Pathophysiological mechanisms of postrevascularization hyperkalemia in orthotopic liver transplantation

The underlying mechanisms of hyperkalemia occurring immediately after revascularization in orthotopic liver transplantation (OLT) are unknown. We investigated the possible pathophysiological mechanisms of hyperkalemia in relation to the donor and recipient. The study included 64 consecutive patients undergoing OLT. Recipients were divided into two groups: Group 1 consisted of 47 patients with serum K(+) concentration <5.5 mmol/L at 1-min postrevascularization, and Group 2 consisted of 17 patients with serum K(+) exceeding 5.5 mmol/L. Increased serum K(+) concentration, more progressive metabolic acidosis, and decreased mean arterial blood pressure and cardiac index during the anhepatic phase were recognized in Group 2. Multiple regression analysis showed that cardiac index, serum lactate, and serum K(+) concentration during the anhepatic phase were independent and significant factors that could predict serum K(+) concentration 1-min postrevascularization. Hyperkalemia at 1-min postrevascularization did not correlate with the extent of preservation injury of the graft liver (represented by the peak value of aspartate aminotransferase measured within the first 72 h after OLT) or the duration of cold ischemia. We conclude that hyperkalemia occurring immediately after revascularization in OLT is mainly caused by metabolic acidosis as a result of insufficient cardiac output during the anhepatic phase.     

Intraoperative hypokalemia in pediatric liver transplantation: incidence and risk factors

In this retrospective study of 268 children undergoing liver transplantation, we investigated the incidence of intraoperative potassium (K+) disturbances and the risk factors for hypokalemia in the preperfusion and postreperfusion periods. Overall, hypokalemia was the predominant disturbance, occurring in 72.0% of pediatric patients during liver transplantation. Hypokalemia was more common during the postreperfusion period than the prereperfusion period. Hyperkalemia, though a commonly cited complication, was infrequent during pediatric liver transplantation. Using multivariate logistic regression analysis, baseline serum K+ < or =3.5 mmol/L, base excess >5 mmol/L, and creatinine < or =0.5 mg/dL were found to be predictors for hypokalemia in the prereperfusion period; and body weight < or =15 kg, K+ < or =3.5 mmol/L, fresh-frozen plasma transfusion >90 mL/kg, and absence of ascites at surgery were independent predictors for hypokalemia in the postreperfusion period. These findings support the use of K+ replacement to maintain normokalemia and avoid the potential complications related to hypokalemia in pediatric liver transplantation, especially in children with the risk factors for hypokalemia.     

Serum calcium increases the incidence of arrhythmias during acetate hemodialysis.

We investigated the occurrence of arrhythmias during maintenance acetate hemodialysis (HD) using a 24-hour continuous electrocardiogram recording system. Three of 22 patients showed augmented increases in both ventricular premature beats and supraventricular premature beats during HD. When we changed the dialysate from one with a Ca2+ concentration of 1.75 mmol/L (3.5 mEq/L), to one with a Ca2+ concentration of 1.25 mmol/L (2.5 mEq/L), the elevation of serum Ca2+ concentration during HD was abolished and the increases in both ventricular premature beats and supraventricular premature beats were significantly decreased. The elevation of serum Ca2+ concentration during HD might induce either extracellular or intracellular increase in Ca2+ concentration in the heart and elicit either reentry- or triggered-activity types of arrhythmias during HD. The present results indicate that the dialysate with a lower Ca2+ concentration is advisable to use in patients with underlying cardiac diseases.     

Renin-Angiotensin System Blockade Is Not Associated with Hyperkalemia in Chronic Hemodialysis Patients

