performed a study in the clinical setting to compare the potassium transport profiles in ninety PD patients who underwent PET using 2.27% and 3.86% glucose-based, lactate-buffered dialysate, as well as to disclose demographic, clinical and biochemical factors which could influence the results of potassium transport analysis in both tests.</p><p class="elsevierStylePara"><span class="elsevierStyleBold">POPULATION AND METHOD</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">General design</span></p><p class="elsevierStylePara">Following a prospective design, ninety PD patients underwent two PET sessions using 2.27% and 3.86% glucose-based solutions in random order. The mean delay between both tests was four months (range 0-6). We compared the saturation profiles for different low molecular weight solutes during both tests, paying particular attention to the behaviour of dialysate potassium concentration. We analysed the correlation between the observed potassium saturation profiles and selected demographic variables (age, gender, time on dialysis, PD modality, diabetes, previous peritonitis, ongoing drug therapies), and laboratory variables (diuresis, glomerular filtration rate [GFR], urinary potassium excretion, haemoglobin, plasma albumin, C-reactive protein [CRP]), PD prescription (peritoneal glucose load, use of icodextrin) and peritoneal function variables (creatinine and glucose transport rates, UF, sodium sieving).</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Population</span></p><p class="elsevierStylePara">All patients from our PD Unit were eligible for the study provided they met two conditions, which were being in stable clinical condition without having experienced peritonitis or any significant events in the previous two months, and giving informed consent for participation. On the other hand, patients suffering peritonitis, haemoperitoneum or peritoneal catheter malfunction, undergoing catheter removal or who presented any significant clinical event in general during the study period were excluded from analysis.</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Study protocol</span></p><p class="elsevierStylePara">PD adequacy and residual renal function were estimated for all patients during the month preceding each PET. All the PET studies followed the general protocol for these tests, with small modifications. In summary, after an overnight dwell with 2.27% dialysate, two litres of 2.27% or 3.86% dialysate were infused into the peritoneal cavity. Dialysate samples were collected according to standardised procedures at 0, 60, 90, 120 and 240 minutes. At the end of the four-hour dwell, the peritoneal cavity was drained completely. We retrieved blood samples for analysis 120 minutes after each test. All patients used conventional lactate-based dialysate made by Baxter (Deerfield, Illinois) (n = 81) or Fresenius (Heidelberg, Germany) (n = 9) laboratories.</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Sample processing and secondary calculations</span></p><p class="elsevierStylePara">Sodium and potassium concentrations in plasma, dialysate and urine were estimated using an indirect ion-selective electrode method. Plasma and dialysate levels of glucose, creatinine (corrected for glucose) and albumin were determined with a standard autoanalyser. Plasma CRP was estimated by immunoturbidimetry (Roche Diag., Mannheim, Germany).</p><p class="elsevierStylePara">GFR was computed as the mean of renal urea and creatinine clearances. Peritoneal transport (D/P creatinine at 240 min, D/P<span class="elsevierStyleInf">Cr-240’ </span>) was categorised according to the results of the 2.27% PET. D/P potassium and D/P creatinine were calculated as the ratio between dialysate potassium or creatinine concentration at any point and plasma potassium or creatinine concentration at the midpoint of the test. Sodium dip was computed as D<span class="elsevierStyleInf">Na-60’</span> – D<span class="elsevierStyleInf">Na-0’</span> glucose was calculated as the ratio of dialysate glucose concentrations at different sampling points versus baseline. UF during the test was estimated as the difference between the weights of the dialysate bag before infusion and after final drainage; UF failure was defined by an UF < 400mL during the 3.86% PET.</p><p class="elsevierStylePara">The main dependent variable of the study was D/P of potassium at 240 minutes (D/P<span class="elsevierStyleInf">K-240’</span>). We compared the performance of this variable in the PET with 2.27% and 3.86% solution. We also searched for correlations between the main variable on the one hand and the demographic, clinical and biochemical variables examined on the other; these included the solute transport characteristics (D/P<span class="elsevierStyleInf">Cr-240’</span>), sodium dip and UF during the corresponding PET.</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Statistical analysis</span></p><p class="elsevierStylePara">Numerical variables are presented as mean or median values (range), as appropriate. Direct comparisons between variables were made using Student’s-t tests, ANOVA (numerical variables) and chi-square distribution (categorical variables). The correlation between numerical variables was calculated according to the Spearman correlation coefficient. Agreement between numerical estimations was evaluated  using Bland-Altman plots, using the paired Student’s t- test to analyse for systematic biases. Forward and stepwise multiple regression strategies were applied for multivariate analysis. We used SPSS version 16.0 for data processing.