Hypokalemia in Chinese Peritoneal Dialysis Patients: Prevalence and Prognostic Implication Cheuk-Chun Szeto, MD, Kai-Ming Chow, MBChB, Bonnie Ching-Ha Kwan, MBBS, Chi-Bon Leung, MBChB, Kwok-Yi Chung, MBChB, Man-Ching Law, BN, RN, and Philip Kam-Tao Li, MD ● Background: Abnormal potassium metabolism may contribute to the increased cardiac morbidity and mortality seen in dialysis patients. We studied the pattern of serum potassium levels in a cohort of Chinese peritoneal dialysis (PD) patients. Methods: We studied serum potassium levels of 266 PD patients during 3 consecutive clinic visits. Dialysis adequacy, residual renal function, and nutritional status also were assessed. Patients were followed up for 33.7 ⴞ 20.7 months. Results: Mean serum potassium level was 3.9 ⴞ 0.5 mEq/L (mmol/L). Five patients (1.9%) had an average serum potassium level less than 3 mEq/L (mmol/L), whereas 54 patients (20.3%) had a serum potassium level less than 3.5 mEq/L (mmol/L). Serum potassium levels correlated with overall Subjective Global Assessment score (r ⴝ 0.276; P < 0.001) and serum albumin level (r ⴝ 0.173; P ⴝ 0.005) and inversely with Charlson comorbidity score (r ⴝ ⴚ0.155; P ⴝ 0.011). There was no correlation between serum potassium level and daily PD exchange volume, total Kt/V, urine volume, or residual glomerular filtration rate. By means of multivariate analysis with Cox proportional hazard model to adjust for confounders, serum potassium level was an independent predictor of actuarial patient survival. PD patients with hypokalemia (serum potassium < 3.5 mEq/L [mmol/L]) had significantly worse actuarial survival (hazard ratio, 1.79; 95% confidence interval, 1.12 to 2.85; P ⴝ 0.015) than those without hypokalemia after adjusting for confounding factors. Conclusion: Hypokalemia is common in Chinese PD patients. Serum potassium level was associated with nutritional status and severity of coexisting comorbid condition. Furthermore, hypokalemia was an independent predictor of survival in PD patients. Additional studies may be needed to investigate the benefit of potassium supplementation for PD patients with hypokalemia. Am J Kidney Dis 46:128-135. © 2005 by the National Kidney Foundation, Inc. INDEX WORDS: Peritoneal dialysis (PD); continuous ambulatory peritoneal dialysis (CAPD); nutrition; cardiovascular disease. P ERITONEAL DIALYSIS (PD) is the treatment modality of 14% of the world’s dialysis population.1 Although the efficacy of potassium removal by PD is low, PD patients more commonly are hypokalemic than hemodialysis patients.2 Hypokalemia is found in 10% to 36% of PD patients.2-5 For example, Oreopoulos et al3 reported that 10% to 15% of PD patients required potassium supplementation for hypokalemia. Spital and Sterns4 noted that 36% of PD patients had a serum potassium level less than 3.5 mEq/L From the Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China. Received December 21, 2004; accepted in revised form March 14, 2005. Originally published online as doi:10.1053/j.ajkd.2005.03.015 on May 23, 2005. Supported in part by Chinese University of Hong Kong research account 6901031. Address reprint requests to Cheuk-Chun Szeto, MD, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China. E-mail: ccszeto@cuhk.edu.hk © 2005 by the National Kidney Foundation, Inc. 0272-6386/05/4601-0016$30.00/0 doi:10.1053/j.ajkd.2005.03.015 128 (mmol/L) at some time during their course and 20% required potassium supplementation. Cellular uptake and bowel loss probably have important roles in the pathogenesis of hypokalemia. Muscle biopsy studies showed that muscle potassium content was increased in PD patients, presumably reflecting intracellular uptake.6 However, ongoing losses of potassium