Background.?Serious hyperkalemia was reported in 10% of chronic hemodialysis (HD) patients that could lead to arrhythmia and death. Angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin II receptor blockers (ARB) are well accepted for cardio-protective benefits. The relationship between renin-angiotensin system blockade (RASB) and hyperkalemia in chronic HD patients remains controversial. The aim of this study was to find the relationship between RASB and hyperkalemia in these patients.?Methods.?Pre-dialysis serum potassium, clinical factors, and drugs were evaluated in 200 chronic HD patients in one HD center. Hyperkalemia was defined as serum K ≥ 5.3 meq/L. Finally, multivariate analysis with logistic regression was used to evaluate the risk of hyperkalemia by RASB and other factors. Results.?In 200 patients, the mean K was 4.93 ± 0.79 meq/L, and 70 (35%) patients had hyperkalemia. Fifty-eight (29%) patients were prescribed with RASB. Seven variables—non-DM, longer HD duration, lower dialysate calcium, lower serum glucose, higher serum iPTH, not using RASB, and not using furosemide—were more frequent in hyperkalemia group. In logistic regression analysis, RASB was associated with decreased odds for hyperkalemia (OR 0.262, p = 0.001 in model A; OR 0.205, p = 0.001 in model B). In addition, furosemide was associated with decreased odds for hyperkalemia (OR 0.068, p = 0.022 in model B).?Conclusions.?RASB is not associated with hyperkalemia in chronic HD patients.     

The faster potassium-lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients.

BACKGROUND: Hyperkalaemia is common in patients with advanced renal disease. In this double-blind, randomized, three-sequence, crossover study, we compared the effect of three dialysate bicarbonate concentrations ([HCO3-]) on the kinetics of serum potassium (K+) reduction during a conventional haemodialysis (HD) session in chronic HD patients. METHODS: We studied eight stable HD patients. The choice of dialysate [HCO3-] followed a previously assigned treatment protocol and the [HCO3-] used were low bicarbonate (LB; 27 mmol/l), standard bicarbonate (SB; 35 mmol/l) and high bicarbonate (HB; 39 mmol/l). Polysulphone dialysers and automated machines provided blood flow rates of 300 ml/min and dialysis flow rates of 500 ml/min for each HD session. Blood samples were drawn at 0 (baseline), 15, 30, 60 and 240 min from the arterial extracorporeal line to assess blood gases and serum electrolytes. In three of the eight patients, we measured serum K+ 1 h post-dialysis as well as K+ removal by the dialysis. The same procedures were followed until the completion of the three arms of the study, with a 1 week interval between each experimental arm. RESULTS: Serum K+ decreased from 5.4+/-0.26 (baseline) to 4.96+/-0.20, 4.90+/-0.19, 4.68+/-0.13 and 4.24+/-0.15 mmol/l at 15, 30, 60 and 240 min, respectively, with LB; from 5.38+/-0.21 to 5.01+/-0.23, 4.70+/-0.25, 4.3+/-0.15 and 3.8+/-0.19 mmol/l, respectively, with SB; and from 5.45+/-0.25 to 4.79+/-0.17, 4.48+/-0.17, 3.86+/-0.16 and 3.34+/-0.11 mmol/l, respectively, with HB (P<0.05 for high vs standard and low [HCO3-] at 60 and 240 min). The decrease in serum K+ correlated with the rise in serum [HCO3-] in all but LB (P<0.05). Potassium rebound was 3.9+/-10.2%, 5.2+/-6.6% and 8.9+/-4.9% for LB, SB and HB dialysates, respectively (P=NS), while total K+ removal (mmol/dialysis) was 116.4+/-21.6 for LB, 73.2+/-12.8 for SB and 80.9+/-15.4 for HB (P=NS). CONCLUSIONS: High dialysate [HCO3-] was associated with a faster decrease in serum K+. Our results strongly suggest that this reduction was due to the enhanced shifting of K+ from the extracellular to the intracellular fluid compartment rather than its removal by dialysis. This finding could have an impact for those patients with life-threatening pre-HD hyperkalaemia.     