</p><p class="elsevierStylePara"><span class="elsevierStyleBold">RESULTS</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Overview</span></p><p class="elsevierStylePara">The main characteristics of the study population are presented in Table 1. Total infused dialysate volume was 6.8 ± 2.2L/day (3.5-14.5) at the time of the 2.27% solution PET and 7.0 ± 2.4L/day (3.5-15.5) at the time of the 3.86% solution PET (p=0.51). The daily peritoneal glucose loads were 87.2 ± 47.0g (27.2-233.7) and 90.4 ± 45.9g (21.2-236.0) respectively (p=0.46). With regard to the PET-related values, the observed D/PCr profiles were very similar in the 2.27% and 3.86% solution tests (not represented). The study population included 17 slow (18.9%), 63 average (70.0%) and 10 fast transporters (11.1%). Mean UF values were 131.4 ± 256.7mL (-480-600) during the 2.27% solution PET and 542.0 ± 344.5mL (-150-1300) during the 3.86% solution PET. Twenty-six patients (28.9%) met the diagnostic criteria for UF failure. Mean plasma potassium levels were 4.74 ± 0.72mM/L (2.8-6.1) during the 2.27% PET and 4.73 ± 0.62mM/L (3.5-6.1) during the 3.86% PET (p=0.70). Mean plasma glucose levels were 111.7 ± 48.6mg/dL (52-269) and 112.5 ± 48.5mg/dL (66-318) respectively (p=0.85).</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Comparison of potassium transport profiles in both</span><span class="elsevierStyleBold">PET sessions</span></p><p class="elsevierStylePara">The dialysate potassium saturation profiles were very similar in the 2.27% and the 3.86% solution PET sessions (Figure 1). There was good agreement between both tests, without systematic biases, at 60 (p = 0.09), 90 (p = 0.71), 120 (p = 0.17) and 240 minutes (Figure 2).</p><p class="elsevierStylePara">There was a marked correlation between potassium and creatinine transport in both PET sessions (Figure 3). The observed correlation between D/P<span class="elsevierStyleInf">K-240’</span> and D/D<span class="elsevierStyleInf">0</span> glucose at 240 minutes was closer during the 2.27% test (r = -0.49, p < 0.0005) than during the 3.86% test (r = -0.29, p = 0.006). At the same time, no apparent univariate correlation was observed between plasma potassium (r = -0.01, p = 0.96 2.27%, r = -0.05, p = 0.64 3.86%), UF (r = 0.13, p = 0.22 2.27%; r = 0.03, p = 0.75 3.86%) or dialysate sodium dip at 60 minutes (r = 0.02, p = 0.88 2.27%, r = 0.10, p = 0.34 3.86%) on the one hand and D/P<span class="elsevierStyleInf">K-240’</span>, on the other.</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Demographic, clinical and biochemical correlates of peritoneal potassium transport</span></p><p class="elsevierStylePara">Table 2 shows the univariate correlations between D/P<span class="elsevierStyleInf">K-240’</span> as well as the different demographic, clinical and biochemical variables that were examined. There was a clear trend toward higher D/P potassium levels in patients treated with ACEI-ARA drugs (Figure 4), particularly during the 3.86% PET (Figure 4b). Mean plasma potassium levels were 4.84 ± 0.69mM/L (2.8-5.8) (ACEI-ARA) vs. 4.64 ± 0.64mM/L (3.1-6.1) (no ACEI-ARA) during the 2.27% PET (p = 0.18), and 4.89 ± 0.68 (3.5-6.1) and 4.61 ± 0.65mM/L (3.6-5.8), respectively, during the 3.86% PET (p = 0.06).</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Multivariate analysis</span></p><p class="elsevierStylePara">Multiple regression analysis (Table 3) identified the overall peritoneal transport category (as estimated from D/P<span class="elsevierStyleInf">Cr-240’</span>) as the most consistent correlate of D/P<span class="elsevierStyleInf">K-240’</span>. Treatment with ACEI/ARA drugs was also a strong predictor of D/P<span class="elsevierStyleInf">K-240’</span>, but only in the 3.86% PET, while a similar but non-significant trend was observed in the 2.27% PET. On the other hand, both GFR (Table 2) and urinary potassium excretion (Figure 5) showed an inverse univariate association with the main study variable. GFR remained an independent correlate of the dependent variable [B = -0.005 (95% CI -0.009, 0.000), p = 0,036 2.27% test; B = -0.005 (-0.010, 0.000), p=0,038 3.86% test] only if urinary potassium was not included in the regression model, but that variable proved to be a far more stable predictor of D/P<span class="elsevierStyleInf">K-240’</span> (Table 3).</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">Our results are consistent with earlier reports<span class="elsevierStyleSup">7,9</span> in that they showed overall agreement between the way the 2.27% and the 3.86% glucose-based PET estimated peritoneal potassium transport. This equivalence may be the result of the interaction of several opposing forces. Free water transport is expected to produce a slower saturation of potassium in the 3.86% test than in the 2.27% test, particularly during the first two hours of the test, but both diffusion and convection of potassium through small pores act to compensate for this effect. Moreover, other mechanisms may potentially influence potassium transport, depending on the concentration of glucose in dialysate. First, the hypertonicity and low pH of glucose-based, lactate-buffered dialysate causes peritoneal vasodilation, thus increasing solute (including potassium) transport. However, this effect appears to be non-linear, meaning that 3.86% glucose solution may not be more vasodilatory than 2.27% glucose solution.