in dialysate are an important contributing factor to hypokalemia. This is compounded further by poor nutritional intake, particularly of such potassium-rich foods as fruits and vegetables. For example, avoidance of fruits and vegetables as a result of ethnocultural food preference has been ascribed as the cause of the high prevalence of hypokalemia in the black race.2 Although a traditional Chinese diet is rich in vegetables, the method of cookery involves extensive boiling and frying, resulting in a substantial reduction in potassium content in the dishes served. A recent survey in Hong Kong indicated that the average dietary potassium intake of elderly subjects with normal renal function taking a traditional Chinese diet was only 30 to 40 mmol/d.7 Nevertheless, the prevalence of hypokalemia in Chinese PD patients has not been reported, and the long-term American Journal of Kidney Diseases, Vol 46, No 1 (July), 2005: pp 128-135 HYPOKALEMIA IN PERITONEAL DIALYSIS PATIENTS implication of hypokalemia in PD patients has not been studied. METHODS Patient Selection We studied 266 unselected Chinese PD patients in the dialysis unit of a single university hospital in Hong Kong from April to June 1999. Baseline data, including age, sex, underlying renal disease, duration of dialysis, PD regimen, and time on dialysis therapy, were recorded. Because excessive glucose load could cause hyperinsulinemia, resulting in a transcellular shift of potassium, we further recorded use of a hypertonic PD exchange, defined as a glucose concentration of 2.27% or more. Total daily exposure to glucose was calculated further from the dialysis regimen as described by Davies et al.8 Comorbid conditions, including coronary artery disease, heart failure, peripheral vascular disease, cerebrovascular disease, dementia, chronic pulmonary disease, connective tissue disorder, peptic ulcer disease, liver disease, diabetes with and without complications, hemiplegia, malignancy, and acquired immunodeficiency syndrome, also were recorded. The modified Charlson Comorbidity Index, which was validated in PD patients,9 was used to calculate a comorbidity score. Results of a peritoneal equilibration test (PET), usually performed a month after the initiation of PD therapy, also were reviewed. Detection and Management of Hypokalemia Serum potassium level was measured by means of a conventional method 3 times within 12 weeks. Hypokalemia is defined as an average serum potassium level less than 3.5 mEq/L (mmol/L). Use of medications that might affect potassium balance, including diuretics, potassium supplements, and angiotensin-converting enzyme (ACE) inhibitors, also were recorded. For the convenience of analysis, only long-term potassium supplementation was counted. In general, we aimed to keep serum potassium levels greater than 3.5 mEq/L (mmol/L) in our patients. Patients with hypokalemia generally were treated with supplemental doses of oral potassium chloride, typically 20 to 40 mmol/d for 1 to 3 days, followed by dietary advice to increase fresh fruit and vegetable intake. Nutritional Assessment and Clearance Study Nutritional status was assessed by means of Subjective Global Assessment (SGA), normalized protein nitrogen appearance (nPNA), anthropometric lean body mass (LBM), serum albumin level, and fat-free edema-free body mass (FEBM). SGA was performed by trained observers who were blinded to biochemical results of patients. The 4-item 7-point system was used.10,11 The 4 items for assessment were change in body weight, degree of anorexia, amount of subcutaneous tissue, and muscle mass. The 4 individual item scores were combined to generate a global score, which also took into account the clinical judgment of the