Effect of preoperative colon preparation on serum potassium

Although surgeons and anesthesiologists are constantly warned of the danger of hypokalemia following mechanical bowel preparations during the peri- and intraoperative periods, the amount and significance of this problem have not been quantitated. Therefore, the magnitude of the potassium (K+) depletion resulting from three to four days of mechanical bowel preparation was measured in a randomized, prospective fashion in 53 patients. The 27 patients in Group I received intravenous and/or oral potassium chloride supplementation during the preoperative bowel preparation, while the 26 patients in Group II received no supplementation. In an additional five patients, renal and colonic excretory potassium losses were measured to determine if they correlated with preoperative serum potassium levels. All patients had a standard preparation consisting of clear liquid diet (15 mmol K+/day), magnesium citrate orally, enemas, and oral antibiotics. Serum K+ levels in patients in Group I decreased from control levels of 4.01 + 0.41 mmol/1 to 3.71 +/- 0.58 (P less than 0.01) despite an average of 60 mmol potassium chloride supplementation during the preparation. The serum potassium levels in patients in Group II decreased from 4.13 + 0.69 mmol/1 to 3.43 +/- 0.53 (P less than 0.001) during the preparation. Measurement of stool K+ content revealed values that varied considerably between patients and that did not correlate with immediate preoperative serum levels. Urinary K+ measurement showed little renal compensation during the preparation and it did not significantly correlate with preoperative serum levels either.     

Dialysate magnesium level and blood pressure

BACKGROUND: We investigated the way dialysate magnesium (dMg) concentrations could affect blood pressure (BP) during hemodialysis (HD). METHODS: Eight HD patients underwent four midweek HD treatments consecutively, using, during each four-hour HD session, one of the following four dialysate formulations, in randomized order, which differed only with regard to dMg and dialysate calcium (dCa) concentrations (in mmol/L): 0.75 dMg, 1.75 dCa (group I); 0.25 dMg, 1.75 dCa (group II); 0.75 dMg, 1.25 dCa (group III); 0.25 dMg, 1.25 dCa (group IV). Before HD and at four 60-minute intervals during the HD sessions, BP and noninvasive measurements of cardiac index (CI) were obtained. Additionally, 14 HD patients were treated for four weeks with 0.5 mmol/L dMg, followed by four weeks with 0.25 mmol/L dMg, and another four weeks with 0.75 mmol/L dMg, in random order. In all treatments dCa was 1.25 mmol/L. BP and symptoms were recorded during each HD session. RESULTS: Mean arterial pressure (MAP) decreased to a significantly (P < 0.05) greater extent in group IV compared to the other groups. This substantial drop in MAP by 15.2% in group IV, paralleled by a 12.1% and 17% drop in CI and stroke index, respectively, was not seen in group II, despite comparable reductions in intradialytic serum Mg (sMg) of about 35% in both groups. In groups I and III, the increase in sMg by 2% did not compromise BP via vasodilatation. In the second study, treatment with 0.75 mmol/L dMg was superior to the other two treatments regarding intradialytic morbidity (P < 0.001) and BP stability (P < 0.05). CONCLUSION: We (1) identified a dialysis solution containing 0.25 mmol/L Mg and 1.25 mmol/L Ca as a major cause of intradialytic hypotension (IDH) due to an impairment of myocardial contractility, and (2) showed that increasing dMg level to 0.75 mmol/L could prevent IDH frequently seen with the use of 1.25 mmol/L dCa. Thus, manipulating dMg levels independently or in concert with dCa levels might have important implications with regard to dialysis tolerance.     

Studies to determine the basis for hyperkalemia in recipients of a renal transplant who are treated with cyclosporine.

Hyperkalemia is commonly encountered in patients who receive a renal transplant and the immunosuppressive drug, cyclosporine. There is also a high incidence of hypertension (which is thought to be due to expansion of the extracellular fluid volume) and hyperchloremic metabolic acidosis in this group of patients. This constellation of findings led to the suspicion of the possibility that their basis might be type II hypoaldosteronism. To test this hypothesis, 12 patients with hyperkalemia (plasma K+, 5.1 +/- 0.2 mmol/L at the time of study) while receiving cyclosporine were studied. Patients who had diabetes mellitus, those receiving drugs known to cause hyperkalemia (e.g., beta blockers, angiotensin-converting enzyme inhibitors, K(+)-sparing diuretics), or those with a serum creatinine greater than 200 mumol/L were excluded. The renal response to hyperkalemia was inappropriate because the transtubular K+ concentration gradient (TTKG) was only 4.3 +/- 0.4 compared with a TTKG of 13 +/- 1, 2 h after 50 mmol of KCl was given to normal subjects. The TTKG, after administration of 200 micrograms of fludrocortisone, was still very low (5.6 +/- 0.6) in the patients compared with that of controls (12 +/- 1). After administration of 250 to 500 mg of acetazolamide to increase the delivery of bicarbonate to the distal nephron, the TTKG rose significantly to 11 +/- 1 in patients on cyclosporine, compared with 17 +/- 1 in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Calcium exposure and removal in chronic hemodialysis patients.