<span class="elsevierStyleSup">10</span> In fact, PET sessions for the peritoneal transport of creatinine are consistent when different glucose concentrations are used.<span class="elsevierStyleSup">3-5</span></p><p class="elsevierStylePara">On the other hand, cellular efflux of potassium may contribute significantly to peritoneal transport of this cation during a PD exchange.<span class="elsevierStyleSup">6,7</span> The reasons for this phenomenon are not totally clear. Local cell breakdown with release of potassium into the peritoneal cavity is a possible explanation, but recent studies<span class="elsevierStyleSup">8</span> suggest that potassium efflux from viable cells may be a more important mechanism. First, low dialysate pH could favour a proton-potassium transcellular exchange<span class="elsevierStyleSup">7</span> although this effect may be self-limited, because pH equilibrates rapidly during a PD dwell. Moreover, hypertonic glucose-based dialysate generates a high local osmolarity, which may induce peritoneal cell dehydration and secondary potassium efflux.<span class="elsevierStyleSup">11</span> If the latter were true, 3.86% dialysate would be expected to produce higher rates of potassium transport than 1.36% or 2.27% dialysate, thus counterbalancing the above-mentioned, putative opposite effect of free water transport. The reported direct correlation between the latter and potassium release from cells<span class="elsevierStyleSup">11</span> lends some support to this hypothesis. Nevertheless, this proposed mechanism deserves further clarification. For instance, hypertonic glucose-based dialysate drives insulin secretion<span class="elsevierStyleSup">12</span> which in turn could favour systemic (and peritoneal) cellular uptake of potassium, with a yet undefined impact on peritoneal potassium transport.<span class="elsevierStyleSup">13</span></p><p class="elsevierStylePara">A remarkable finding in our study was the observation of higher potassium transport rates in patients treated with ACEI-ARA, an effect which was particularly evident during the 3.86% solution PET (Figure 4). The effect of this family of drugs on peritoneal function and structure is still a matter of controversy. First, patients treated with ACEI-ARA may have specific comorbidity profiles, and present intrinsically higher solute transport rates since beginning PD.<span class="elsevierStyleSup">14</span> On the other hand, short-term administration of ACEI-ARA to PD patients may induce vasodilation of peritoneal vessels,<span class="elsevierStyleSup">15</span> but this effect does not appear to significantly modify peritoneal solute transport characteristics.<span class="elsevierStyleSup">16-18</span> Long-term therapy with ACEI-ARA may prevent PD-induced changes in the peritoneal membrane,<span class="elsevierStyleSup">19,20</span> resulting at least partially from these drugs’ ability to prevent fibrosis and stabilize the peritoneal vascular surface<span class="elsevierStyleSup">20-22</span>. The specific effect of ACEI-ARA on potassium transport has been a subject of limited attention. A study by Rojas-Campos et al<span class="elsevierStyleSup">18</span> could not find that losartan had a significant impact on potassium transport. However, the study was a short-term one, and 2.5% glucose dialysate was used for solute transport analysis. Moreover, a non-significant trend toward a D/P potassium increase could be observed after losartan, but not after prazosin or verapamil therapy.<span class="elsevierStyleSup">18</span> In our study, the impact of ACEI-ARA therapy on potassium transport was more evident during the 3.86% (Figure 4b) than during the 2.27% PET (Figure 4a) (Table 3). Again, the explanation for this finding is not totally clear. ACEI-ARA drugs could increase potassium release by inducing apoptosis of peritoneal cells, in a similar way to what happens in other tissues,<span class="elsevierStyleSup">23,24 </span>but this hypothesis is rather speculative. ACEI-ARA could also hamper general compensatory mechanisms oriented toward attenuating potassium efflux from cells, and this effect should be more evident at the peritoneal level in the presence of a stronger drive for potassium efflux (as in a 3.86% PET). Hyperkalaemia is a well-known consequence of ACEI-ARA therapy.<span class="elsevierStyleSup">25,26</span> Inhibition of renal potassium excretion is the main mechanism underlying this effect; however, in patients on dialysis with a low or absent residual renal function, antagonizing the renin-angiotensin-aldosterone axis may block compensatory mechanisms oriented toward facilitating faecal excretion and cellular uptake of potassium.