observers and thus did not represent the simple arithmetic aggregate of the 4 individual item scores. All SGA items were rated subjectively on a scale from 1 to 7, in which 1 or 2 is severe 129 malnutrition, 3 to 5 is moderate to mild malnutrition, and 6 or 7 is mild malnutrition to normal nutritional status.10 Anthropometric measurements were performed by trained observers. Measurements included biceps, triceps, subscapular, and suprailiac skinfold thickness. Anthropometric LBM was computed using the formula described by Durnin and Rahaman.12 Interobserver coefficient of variation of LBM was approximately 10%. Routine serum biochemical tests were performed at the baseline study. Serum albumin level was measured using the bromcresol purple method. FEBM was calculated from 24-hour urine and dialysate biochemistry according to the formula described by Forbes and Brunining.13 nPNA was calculated using the modified Bergstrom formula14 and normalized by ideal body weight, which was determined by means of body height and sex according to a standard formula validated in southern Chinese patients.15 Kt/V and weekly creatinine clearance were determined by using standard methods.16 Residual glomerular filtration rate (GFR) was calculated as the average of 24-hour urinary urea and creatinine clearance, as described.17 Clinical Follow-Up All patients were followed up until June 2004 (ie, up to 60 months). Clinical management and dialysis regimen were decided by individual nephrologists and not affected by the study. Clinical outcome in this study is actuarial patient survival. Censoring events for survival analysis include transfer to long-term hemodialysis therapy, kidney transplantation, loss to follow-up, and transfer to other dialysis centers. Statistical Analysis Statistical analysis was performed using SPSS for Windows software, version 11.0 (SPSS Inc, Chicago, IL). Results are expressed as mean ⫾ SD unless otherwise specified. Comparisons between parameters were performed using chi-square test, Student t-test, or Pearson correlation coefficient, as appropriate. P less than 0.05 is considered statistically significant. All probabilities are 2 tailed. Actuarial survival between patients with and without hypokalemia (defined as serum potassium level ⬍ 3.5 mEq/L [mmol/L]) was compared by using log-rank test. The Cox proportional hazards model was used further for statistical analysis of serum potassium level on actuarial patient survival.18 For survival analysis, all patients who remained alive and on PD therapy at the end of the study were administratively censored on June 30, 2004. In addition to serum potassium level, the Cox models were constructed by age, time on dialysis, diabetic status, Charlson comorbidity score, overall SGA score, serum albumin level, anthropometric LBM, total Kt/V, nPNA, FEBM, and residual GFR. These parameters were selected for construction of the Cox model because of their importance in determining patient survival according to previous studies. The analysis was repeated to compare patients with and without hypokalemia, rather than actual serum potassium level. 130 SZETO ET AL Table 1. Patient Demographic and Baseline Clinical Data No. of patients Sex (M/F) Age (y) Duration of dialysis (mo) Body height (cm) Body weight (kg) Mean blood pressure (mm Hg) Renal diagnosis Glomerulonephritis Diabetic nephropathy Hypertension Polycystic kidney Obstructive uropathy Others/unknown Major comorbidity Coronary heart disease Congestive heart failure Peripheral vascular disease Dementia Chronic pulmonary disease Connective tissue disorder Peptic ulcer disease Mild liver disease Hemiplegia Moderate or severe renal disease Diabetes with end-organ damage Any