The risks associated with calcium exposure in chronic hemodialysis (HD) patients are becoming increasingly apparent. Current K/DOQI guidelines recommend an absolute maximum elemental calcium load of 2,000 mg/d, including calcium-containing medication and a maximum dialysate calcium concentration of 1.25 mmol/L (to avoid intradialytic calcium loading). The goal of this study was to characterize the total exposure to calcium from all sources that chronic HD patients are exposed to. We studied 52 patients. Each was requested to complete a 3-day food diary for analysis of daily calcium intake; 24-hour urine collections were taken and analyzed for calcium content. All patients underwent HD using Hospal Integra (Lyon, France) dialysis monitors, bicarbonate buffering, and dialysate sodium and calcium concentrations of 134 mmol/L and 1.25 mmol/L, respectively. Blood was sampled before and after HD for total serum calcium, albumin, bicarbonate, and phosphate, in addition to ionized calcium level measured at the bedside using a portable electrolyte analyzer. Calcium flux was determined from measurements of ionized calcium levels in dialyzer inlet samples and those in continuous partial waste dialysis collection (with reference to total waste dialysate and ultrafiltration volumes). There was marked interpatient variability of total calcium exposure; the mean was 2,346 +/- 293 mg (range, 230 to 7,309 mg) per day. The majority of enteral calcium exposure was from calcium-containing phosphate binders, with diet providing only a mean load of 581 +/- 34 mg (range, 230 to 1,309 mg). Calcium removal was evident in 83% of patients. Mean calcium flux was -187 +/- 232 mg (range, -486 to 784 mg). There was a linear correlation observed between the amount of calcium removed during dialysis and the predialysis ionized plasma calcium concentration, r2 = 0.42, P < .001 (calculated from actual measured dialysate ionized calcium concentration). This shows that calcium flux across the dialysis membrane is determined by the diffusion gradient. The amount of calcium removed during dialysis was found to be independent of exogenous calcium load. These results support previous reported data showing that the majority of HD patients are continually experiencing calcium overload. This may have a contributory role in the development of vascular calcification. In contrast to recent K/DOQI recommendations, an upper dialysate concentration of 1.25 mmol/L may not be ideal for every patient. To minimize the effects of exogenous calcium overload, dialysate concentrations should be prescribed with reference to plasma calcium levels.     

QTc dispersion increases during hemodialysis with low-calcium dialysate

BACKGROUND: The risk of ventricular arrhythmias is known to increase during hemodialysis (HD) treatment, but the cause of this phenomenon has remained unidentified. QT dispersion (= QTmax - QTmin) reflects heterogeneity of cardiac repolarization, and increased dispersion is known to predispose the heart to ventricular arrhythmias and sudden cardiac death. METHODS: We studied the effect of dialysate calcium concentration on cardiac electrical stability during HD treatment in 23 end-stage renal disease patients. Three HD treatments were applied with dialysate Ca++ concentrations of 1.25 mmol/L (dCa++1.25), 1.5 mmol/L (dCa++1.5), and 1.75 mmol/L (dCa++1.75). The QTc interval and QTc dispersion were measured before and after the three sessions. RESULTS: With the dCa++1.5 and dCa++1.75 dialyses, serum Ca++ increased and the QTc interval remained stable (dCa++1.5) or decreased (dCa++1.75), but no significant change was noted in QTc dispersion. With dCa++1.25 HD, serum Ca++ decreased (1.24 +/- 0.11 vs. 1.20 +/- 0.09 mmol/L, P < 0. 05), and both the QTc interval (403 +/- 27 vs. 419 +/- 33 ms, P < 0. 05) and QTc dispersion increased (38 +/- 19 vs. 49 +/- 18 ms, P < 0. 05). The change in the QTc interval correlated inversely with the change in serum Ca++ (r = -0.68, P < 0.0001). Except for serum Ca++ and plasma intact parathyroid hormone, predialysis and postdialysis values in other blood chemistry, blood pressure, heart rate, body weight, and total ultrafiltration were equal in the three dialysis sessions. CONCLUSION: This study is the first, to our knowledge, to demonstrate that HD increases QTc dispersion if a low-calcium (dCa++1.25) dialysate is used. This indicates that the use of low-calcium dialysate may predispose HD patients to ventricular arrhythmias and that perhaps it should be avoided, at least when treating patients with pre-existing cardiac disease.     