<span class="elsevierStyleSup">27-29</span></p><p class="elsevierStylePara">GFR and urinary potassium excretion were both inverse correlates of peritoneal potassium transport, but urinary potassium showed a far more consistent association with the study variable. This latter correlation could be adequately explored because only seven patients (7.8%) were anuric at the start of our study. An inverse association between residual renal function and peritoneal potassium transport may at first seem paradoxical because decaying GFR should activate mechanisms of potassium adaptation, favouring cell uptake and consequently decreasing transcellular peritoneal transport. On the contrary, it is tempting to speculate that urinary potassium excretion may be an indirect marker of aldosterone activity, although plasma levels of this hormone were not estimated. As previously hypothesised, high aldosterone levels could favour cell potassium uptake,<span class="elsevierStyleSup">28</span> thus opposing efflux from peritoneal cells in response to dialysate acidity and hypertonicity.</p><p class="elsevierStylePara">Treatment with calcium antagonists showed a degree of direct association with potassium transport in the univariate analysis, but the relationship did not persist after verifying for other variables. These drugs were examined due to their ability to block calcium-dependent potassium efflux from endothelial cells.<span class="elsevierStyleSup">30</span> This type of channel has also been identified in the peritoneal mesothelium.<span class="elsevierStyleSup">31</span> In PD patients, short-term treatment with verapamil does not appear to modify peritoneal solute transport characteristics although, for unclear reasons, it can increase UF.<span class="elsevierStyleSup">18</span></p><p class="elsevierStylePara">In conclusion, the classic 2.27% and the modified 3.86% solution PET show good agreement for estimating D/P of potassium. Urinary potassium excretion and ongoing treatment with ACEI-ARA (3.86% PET) are independent correlates of peritoneal potassium transport rates. Further studies will be necessary to clarify the interactions between systemic mechanisms of adaptation to renal failure and the physiopathology of the peritoneal membrane during PD.</p><p class="elsevierStylePara"><a href="grande/1003618078_t1_pag97.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_t1_pag97.jpg" alt="Study population"></img></a></p><p class="elsevierStylePara">Table 1. Study population</p><p class="elsevierStylePara"><a href="grande/1003618078_f1_pag98.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_f1_pag98.jpg"></img></a></p><p class="elsevierStylePara">Figure 1. </p><p class="elsevierStylePara"><a href="grande/1003618078_f2_pag98.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_f2_pag98.jpg"></img></a></p><p class="elsevierStylePara">Figure 2. </p><p class="elsevierStylePara"><a href="grande/1003618078_f3_pag98.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_f3_pag98.jpg"></img></a></p><p class="elsevierStylePara">Figure 3. </p><p class="elsevierStylePara"><a href="grande/1003618078_t2_pag99.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_t2_pag99.jpg" alt="Clinical correlates of potassium transport during PET. Univariate."></img></a></p><p class="elsevierStylePara">Table 2. Clinical correlates of potassium transport during PET. Univariate.</p><p class="elsevierStylePara"><a href="grande/1003618078_t3_pag100.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_t3_pag100.jpg" alt="Clinical correlates of potassium transport. Multivariate"></img></a></p><p class="elsevierStylePara">Table 3. Clinical correlates of potassium transport. Multivariate</p><p class="elsevierStylePara"><a href="grande/1003618078_f4_pag100.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_f4_pag100.jpg"></img></a></p><p class="elsevierStylePara">Figure 4. </p><p class="elsevierStylePara"><a href="grande/1003618078_f5_pag101.jpg" class="elsevierStyleCrossRefs"><img src="1003618078_f5_pag101.jpg"></img></a></p><p class="elsevierStylePara">Figure 5. </p>" "pdfFichero" => "P1-E43-S1785-A10036-EN.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "es" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437813" "palabras" => array:1 [ 0 => "Potasio urinario" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437815" "palabras" => array:1 [ 0 => "IECA-ARA" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437817" "palabras" => array:1 [ 0 => "Potasio" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437819" "palabras" => array:1 [ 0 => "Prueba de equilibrio peritoneal" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437821" "palabras" => array:1 [ 0 => "Diálisis peritoneal" ] ] ] "en" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437814" "palabras" => array:1 [ 0 => "Urinary potassium" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437816" "palabras" => array:1 [ 0 => "ACEI-ARA" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437818" "palabras" => array:1 [ 0 => "Potassium" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437820" "palabras" => array:1 [ 0 => "Peritoneal equilibration test" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437822" "palabras" => array:1 [ 0 => "Peritoneal dialysis" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:1 [ "resumen" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Background: </span>There are gaps in the knowledge of factors which influence peritoneal potassium transport in peritoneal dialysis (PD). The aims of this study were to compare peritoneal potassium transport in PD patients undergoing 2.27% and 3.86% peritoneal equilibration