tumor, leukemia, lymphoma Moderate or severe liver disease Metastatic solid tumor Acquired immunodeficiency syndrome Charlson index score Daily exchange volume (L/d) 266 135:131 51.2 ⫾ 15.0 38.1 ⫾ 28.9 159.1 ⫾ 7.7 58.4 ⫾ 9.2 101.3 ⫾ 12.6 99 (37.2) 65 (24.4) 13 (4.9) 12 (4.5) 15 (5.6) 62 (23.3) 79 (29.7) 41 (15.4) 24 (9.0) 22 (8.3) 9 (3.4) 7 (2.6) 30 (11.3) 36 (13.6) 39 (14.7) 266 (100) 79 (29.7) 6 (2.3) 5 (1.9) 0 0 4.9 ⫾ 2.3 6.9 ⫾ 1.4 long-term potassium supplementation (average dose, 11.6 ⫾ 4.0 mmol/d). Forty-six (17.3%) and 140 patients (52.6%) had 1 or more serum potassium levels less than 3 mEq/L (mmol/L) and 3.5 mEq/L (mmol/L), respectively. In addition, another 12 patients (4.5%) required long-term potassium supplementation, although average serum potassium level was greater than 3.5 mEq/L (mmol/L; average dose, 16.0 ⫾ 8.0 mmol/d). A total of 128 patients (48.1%) were administered furosemide, and 36 patients (13.5%) were administered an ACE inhibitor. However, treatment with furosemide or ACE inhibitor did not affect serum potassium level (details not shown). Additional analysis showed that serum potassium level had a modest inverse correlation with PET ultrafiltration volume (r ⫽ ⫺0.161; P ⫽ 0.025). When hypokalemia is defined as an average serum potassium level less than 3.5 mEq/L (mmol/L), patients with hypokalemia had significantly greater PET ultrafiltration volumes (0.42 ⫾ 0.17 versus 0.35 ⫾ 0.20 L; P ⫽ 0.044). However, serum potassium levels did not correlate with other parameters of peritoneal transport of small solutes, such as dialysate-plasma creatinine ratio at 4 hours (r ⫽ ⫺0.101; P ⫽ 0.16) and mass transfer area coefficient of creatinine (r ⫽ ⫺0.105; P ⫽ 0.15). Serum potassium levels also did not correlate with urine volume (r ⫽ 0.053; P ⫽ 0.4), residual GFR (r ⫽ 0.007; P ⫽ 0.9), or daily PD exchange volume (r ⫽ ⫺0.061; P ⫽ 0.3). There were no significant differences in the NOTE. Values expressed as mean ⫾ SD or number of patients (percent). RESULTS We studied 266 PD patients. Their baseline demographic and clinical characteristics are listed in Table 1. Prevalence of Hypokalemia The distribution histogram of average serum potassium levels in the study population is shown in Fig 1. Mean serum potassium level was 3.9 ⫾ 0.5 mEq/L (mmol/L). Five patients (1.9%) had an average serum potassium level less than 3 mEq/L (mmol/L), whereas 54 patients (20.3%) had an average serum potassium level less than 3.5 mEq/L (mmol/L); 9 patients (3.4%) required Fig 1. Distribution histogram of serum potassium levels among patients. To convert potassium in mmol to mEq/L, multiply by 1. HYPOKALEMIA IN PERITONEAL DIALYSIS PATIENTS Table 2. Use of Hypertonic Exchange and Daily Glucose Exposure in Patients With and Without Hypokalemia All patients Hypertonic exchange (L/d)* 0 2 4 ⱖ6 Daily glucose load (g/d)† Without Hypokalemia With Hypokalemia 212 54 70 (30.0) 43 (20.3) 43 (20.3) 56 (26.4) 120.6 ⫾ 37.2 14 (25.9) 14 (25.9) 13 (24.1) 13 (24.1) 123.8 ⫾ 37.7 NOTE. Values expressed as number of patients (percent) or mean ⫾ SD. *Overall chi-square test, P ⫽ 0.73. †Unpaired Student t-test, P ⫽ 0.58. use of hypertonic exchange or daily glucose exposure between patients with and without hypokalemia (Table 2). Peritoneal transport characteristics of small solutes, residual renal function, or daily PD exchange volume did not differ significantly between patients with and without hypokalemia (Fig 2). Relation to Malnutrition The presence of hypokalemia was associated with features of malnutrition. Serum potassium levels correlated with serum albumin level (Pearson r ⫽ 0.173; P ⫽ 0.005) and overall SGA score (r ⫽ 0.276; P ⬍ 0.001). Among SGA subscores, serum potassium levels correlated with weight