Plasma potassium in patients with terminal renal failure during and after haemodialysis; relationship with dialytic potassium removal and total body potassium

Background: Chronic haemodialysis (HD) patients may present with severe predialysis hyperkalaemia which is improved by dialytic treatment. However, factors influencing the behaviour of postdialysis plasma potassium (plasma K) are not well known. Method: In this prospective study 14 patients (7 female, 7 male) on chronic HD were investigated during a standardized 4-h HD with a 2 m² high-flux dialyser and up to 6 h postdialysis. Dialytic potassium removal was measured by dialysate collection. Total body potassium (TBK) was measured by whole-body counting of ⁴⁰K. Results: Plasma K declined from 5.65 to 3.62 mmol/l of HD. In spite of a total dialytic removal of 107 mmol of potassium plasma K rose to 5.01 mmol/16 h postdialysis. TBK, as adjusted for age, was 38.2 and 49.0 mmol/kg B2 in female and male patients respectively, i.e. in the normal range. Of a total potassium removal of 107 mmol on HD only 42% originated from the extracellular space. Dialytic potassium removal was best correlated with removal of intracellular potassium but also with extracellular potassium content and with the product of plasma K x TBK. The 6-h postdialysis plasma K was correlated with the predialysis value but not with TBK or dialytic potassium removal. Conclusion: A rather high dialytic removal of potassium (which is correlated with plasma K x TBK) does not necessarily prevent a rapid postdialysis rebound of plasma K. Therefore patients with marked hyperkalaemia should be monitored closely postdialysis. TBK can be normal in haemodialysis patients who are well nourished.     

Iodine-induced thyrotoxic hypokalemic paralysis after ingestion of Salicornia herbace

A 56-year-old Korean man visited to emergency room due to paroxysmal flaccid paralysis in his lower extremities. There was no family or personal history of periodic paralysis. His initial potassium levels were 1.8?mmol/L. The patient had been taking Salicornia herbacea for the treatment of diabetes and hypertension. Results of a thyroid function test were as follows: T3?=?130.40?ng/dL, TSH?=?0.06?mIU/L, and free T4?=?1.73?ng/dL. A thyroid scan exhibited a decreased uptake (0.6%). His symptoms clearly improved and serum potassium levels increased to 4.4?mmol/L by intravenous infusion of only 40?mmol of potassium chloride. Eight months after the discontinuation of only Salicornia herbacea, the patient’s thyroid function tests were normalized. Large amounts of iodine can induce hypokalemic thyrotoxic paralysis and it may be necessary to inquire about the ingestion of iatrogenic iodine compounds, such as Salicornia herbacea.     

Intraoperative bradycardia and postoperative hyperkalemia in patients undergoing endoscopic third ventriculostomy.