tests (PET), and to disclose clinical correlates of this phenomenon. <span class="elsevierStyleBold">Method: </span>Ninety PD patients underwent 2.27% and 3.86% PET, in a random order. We compared peritoneal potassium transport in both tests, and searched for correlations between D/P potassium at 240 minutes (main study variable) and PET-derived markers of peritoneal function and selected demographic, clinical and biochemical variables, using a multivariate approach. <span class="elsevierStyleBold">Main results: </span>D/P potassium showed a good agreement between both PET, and presented a univariate association with creatinine transport, but not with plasma potassium, ultrafiltration or sodium dip. Age, PD modality, peritoneal glucose load, icodextrin, ACEI-ARA and calcium antagonist therapy, urinary potassium and glomerular filtration rate were other univariate correlates of potassium transport. Multivariate analysis confirmed D/P creatinine at 240 minutes (B = 0.40 [95% CI 0.26-0.53] 2.27%, B = 0.36 [0.21-0.51] 3.86%,p <0.0005) as the main predictor of D/P potassium at 240’. Urinary potassium, rather than glomerular filtration rate, sustained also an inverse correlation with the dependent variable. Treatment with ACEI-ARA was consistently associated with peritoneal potassium transport (3.86% PET) (B = 0,08 [0.04-0.12], p <0.0005). <span class="elsevierStyleBold">Conclusions: </span>The 2.27% and the 3.86% PET show a good agreement at the time of estimating peritoneal potassium transport. Urinary potassium excretion and treatment with ACEI-ARA (3.86% test) show an independent association with peritoneal potassium transport rates.</p>" ] "es" => array:1 [ "resumen" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Introducción: </span>El conocimiento de los factores que determinan el transporte peritoneal de potasio en diálisis peritoneal (DP) es incompleto. Los objetivos de este estudio fueron comparar el transporte peritoneal de potasio en pruebas de equilibrio peritoneal (PEP) con soluciones de glucosa al 2,27 y al 3,86%, y desvelar factores con influencia en este fenómeno. <span class="elsevierStyleBold">Método: </span>Noventa pacientes en DP fueron sometidos a PEP al 2,27 y al 3,86%, en orden aleatorio. Comparamos el transporte de potasio en ambas pruebas, buscando correlaciones del cociente D/P de potasio a 240 minutos (variable principal) con marcadores de función peritoneal durante PEP, y con diferentes variables demográficas, clínicas y bioquímicas, usando una estrategia multivariante. <span class="elsevierStyleBold">Resultados: </span>El D/P de potasio presentó buena concordancia en ambas PEP, mostrando asociación univariante con el D/P de creatinina, pero no con potasio plasmático, ultrafiltración o descenso de sodio. La edad, tipo de DP, carga peritoneal de glucosa, icodextrina, tratamiento con IECA-ARA o calcioantagonistas, potasio urinario y filtrado glomerular tuvieron una correlación univariante con el transporte de potasio. En el análisis multivariante, el D/P de creatinina a 240 minutos (B = 0,40 [IC 95%: 0,26-0,53] 2,27%; B = 0,36 [0,21-0,51] 3,86%; p <0,0005) fue el predictor esencial del D/P de potasio a 240’. La excreción urinaria de potasio también tuvo una correlación inversa con la variable principal. Asimismo, el tratamiento con IECA-ARA se asoció de forma consistente con el transporte peritoneal de potasio, pero sólo en la PEP al 3,86% (B = 0,08 [0,04-0,12]; p <0,0005). <span class="elsevierStyleBold">Conclusiones: </span>Las PEP al 2,27 y al 3,86% estiman de manera concordante el transporte peritoneal de potasio. Aunque el transporte de creatinina es el predictor principal del de potasio, la excreción urinaria de potasio y el tratamiento con IECA-ARA se asocian de manera independiente con el fenómeno citado.</p>" ] ] "multimedia" => array:8 [ 0 => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_t1_pag97.jpg" "Alto" => 382 "Ancho" => 403 "Tamanyo" => 43782 ] ] "descripcion" => array:1 [ "en" => "Study population" ] ] 1 => array:7 [ "identificador" => "fig2" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_f1_pag98.jpg" "Alto" => 451 "Ancho" => 400 "Tamanyo" => 17882 ] ] ] 2 => array:7 [ "identificador" => "fig3" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_f2_pag98.jpg" "Alto" => 344 "Ancho" => 400 "Tamanyo" => 20088 ] ] ] 3 => array:7 [ "identificador" => "fig4" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_f3_pag98.jpg" "Alto" => 354 "Ancho" => 400 "Tamanyo" => 23456 ] ] ] 4 => array:8 [ "identificador" => "fig5" "etiqueta" => "Tab. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_t2_pag99.jpg" "Alto" => 388 "Ancho" => 828 "Tamanyo" => 84946 ] ] "descripcion" => array:1 [ "en" => "Clinical correlates of potassium transport during PET. Univariate." ] ] 5 => array:8 [ "identificador" => "fig6" "etiqueta" => "Tab. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_t3_pag100.jpg" "Alto" => 377 "Ancho" => 828 "Tamanyo" => 77974 ] ] "descripcion" => array:1 [ "en" => "Clinical correlates of potassium transport. Multivariate" ] ] 6 => array:7 [ "identificador" => "fig7" "etiqueta" => "Fig. 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_f4_pag100.jpg" "Alto" => 368 "Ancho" => 825 "Tamanyo" => 30107 ] ] ] 7 => array:7 [ "identificador" => "fig8" "etiqueta" => "Fig. 