change (r ⫽ 0.235; P ⫽ 0.001), anorexia (r ⫽ 0.168; P ⫽ 0.02), and muscle mass (r ⫽ 0.180; P ⫽ 0.012), but not subcutaneous fat (r ⫽ 0.112; P ⫽ 0.12). When hypokalemia is defined as average serum potassium level less than 3.5 mEq/L (mmol/L), patients with hypokalemia had significantly lower serum albumin levels (2.76 ⫾ 0.44 versus 2.91 ⫾ 0.41 g/dL [27.6 ⫾ 4.4 versus 29.1 ⫾ 4.1 g/L]; P ⫽ 0.019) and overall SGA scores (4.93 ⫾ 1.01 versus 5.43 ⫾ 1.03; P ⫽ 0.005) than patients without hypokalemia. Conversely, serum potassium levels did not correlate with anthropometric LBM (r ⫽ 0.080; P ⫽ 0.27), FEBM by means of creatinine kinetics (r ⫽ ⫺0.023; P ⫽ 0.7), or nPNA (r ⫽ 0.107; P ⫽ 0.1). In addition to traditional nutritional markers, serum potassium levels also correlated signifi- 131 cantly with serum phosphate level (r ⫽ 0.336; P ⬍ 0.001) and inversely with fasting total serum cholesterol level (r ⫽ ⫺0.139; P ⫽ 0.028) and Charlson comorbidity score (r ⫽ ⫺0.155; P ⫽ 0.011). Patients with hypokalemia had significantly lower serum phosphate levels (4.68 ⫾ 1.39 versus 5.30 ⫾ 1.27 mg/dL [1.51 ⫾ 0.45 versus 1.71 ⫾ 0.41 mmol/L]; P ⫽ 0.002), but marginally higher Charlson comorbidity scores (5.4 ⫾ 2.2 versus 4.7 ⫾ 2.3; P ⫽ 0.07) than patients without hypokalemia. Relation to Patient Survival Patients were followed up for a total of 8,970 patient-months. Average duration of follow-up was 33.7 ⫾ 20.7 months. During the study period, there were 139 deaths. During the same period, there were 27 transplantations, 28 patients changed to hemodialysis therapy, and 7 patients transferred to other centers. Causes of death of patients with and without hypokalemia are listed in Table 3. There was no significant difference in distribution of causes of death between groups. The Kaplan-Meier survival plot is shown in Fig 3. Actuarial patient survival at 36 months was 44.9% and 62.4% for patients with and without hypokalemia (log-rank test, P ⫽ 0.03). By means of univariate analysis with the Cox proportional hazard model, serum potassium level was associated significantly with actuarial survival (hazard ratio, 0.64; 95% confidence interval, 0.44 to 0.92; P ⫽ 0.017). By means of multivariate analysis with the Cox proportional hazard model to adjust for confounders, independent factors for actuarial survival were serum potassium level, Charlson comorbidity score, serum albumin level, and residual GFR. Results of the Cox model analysis are listed in Table 4. In this model, for every 1-mEq/L (-mmol/L) increase in serum potassium level, the adjusted hazard ratio for all-cause mortality was 0.59 (95% confidence interval, 0.37 to 0.94; P ⫽ 0.026). Similarly, when patients with and without hypokalemia were compared by means of multivariate Cox model, the former had significantly worse actuarial survival (hazard ratio, 1.79; 95% confidence interval, 1.12 to 2.85; P ⫽ 0.015) after adjusting for confounding factors. 132 SZETO ET AL Fig 2. Comparison of peritoneal transport, dialysis adequacy, and residual renal function between patients with and without hypokalemia. Data compared by using Student t-test. Error bars denote SDs. Abbreviation: MTAC, mass transfer area coefficient. To convert potassium in mmol to mEq/L, multiply by 1; GFR in mL/ min to mL/s, multiply by 0.01667. DISCUSSION In the present study, we found that hypokalemia was common in Chinese PD patients. Serum potassium level in PD patients was associated with nutritional status or severity of coexisting comorbid conditions. Hypokalemia was an independent prognostic indicator of PD patients. Unfortunately, we did not examine the cause of hypokalemia in our patients, which would, in theory, require detailed dietary assessment and quantification of potassium