During our initial experience with endoscopic third ventriculostomies, we observed intraoperative bradycardia and postoperative hyperkalemia. The present study was carried out to verify the consistency of these initial observations. Intraoperative heart rate (HR) changes and postoperative serum K + changes were studied prospectively in 20 patients of endoscopic third ventriculostomy. Another 6 patients who underwent endoscopic procedures other than ventriculostomy acted as controls. The anaesthetic technique and intraoperative and postoperative fluid regimen were similar in all patients. Serum K + concentrations were measured intraoperatively and once a day for the next 5 days. The third ventriculostomy group exhibited a significant slowing of the heart rate during the fenestration of the floor of the third ventricle (112 +/- 26 to 101 +/- 28 bpm, p < 0.001) and also at the time of the reversal of the neuromuscular block at the end of surgery (104 +/- 29 to 96 +/- 33 bpm, p < 0.01). The control group did not exhibit similar changes in the heart rate. The postoperative increase in serum K + values in the ventriculostomy group (0.82 +/- 0.55 mmol/L) was higher than that in the control group (0.10 +/- 0.44 mmol/L) (p < 0.01). Endoscopic third ventriculostomy is associated with a significant bradycardia at the time of fenestration and at the time of reversal of the neuromuscular block. The procedure is also associated with a postoperative increase in serum K + values. We propose a mechanism involving distortion of the posterior hypothalamus, which accounts for the bradycardia and postoperative hyperkalemia.     

Ion-channel currents of smooth muscle cells isolated from the prostate of guinea-pig

OBJECTIVE: To characterize the voltage-activated ion-channel currents in guinea-pig prostate smooth muscle cells (GPSMCs). MATERIALS AND METHODS: GPSMCs were isolated using collagenase, and used in a whole-cell patch clamp study. RESULTS: When GPSMCs were dialysed with a CsCl solution all the outward K+ currents were blocked and the step-like depolarization (holding voltage -70 mV) of the cell membrane evoked inward currents that were completely blocked by nifedipine (1 micromol/L). With KCl solution, step depolarizations showed outward K+ currents composed of fast, transient outward current (Ito) and outward currents that did not inactivate. Ito was resistant to a high concentration of tetraethylammonium (TEA, 5 mmol/L) but was blocked by 4-aminopyridine (5 mmol/L). The half-activation and half-inactivation voltages of Ito were 6 mV and -58 mV, respectively. With low Ca2+ buffer (0.1 mmol/L EGTA) in the solution, there were spontaneous transient outward currents (STOCs) at depolarized membrane voltages (0 mV). STOCs were blocked by TEA (1 mmol/L) or iberiotoxin (10 nmol/L) but were insensitive to apamin (100 nmol/L). CONCLUSION: This voltage-clamp study showed that GPSMCs have l-type Ca2+ channels and more than two types of K+ channels. The voltage- and time-dependent changes of these ion channels and their interactions might be important in forming action potentials and regulating contractility.     

Intracellular free calcium accumulation in ferret vascular smooth muscle during crystalloid and blood cardioplegic infusions.

OBJECTIVE: The effects of magnesium- and potassium-based crystalloid and blood-containing cardioplegic solutions on coronary smooth muscle intracellular free calcium ([Ca2+]i) accumulation and microvascular contractile function were examined. METHODS: Isolated ferret hearts were subjected to hyperkalemic (25 mmol/L K+) blood cardioplegic infusion, hypermagnesemic (25 mmol/L Mg2+, K+-free) crystalloid cardioplegic infusion, or hyperkalemic crystalloid cardioplegic infusion for 1 hour. Coronary arterioles were isolated, cannulated, and loaded with fura 2. Reactivity and [Ca2+]i were assessed with videomicroscopy. [Ca2+]i was measured at baseline and after application of 50 mmol/L KCl. In addition, [Ca2+]i and vascular contraction were measured during exposure to Mg2+ and K+ cardioplegic solution at both 4 degrees C and 37 degrees C. RESULTS: From a baseline [Ca2+]i of 177 +/- 52 nmol/L, K+ cardioplegic infusion (302 +/- 80 nmol/L potassium) markedly increased [Ca2+]i, whereas blood cardioplegic infusion (214 +/- 53 nmol/L) and Mg2+ cardioplegic infusion (180 +/- 42 nmol/L) did not alter [Ca2+]i. Although a difference between groups in percentage contraction after application of 50 mmol/L KCl was not observed, [Ca2+]i increased significantly more in vessels in the control group (764 +/- 327 nmol/L) and the K+ crystalloid cardioplegic infusion group (698 +/- 215 nmol/L) than in vessels in the blood cardioplegic infusion group (402 +/- 45 nmol/L) and the Mg2+ cardioplegic infusion group (389 +/- 80 nmol/L). Mg2+ cardioplegic solution induced no microvascular contraction at either 4 degrees C or 37 degrees C, nor was an increase in [Ca2+]i observed. K+ cardioplegic solution induced microvascular contraction at 37 degrees C but not at 4 degrees C; it increased [Ca2+]i at both 4 degrees C and 37 degrees C. CONCLUSION: An Mg2+-based cardioplegic solution, or appropriate Mg2+ or blood supplementation of a K+ crystalloid cardioplegic solution, may decrease the accumulation of [Ca2+]i in the vascular smooth muscle during ischemic arrest.     