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "1003618078_f5_pag101.jpg" "Alto" => 345 "Ancho" => 398 "Tamanyo" => 23289 ] ] ] ] "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:31 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Smit W, Van Dijk P, Langedijk M, Schouten N, Van der Berg N, Struijk D, Krediet R. Peritoneal function and assessment of reference values using a 3.86% glucose solution. Perit Dial Int 2003;23:440-9." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 1 => array:3 [ "identificador" => "bib2" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Mujais S, Nolph KD, Gokal R, Blake P, Burkart J, Coles G, et al. Evaluation and management of ultrafiltration problems in peritoneal dialysis. Perit Dial Int 2000;20(Supl. 4):S5-S21. <a href="http://www.ncbi.nlm.nih.gov/pubmed/11098926" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 2 => array:3 [ "identificador" => "bib3" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "La Milia V, Pozzoni P, Virga G, Crepaldi M, Del Vecchio L, Locatelli F. Peritoneal transport assessment by peritoneal equilibration test with 3.86% glucose: a long-term prospective evaluation. Kidney Int 2006;69:927-33." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 3 => array:3 [ "identificador" => "bib4" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Smit W, Langedijk M, Schouten N, Van der Berg N, Struijk D, Krediet R. A comparison between 1.36% and 3.86% dextrose dialysis solution for the assessment of peritoneal membrane function. Perit Dial Int 2000;20:734-41." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 4 => array:3 [ "identificador" => "bib5" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Pride E, Gustafson J, Graham A, Spainhour L, Mauck V, Brown P, et al. Comparison of a 2.5% and a 4.25% dextrose peritoneal equilibration test. Perit Dial Int 2002;22:365-70." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 5 => array:3 [ "identificador" => "bib6" "etiqueta" => "6" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Imholz AL, Koomen GC, Struijk DG, Arisz L, Krediet RT. Fluid and solute transport in CAPD patients using ultralow sodium dialysate. Kidney Int 1994;46:333-40. <a href="http://www.ncbi.nlm.nih.gov/pubmed/7967344" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 6 => array:3 [ "identificador" => "bib7" "etiqueta" => "7" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Rippe B, Venturoli D, Simonsen O, De Arteaga J. Fluid and electrolyte transport across the peritoneal membrane during CAPD according to the three-pore model. Perit Dial Int 2004;24:10-27. <a href="http://www.ncbi.nlm.nih.gov/pubmed/15104333" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 7 => array:3 [ "identificador" => "bib8" "etiqueta" => "8" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Coester AM, Struijk DG, Smit W, De Waart DR, Krediet RT. The cellular contribution to effluent potassium and its relation to free water transport during peritoneal dialysis. Nephrol, Dial & Transplant 2007;22:3593-600." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 8 => array:3 [ "identificador" => "bib9" "etiqueta" => "9" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Heimbürger O, Waniewski J, Werynski A, Lindholm B. A quantitative description of solute and fluid transport during peritoneal dialysis. Kidney Int 1992;41:1320-2." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 9 => array:3 [ "identificador" => "bib10" "etiqueta" => "10" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Zakaria ER, Patel AA, Li N, Matheson PJ, Garrison RN. Vasoactive components of dialysis solution. Perit Dial Int 2008;28:283-95. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18474922" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 10 => array:3 [ "identificador" => "bib11" "etiqueta" => "11" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Krediet RT, Coester AM, Parikova A, Smit W, Struijk DG. New insights into the physiology of peritoneal fluid transport. Perit Dial Int 2008;28(Supl. 3):S144-S149. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18552245" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 11 => array:3 [ "identificador" => "bib12" "etiqueta" => "12" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Pérez-Fontán M, Cordido F, Rodríguez-Carmona A, García-Naveiro R, Isidro ML, Villaverde P, et al. Acute plasma Ghrelin and Leptin responses to oral feeding or intraperitoneal hypertonic glucose-based dialysate in patients with chronic renal failure. Kidney Int 2005;68:2877-85. <a href="http://www.ncbi.nlm.nih.gov/pubmed/16316365" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 12 => array:3 [ "identificador" => "bib13" "etiqueta" => "13" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Sem Dial 2001;14:348-56." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 13 => array:3 [ "identificador" => "bib14" "etiqueta" => "14" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Clerbaux G, Francart J, Wallemacq P, Robert A, Goffi. Evaluation of peritoneal transport properties at onset of peritoneal dialysis and longitudinal follow-up. Nephrol, Dial & Transplant 2006;21:1032-9." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 14 => array:3 [ "identificador" => "bib15" "etiqueta" => "15" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Ishida Y, Tomori K, Nakamoto H, Imai H, Suzuki H. Effects of antihypertensive drugs on peritoneal vessels in hypertensive dogs with mild renal insufficiency. Adv Perit Dial 2003;19:10-4. <a href="http://www.ncbi.nlm.nih.gov/pubmed/14763026" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 15 => array:3 [ "identificador" => "bib16" "etiqueta" => "16" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Ripley EBD, Gehr TWB, Kish CW, Sica DA. Hormonal, blood pressure and peritoneal transport response to short-term ACE inhibition. Perit Dial Int 1994;14:378-83. <a href="http://www.ncbi.nlm.nih.gov/pubmed/7827189" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 16 => array:3 [ "identificador" => "bib17" "etiqueta" => "17" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Coronel F, Berni A, Cigarrán S, Calvo N, Herrero JA. Effects of angiotensin II receptor blocker (irbesartan) on peritoneal membrane functions. Adv Perit Dial 2004;20:27-30. <a href="http://www.ncbi.nlm.nih.gov/pubmed/15384790" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 17 => array:3 [ "identificador" => "bib18" "etiqueta" => "18" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Rojas-Campos E, Cortés-Sanabria L, Martínez-Ramírez HR, González L, Martín del Campo F, González Ortíz M, et a..: Effect of oral administration of losartan, prazosin and verapamil on peritoneal solute transport in CAPD patients. Perit Dial Int 2005;25:576-82. <a href="http://www.ncbi.nlm.nih.gov/pubmed/16411525" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 18 => array:3 [ "identificador" => "bib19" "etiqueta" => "19" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Kolesnyk I, Dekker FW, Noordzij M, Le Cessie S, Struijk D, Krediet RT. Impact of ACE inhibitors and AII receptor blockers on peritoneal membrane transport characteristics in long-term peritoneal dialysis patients. Perit Dial Int 2007;27:44-53." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 19 => array:3 [ "identificador" => "bib20" "etiqueta" => "20" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Nakamoto H, Imai H, Fukushima R, Ishida Y, Yamanouchi Y, Suzuki H. Role of the renin-angiotensin system in the pathogenesis of peritoneal fibrosis. Perit Dial Int 2008;28(Supl. 3):S83-S87. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18552271" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 20 => array:3 [ "identificador" => "bib21" "etiqueta" => "21" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Duman S, Günal AI, Sen S, Asci G, Ozkahya M, Terzioglu E, et al.Does enalapril prevent peritoneal fibrosis induced by hypertonic (3.86%) peritoneal dialysis solution? Perit Dial Int 2001;21:219-24." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 21 => array:3 [ "identificador" => "bib22" "etiqueta" => "22" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Kyuden Y, Ito T, Masaki T, Yorioka N, Kohno N. TGF¿1 induced by high glucose incontrolled by angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker on cultured human peritoneal mesothelial cells. Perit Dial Int 2005;25:483-91. <a href="http://www.ncbi.nlm.nih.gov/pubmed/16178483" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 22 => array:3 [ "identificador" => "bib23" "etiqueta" => "23" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Buemi M, Allegra A, Marino D, Marino MT, Medici MA, De Pasquale G, et al. Does captopril have a direct pro-apoptotic effect? Nephron 1999;81:99-101. <a href="http://www.ncbi.nlm.nih.gov/pubmed/9884429" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 23 => array:3 [ "identificador" => "bib24" "etiqueta" => "24" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Gliklich D, Burris L, Urban A, Tellis V, Greenstein S, Schechner R, et al. Angiotensin-converting enzyme inhibition induces apoptosis in erhthroid precursors and affects insulin-like growth factor-1 in posttransplantation erythrocytosis. J Am Soc Nephrol 2001;12:1958-64. <a href="http://www.ncbi.nlm.nih.gov/pubmed/11518790" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 24 => array:3 [ "identificador" => "bib25" "etiqueta" => "25" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Sica DA, Gehr TWB. Angiotensin-converting enzyme inhibitors. En: Oparil S, Weber MA (eds.). Hypertension. Philadelphia: Elsevier-Saunders, 2005;669-82." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 25 => array:3 [ "identificador" => "bib26" "etiqueta" => "26" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Ruddy MC, Kostis JB. Angiotensin II receptor antagonists. En: En: Oparil S, Weber MA (eds.). Hypertension. Philadelphia: Elsevier-Saunders, 2005;705-24." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 26 => array:3 [ "identificador" => "bib27" "etiqueta" => "27" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Panese S, Martin RS, Virginillo M, Litardo M, Siga E, Arrizurieta E, et al. Mechanism of enhanced transcellular potassium secretion in man with chronic renal failure. Kidney Int 1987;31:1377-82. <a href="http://www.ncbi.nlm.nih.gov/pubmed/3613409" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 27 => array:3 [ "identificador" => "bib28" "etiqueta" => "28" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Sugarman A, Brown RS. The role of aldosterone in potassium tolerance: Studies in anephric humans. Kidney Int 1988;34:397-403. <a href="http://www.ncbi.nlm.nih.gov/pubmed/3172648" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 28 => array:3 [ "identificador" => "bib29" "etiqueta" => "29" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Phakdeekitcharoen B, Leelasa-Nguan P. Effects of an ACE inhibitor or angiotensin receptor blocker on potassium in CAPD patients. Am J Kidney Dis 2004;44:738-46. <a href="http://www.ncbi.nlm.nih.gov/pubmed/15384026" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 29 => array:3 [ "identificador" => "bib30" "etiqueta" => "30" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Smith JM, Jones AW. Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats. Hypertension 1990;15:78-83. <a href="http://www.ncbi.nlm.nih.gov/pubmed/2295515" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 30 => array:3 [ "identificador" => "bib31" "etiqueta" => "31" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Thompson-Vest N, Shimizu Y, Hunne B, Furness JB. The distribution of\u{A0} intermediate conductance, calcium-activated, potassium channels in epithelial cells. J Anat 2006;208:219-29. <a href="http://www.ncbi.nlm.nih.gov/pubmed/16441566" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/20132514/0000003000000001/v0_201502091608/X2013251410033800/v0_201502091609/en/main.assets" "Apartado" => array:4 [ "identificador" => "35441" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Originals" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/20132514/0000003000000001/v0_201502091608/X2013251410033800/v0_201502091609/en/P1-E43-S1785-A10036-EN.pdf?idApp=UINPBA000064&text.app=https://revistanefrologia.com/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X2013251410033800?idApp=UINPBA000064" ]
| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 5 | 6 | 11 |
| 2024 October | 52 | 31 | 83 |
| 2024 September | 44 | 23 | 67 |
| 2024 August | 75 | 48 | 123 |
| 2024 July | 50 | 19 | 69 |
| 2024 June | 67 | 36 | 103 |
| 2024 May | 70 | 29 | 99 |
| 2024 April | 55 | 38 | 93 |
| 2024 March | 60 | 31 | 91 |
| 2024 February | 50 | 36 | 86 |
| 2024 January | 42 | 36 | 78 |
| 2023 December | 47 | 27 | 74 |
| 2023 November | 33 | 34 | 67 |
| 2023 October | 70 | 24 | 94 |
| 2023 September | 57 | 37 | 94 |
| 2023 August | 24 | 20 | 44 |
| 2023 July | 47 | 26 | 73 |
| 2023 June | 37 | 23 | 60 |
| 2023 May | 50 | 35 | 85 |
| 2023 April | 37 | 32 | 69 |
| 2023 March | 44 | 26 | 70 |
| 2023 February | 44 | 21 | 65 |
| 2023 January | 36 | 18 | 54 |
| 2022 December | 44 | 35 | 79 |
| 2022 November | 70 | 22 | 92 |
| 2022 October | 46 | 27 | 73 |
| 2022 September | 43 | 35 | 78 |
| 2022 August | 60 | 44 | 104 |
| 2022 July | 38 | 47 | 85 |
| 2022 June | 46 | 37 | 83 |
| 2022 May | 57 | 38 | 95 |
| 2022 April | 49 | 33 | 82 |
| 2022 March | 66 | 46 | 112 |
| 2022 February | 37 | 40 | 77 |
| 2022 January | 56 | 30 | 86 |
| 2021 December | 40 | 48 | 88 |
| 2021 November | 43 | 32 | 75 |
| 2021 October | 61 | 49 | 110 |
| 2021 September | 26 | 36 | 62 |
| 2021 August | 39 | 27 | 66 |
| 2021 July | 52 | 34 | 86 |
| 2021 June | 32 | 17 | 49 |
| 2021 May | 39 | 24 | 63 |
| 2021 April | 49 | 58 | 107 |
| 2021 March | 26 | 8 | 34 |
| 2021 February | 57 | 17 | 74 |
| 2021 January | 29 | 27 | 56 |
| 2020 December | 34 | 12 | 46 |
| 2020 November | 41 | 10 | 51 |
| 2020 October | 19 | 11 | 30 |
| 2020 September | 28 | 5 | 33 |
| 2020 August | 39 | 7 | 46 |
| 2020 July | 45 | 14 | 59 |
| 2020 June | 30 | 6 | 36 |
| 2020 May | 69 | 12 | 81 |
| 2020 April | 33 | 11 | 44 |
| 2020 March | 48 | 21 | 69 |
| 2020 February | 31 | 15 | 46 |
| 2020 January | 48 | 12 | 60 |
| 2019 December | 39 | 19 | 58 |
| 2019 November | 58 | 23 | 81 |
| 2019 October | 36 | 14 | 50 |
| 2019 September | 32 | 19 | 51 |
| 2019 August | 27 | 14 | 41 |
| 2019 July | 32 | 19 | 51 |
| 2019 June | 44 | 16 | 60 |
| 2019 May | 43 | 17 | 60 |
| 2019 April | 66 | 28 | 94 |
| 2019 March | 30 | 28 | 58 |
| 2019 February | 31 | 20 | 51 |
| 2019 January | 56 | 21 | 77 |
| 2018 December | 104 | 37 | 141 |
| 2018 November | 108 | 14 | 122 |
| 2018 October | 105 | 14 | 119 |
| 2018 September | 85 | 14 | 99 |
| 2018 August | 59 | 15 | 74 |
| 2018 July | 55 | 13 | 68 |
| 2018 June | 44 | 8 | 52 |
| 2018 May | 61 | 17 | 78 |
| 2018 April | 51 | 7 | 58 |
| 2018 March | 35 | 13 | 48 |
| 2018 February | 46 | 8 | 54 |
| 2018 January | 37 | 9 | 46 |
| 2017 December | 47 | 9 | 56 |
| 2017 November | 35 | 15 | 50 |
| 2017 October | 37 | 13 | 50 |
| 2017 September | 35 | 12 | 47 |
| 2017 August | 29 | 6 | 35 |
| 2017 July | 38 | 9 | 47 |
| 2017 June | 38 | 16 | 54 |
| 2017 May | 54 | 11 | 65 |
| 2017 April | 34 | 5 | 39 |
| 2017 March | 34 | 9 | 43 |
| 2017 February | 47 | 13 | 60 |
| 2017 January | 18 | 9 | 27 |
| 2016 December | 55 | 10 | 65 |
| 2016 November | 74 | 6 | 80 |
| 2016 October | 98 | 7 | 105 |
| 2016 September | 146 | 5 | 151 |
| 2016 August | 162 | 0 | 162 |
| 2016 July | 160 | 4 | 164 |
| 2016 June | 128 | 0 | 128 |
| 2016 May | 141 | 0 | 141 |
| 2016 April | 97 | 0 | 97 |
| 2016 March | 89 | 0 | 89 |
| 2016 February | 115 | 0 | 115 |
| 2016 January | 116 | 0 | 116 |
| 2015 December | 130 | 0 | 130 |
| 2015 November | 106 | 0 | 106 |
| 2015 October | 82 | 0 | 82 |
| 2015 September | 87 | 0 | 87 |
| 2015 August | 75 | 0 | 75 |
| 2015 July | 81 | 0 | 81 |
| 2015 June | 40 | 0 | 40 |
| 2015 May | 56 | 0 | 56 |
| 2015 April | 6 | 0 | 6 |
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