loss in dialysate and urine. Proper evaluation of potassium balance requires careful study of intake and output, which nevertheless is practically difficult in a large cohort of patients. We believe that low dietary potassium intake is the major factor for the high prevalence of hypokalemia. Although a traditional Chinese diet is rich in vegetables, the method of cookery involves extensive boiling and frying, resulting in a substantial reduction in potassium content in the dishes being served. Recent data suggest that the average dietary potassium intake of Hong Kong Chinese was only 30 to 40 mmol/d,7,19 substantially less than that in white populations. We observed that serum potassium level was associated with serum phosphate level, indirectly suggesting that hypokalemic patients had an overall reduction in HYPOKALEMIA IN PERITONEAL DIALYSIS PATIENTS Table 3. Causes of Death in Patients With and Without Hypokalemia All patients All deaths Cause of death Vascular diseases Cardiovascular Cerebrovascular Peripheral vascular Infections Nonperitonitis Peritonitis Others Liver cirrhosis Malignancy Miscellaneous Termination of dialysis Unknown Without Hypokalemia With Hypokalemia 212 104 (49.1) 54 35 (64.8) 40 (18.9) 13 (6.1) 5 (2.4) 8 (14.8) 4 (7.4) 2 (3.7) 13 (6.1) 13 (6.1) 4 (7.4) 8 (14.8) 2 (0.9) 5 (2.4) 2 (0.9) 10 (4.7) 1 (0.5) 0 (0) 2 (3.7) 1 (1.9) 4 (7.4) 2 (3.7) NOTE. Values expressed as number of patients (percent). oral intake. Although we did not quantify the amount of potassium loss in dialysate, it is interesting to note that average PD exchange volume in our patients was 6.9 L/d, and serum potassium level was 3.9 mEq/L (mmol/L). Daily dialysate potassium loss therefore would be approximately 28 mmol if complete equilibration is Fig 3. Actuarial survival by Kaplan-Meier plot of patients with (serum potassium < 3.5 mEq/L [mmol/L]) and without hypokalemia (serum potassium > 3.5 mEq/L [mmol/L]). Patients without hypokalemia had significantly better survival than those with hypokalemia (logrank test, P ⴝ 0.03). 133 assumed. Contrary to the general expectation,2-5 urine volume or diuretic treatment was not associated with hypokalemia in our patients. It recently was suggested that improving the adequacy index of dialysis would inevitably increase the incidence of hypokalemia in PD patients.20 We did not find that serum potassium level correlated with daily exchange volume or any dialysis adequacy index. Unfortunately, we did not analyze serial serum potassium levels of our patients during follow-up, and it remains probable that for any individual patient with fixed dietary potassium intake, increasing the daily exchange volume to achieve dialysis adequacy index would result in a decline in serum potassium level. We found that serum potassium levels were associated with serum albumin level, overall SGA score, and Charlson comorbidity score. It therefore seems probable that hypokalemia is a surrogate marker of malnutrition or severe comorbid illness, both related to poor dietary intake. As noted, hypokalemic patients also had lower serum phosphate levels, which further supports the role of overall dietary intake. However, it is important to note that correlation coefficients were weak, although statistically significant, suggesting that neither comorbidity nor nutritional status was the major governing factor of serum 134 SZETO ET AL Table 4. Cox Proportional Hazards Model of Actuarial Survival Variable Adjusted Hazard Ratio 95% Confidence Interval P Serum potassium (11 mEq/L) Charlson comorbidity score (11 point) Serum albumin (10.1 g/dL) Residual GFR (11 mL/min/1.73 m2) 0.59 1.21 0.93 0.81 0.37-0.94 1.11-1.33 0.89-0.98 0.69-0.95 0.026 ⬍0.001 0.008 0.011 NOTE. To convert