Dialysate bath and QTc interval in patients on chronic maintenance hemodialysis: pilot study of single dialysis effects

Introduction: Serum concentrations of potassium (K) and calcium (Ca) influence ionic currents and play an important role in the duration of ventricular action potential. Further, the influence of alkalosis in reducing ionized calcium has been well known for a long time. The aim of this study was to assess the effects of different dialysate electrolytes and bicarbonate concentrations on changes of QTc interval in patients on chronic hemodialysis. Methods: The study hemodialysis sessions were performed in 22 patients, with different electrolyte and bicarbonate concentrations in dialysate. Tested dialysate concentrations were K of 2 and 3 mmol/L; Ca 1.25, 1.5 and 1.75 mmol/L; and bicarbonate 30 and 34 mmol/L. An electrocardiogram (ECG) was recorded 1 hour before, at the end and every hour for 4 hours after each study dialysis session. QTc interval was measured from the beginning of the QRS complex to the end of a T wave on a 12-lead ECG. Blood was collected and K, total Ca, ionic Ca and pH evaluated. Results: At the end of the study hemodialysis session with dialysate containing low K (2 mmol/L), low Ca (1.25 mmol/L) and high bicarbonate concentration (34 mmol), mean QTc interval was significantly prolonged compared with that recorded with dialysate containing high K (3 mmol/L), high Ca (1.75 mmol/L) and bicarbonate (30 mmol) (40 ± 10 milliseconds vs. 2 ± 2 milliseconds; p<0.01). Dialysate with low concentration of low Ca, K and high concentration of bicarbonate was an independent predictor of QTc; the combination of low Ca and K and high bicarbonate strongly increased the risk of prolonged QTc interval. Conclusion: The present pilot study shows that changes in QTc interval during hemodialysis depend on both electrolyte and bicarbonate concentrations in dialysate.     

库存红细胞清洗在新生儿及小婴儿体外循环手术中的应用

目的 对比体外循环(CPB)心脏手术中接受洗涤及未洗涤的库存红细胞(PRBC)对血清钾离子浓度(K+)及乳酸浓度(LAC)的影响.方法 选取复杂先天性心脏病(先心病)行CPB心脏手术的新生儿及小婴儿为研究对象,排除术前血乳酸大于3.0mmol/L的病婴.对照组(15例)接受未洗涤的PRBC进行CPB预充及术中添加,试验组(15例)接受用血液回收机(Medtronic Autolog)洗涤过的PRBC.在CPB前、CPB 3、15min、CPB复温、停止CPB前、术毕、术后4、24h比较血K+及LAC浓度.结果 洗涤PRBC显著降低供血中K+浓度[从(19.3±0.9)mmol/L降至(1.1±0.3)mmol/L,p<0.001]及IAC浓度[从>15mmol/L降至(7.8±1.2)mmol/L,P<0.001].对照组预充液的K+及ILAC浓度显著高于试验组[K+(9.0±0.5)rranol/L对(2.6±0.1)mmol/L,P<0.001;LAC浓度(9.5±0.5)mmol/L对(4.7±1.1)nrml/L,P<0.001].CPB 3min、CPB复温时对照组血清K+浓度显著高于试验组[CPB 3 min(5.6±0.9)mmol/L对(3.5±0.4)mmol/L,P<0.01;CPB复温时(4.8±0.7)mmol/L对(3.7±0.6)mmol/L,P<0.01];其余时点对照组K+浓度高于试验组,差异无统计学意义.CPB 3、15 min、CPB复温、停止CPB前、术毕、术后4 h对照组IAC浓度高于试验组,但差异无统计学意义.结论 洗涤PRBC降低血清钾及乳酸负荷,可预防cPB中高血钾.在新生儿及小婴儿复杂先心病CPB手术中应考虑应用清洗PRBC.     

Low-potassium and glucose-free dialysis maintains urea but enhances potassium removal.

BACKGROUND: The influence of potassium (K) removal on dialysis efficiency as measured by urea elimination is not clear. In this prospective, randomized, cross-over study we investigated the magnitude of K removal and its effect on urea (u) elimination during high-flux haemodialysis (HD). METHODS: Twelve stable, non-diabetic HD patients were investigated during three one-week standardized HD periods (1.8 m(2) high-flux polysulphone dialyser, treatment time 240 min, Qb = 300 ml/min, Qd = 500 ml/min, dialysate without glucose, bicarbonate 40 mmol/l), using dialysates containing 0 (0K), 1 (1K), and 2 (2K) mmol/l of K. Mass removal of K (M(K)) and u (M(U)) were measured during the mid-week treatment by partial dialysate collection. Urea reduction rate (URR) and Kt/V were determined. RESULTS: 0K, 1K and 2K treatments were perfectly comparable. Plasma K (PK) continuously declined reaching stable concentrations after 180 min. While 0K dialysate removed 117.1 mmol, 80.2 and 63.3 mmol (P < 0.001) were removed by 1K and 2K baths respectively. M(U) was not influenced by M(K) (r = 0.22) and amounted to 491.1 (0K), 508.6 (1K), and 506.2 (2K) mmol (NS) respectively. Accordingly, urea clearance, URR and Kt/V were constant during 0K, 1K and 2K treatments. CONCLUSIONS: Potassium-free dialysate significantly enhances potassium elimination. Potassium removal has no influence on urea elimination. High potassium removal, when needed, does not impair dialysis efficiency as measured by urea kinetics in high-flux, glucose-free, 40 mmol/l bicarbonate HD.     

Influence of sevelamer hydrochloride on serum concentration of whole (1-84) and N-terminally truncated (7-84) parathyroid hormone fragments in hemodialysis uremic patients

Phosphate retention stimulates parathyroid hormone (PTH) secretion in uremic patients. Sevelamer hydrochloride is an aluminium- and calcium-free phosphate binder used in the treatment of secondary hyperparathyroidism in uremic patients. The influence of the phosphate lowering effect on serum levels of whole PTH-1-84 and N-terminally truncated PTH-7-84 has not been studied. Seventeen hemodialysis (HD) patients (nine male, eight female) with chronic renal failure and serum phosphorus concentrations, despite calcium carbonate treatment, >2.0 mmol/L were enrolled in this study. Patients did not receive aluminium containing binders. Blood samples for serum concentration assessments of calcium, phosphorus, PTH-1-84 and N-terminally truncated PTH-7-84, carboxyterminal cross-linked collagen fragments (Ctx), total (AP) and bone specific alkaline phosphatase activity (BAP) were drawn twice: before and after 5-week sevelamer administration (in addition to calcium carbonate). Sevelamer treatment was followed by a significant reduction in serum phosphorus level (from 2.46 +/- 0.09 to 2.07 +/- 0.10 mmol/L; p=0.009), PTH-1-84 level (from 396 +/- 75 to 298 +/- 64 pg/mL; p=0.03) and PTH-1-84/PTH-7-84 ratio (from 1.78 +/- 0.18 to 1.55 +/- 0.19; p=0.01), while serum PTH-7-84 levels declined only slightly (from 220 +/- 35 to 183 +/- 25 pg/mL; p=0.11). Serum calcium, Ctx concentrations, AP and BAP activity did not change markedly. There was a significant positive correlation between changes of phosphorus and PTH-1-84 (tau=0.48; p=0.007) or PTH-7-84 concentration (tau=0.43; p=0.02). A 5-week sevelamer treatment suppressed both PTH-1-84 (change statistically significant) and PTH-7-84 (change statistically non-significant) serum concentration in HD uremic patients seemingly related to changes in phosphatemia.