potassium in mEq/L to mmol/L, multiply by 1; albumin in g/dL to g/L, multiply by 10; GFR in mL/min to mL/s, multiply by 0.01667. potassium level. Although low phosphate intake, serum albumin level, and SGA score point to poor caloric and protein intake, dietary potassium intake was not necessarily low. We found no relation between serum potassium level and body muscle mass (either anthropometric LBM or FEBM by means of creatinine kinetics) or nPNA. Although the latter often is regarded as an indicator of dietary protein intake, the reliability of nPNA has been heavily criticized, particularly in hypercatabolic patients.21 In the present study, hypokalemic PD patients had excess mortality, even after adjusting for multiple confounding factors. Unfortunately, we did not measure serum C-reactive protein in our cohort. Because C-reactive protein level is an important predictor of mortality in PD patients,22 it theoretically would be interesting to explore the relationship and interaction between Creactive protein level and hypokalemia. The abnormal potassium metabolism of patients with end-stage renal disease may contribute to the increased cardiac morbidity and mortality in dialysis patients.23 However, to the best of our knowledge, this hypothesis has not been tested by a prospective study. We did not observe an excess in cardiac mortality in hypokalemic PD patients. Hypokalemic patients had increased mortality from almost all causes (Table 3), which probably was contributed to by abnormal cardiac function,24,25 predisposition to stroke,26 respiratory muscle weakness,24 and complications of the associated malnutrition. Although serum potassium level was associated with serum phosphate level and the latter has important implications in the clinical outcome of PD patients,27 serum phosphate level was not associated with patient survival in our present study. In theory, if cardiac arrhythmia is a major cause of mortality in hypokalemic patients, excess mortality would be observed similarly in patients with intermit- tent hypokalemia. Because the number of patients with intermittent hypokalemia was small in our series, meaningful subgroup analysis to test this hypothesis was not possible. It remains unknown whether potassium supplementation in hypokalemic patients, including those with borderline hypokalemia, would improve survival. Because hypokalemia may merely be a surrogate marker of malnutrition and/or severe comorbid illness, potassium supplementation may not be of benefit, and formal prospective study is needed in this respect. Because of poor renal function, therapeutic measures targeted at the renin-angiotensin axis have very little effect on potassium balance in PD patients. In a previous study by our group,28 ACE inhibitor therapy preserved residual renal function in PD patients, but the treatment affects neither serum potassium level nor all-cause mortality in 12 months. REFERENCES 1. Nolph KD: What’s new in peritoneal dialysis—An overview. Kidney Int Suppl 38:S148-S152, 1992 2. Khan AN, Bernardini J, Johnston JR, Piraino B: Hypokalemia in peritoneal dialysis patients. Perit Dial Int 16:652653, 1996 3. Oreopoulos D, Khanna R, Williams P, Vas S: Continuous ambulatory peritoneal dialysis—1981. Nephron 30:293303, 1982 4. Spital A, Sterns RH: Potassium supplementation via the dialysate in continuous ambulatory peritoneal dialysis. Am J Kidney Dis 6:173-176, 1985 5. Rostand SG: Profound hypokalemia in continuous ambulatory peritoneal dialysis. Arch Intern Med 143:377378, 1983 6. Lindholm B, Alvestrand A, Hultman E, Bergstrom J: Muscle water and electrolytes in patients undergoing continuous ambulatory peritoneal dialysis. Acta Med Scand 219:323330, 1986 7. Kwok TC, Chan TY, Woo J: Relationship of urinary sodium/potassium excretion and calcium intake to blood pressure and prevalence of hypertension among older Chinese vegetarians. Eur J Clin Nutr 57:299-304, 2003 HYPOKALEMIA IN PERITONEAL DIALYSIS PATIENTS 8. Davies SJ, Phillips L, Naish PF, Russell GI: Peritoneal glucose exposure and changes in membrane solute transport with time on peritoneal dialysis. J Am Soc Nephrol 12:10461051, 2001 9. Beddhu S, Zeidel ML, Saul M, et al: The effects of comorbid conditions on the outcomes of patients undergoing peritoneal dialysis. Am J Med 112:696-701, 2002 10. National Kidney Foundation: K/DOQI Clinical Practice Guidelines for Peritoneal Dialysis Adequacy: Update 2000. Am J Kidney Dis 37: S65-S136, 2001(suppl 1) 11. Enia G, Sicus C, Alati G, Zoccali C: Subjective Global Assessment of nutrition in dialysis patients. Nephrol Dial Transplant 8:1094-1098, 1993 12. Durnin JV, Rahaman MM: The assessment of amount of fat in human body from measurement of skin fold thickness. Br J Nutr 21:681-689, 1967 13. Forbes GB, Brunining GJ: Urinary creatinine excretion and lean body mass. Am J Clin Nutr 29:1359-1366, 1976 14. Bergstrom J, Heimburger O, Lindholm B: Calculation of the protein equivalent of total nitrogen appearance from urea appearance. Which formulas should be used? Perit Dial Int 18:467-473, 1998 15. Department of Health, Republic of China (Taiwan). The ROC’s Handbook of Diet (ed 2). Taipei, Taiwan, Department of Health, pp 20-21, 1994 16. Nolph KD, Moore HL, Twardowski ZJ, et al: Crosssectional assessment of weekly urea and creatinine clearances in patients on continuous ambulatory peritoneal dialysis. ASAIO J 38:M139-M142, 1992 17. Van Olden RW, Krediet RT, Struijk DG, Arisz L: Measurement of residual renal function in patients treated with continuous peritoneal dialysis. J Am Soc Nephrol 7:745-748, 1996 18. Cox D: Regression models and life-tables. J R Stat Soc 34:187-201, 1972 135 19. Chow KM, Szeto CC, Wong TY, Leung CB, Li PK: Risk factors of thiazide-induced hyponatraemia. Q J Med 96:911-917, 2003 20. Newman LN, Weiss MF, Berger J, Priester A, Negrea LA, Cacho CP: The law of unintended consequences in action: Increase in incidence of hypokalemia with improved adequacy of dialysis. Adv Perit Dial 16:134-137, 2000 21. Harty JC, Boulton H, Curwell J, et al: The normalized protein catabolic rate is a flawed marker of nutrition in CAPD patients. Kidney Int 45:103-109, 1994 22. Wang AY, Woo J, Lam CW, et al: Is a single time point C-reactive protein predictive of outcome in peritoneal dialysis patients? J Am Soc Nephrol 14:1871-1879, 2003 23. Dolson GM: Do potassium deficient diets and K⫹ removal by dialysis contribute to the cardiovascular morbidity and mortality of patients with end stage renal disease? Int J Artif Organ 20:134-135, 1997 24. Lindinger MI: Potassium regulation during exercise and recovery in humans: Implications for skeletal and cardiac muscle. J Mol Cell Cardiol 27:1011-1022, 1995 25. Fitzovich DE, Hamaguchi M, Tull WB, Young DB: Chronic hypokalemia and the left ventricular responses to epinephrine and preload. J Am Coll Cardiol 18:1105-1111, 1991 26. Smith NL, Lemaitre RN, Heckbert SR, et al: Serum potassium and stroke risk among treated hypertensive adults. Am J Hypertens 16:806-813, 2003 27. Wang AY, Woo J, Sea MM, Law MC, Lui SF, Li PK: Hyperphosphatemia in Chinese peritoneal dialysis patients with and without residual kidney function: What are the implications? Am J Kidney Dis 43:712-720, 2004 28. Li PK, Chow KM, Wong TY, Leung CB, Szeto CC: Effects of an angiotensin-converting enzyme inhibitor on residual renal function in patients receiving peritoneal dialysis: A prospective randomized study. Ann Intern Med 139: 105-112, 2003