Dialysis New-Onset Hyperglycemia in Nondiabetic Chinese Patients Started on Peritoneal Dialysis Cheuk-Chun Szeto, MD, FRCP(Edin), Kai-Ming Chow, MBChB, MRCP(UK), Bonnie Ching-Ha Kwan, MBBS, MRCP(UK), Kwok-Yi Chung, MBChB, MRCP(UK), Chi-Bon Leung, MBChB, FRCP(Edin), and Philip Kam-Tao Li, MD, FRCP Background: Glucose has been used as the osmotic agent added to standard peritoneal dialysis (PD) solutions since its inception. Patients who have no history of glucose intolerance may develop hyperglycemia after the initiation of PD therapy. However, the prevalence and long-term implications of new-onset hyperglycemia in PD patients has not been studied. Methods: We studied 405 consecutive patients with renal failure newly started on PD therapy. Fasting plasma glucose levels 1 month after being stable on PD therapy were reviewed. Clinical factors affecting fasting plasma glucose levels were explored. Patients were followed up for 49.7  28.4 months. Results: Of 405 patients, 136 had underlying diabetic nephropathy and another 17 had preexisting diabetes before starting PD therapy. Of the remaining 252 patients, fasting plasma glucose levels were greater than 200 mg/dL (11.1 mmol/L) in 21 (8.3%) and 126 to 200 mg/dL (7.0 to 11.1 mmol/L) in 48 patients (19.0%). Seven patients required insulin therapy, 3 required low-dose sulfonylurea therapy, and all other patients had glucose levels controlled by means of dietary restriction only. Fasting plasma glucose levels significantly correlated with patient age (Pearson r = 0.278; P  0.001), Charlson comorbidity score (r = 0.484; P  0.001), baseline serum C-reactive protein level (r = 0.390; P  0.001), and serum albumin level (r =-0.182; P  0.001). However, patients with new-onset hyperglycemia had similar values for body weight, body mass index, peritoneal transport parameters, and ultrafiltration profile compared with other patients. At 36 months, actuarial survival rates were 93.7%, 85.3%, 81.6%, and 66.7% for patients with fasting glucose levels less than 100, 100 to less than 126, 126 to less than 200, and 200 mg/dL or greater (5.6, 5.6 to 7.0, 7.0 to 11.1, and 11.1 mmol/L) and 65.9% for patients with preexisting diabetes, respectively (overall log rank test, P  0.001). Conclusion: New-onset hyperglycemia is common in patients without diabetes started on PD therapy. Contrary to common belief, obese patients do not appear to have a greater risk of hyperglyce- mia. Our results suggest that even mild hyperglycemia, with fasting plasma glucose level greater than 100 mg/dL (5.6 mmol/L), is associated with worse survival in PD patients. Am J Kidney Dis 49:524-532. © 2007 by the National Kidney Foundation, Inc. INDEX WORDS: Renal failure; glucose; patient survival. G lucose is the most commonly used osmotic agent in commercial peritoneal dialysis (PD) solutions. It was estimated that PD patients derive about 20% of their total daily energy intake from the glucose in dialysate, correspond- ing to a daily peritoneal energy intake of 4 to 13 kcal/kg of body weight. 1 The high daily glucose absorption raises concern for the possible development of de novo diabetes mellitus. In patients with impending diabetes, the extra glucose load from PD may be responsible for the appearance of the disease, necessitating the institution of insulin therapy. Previous studies sug- gested that exchanges with a 1.5% glucose dialy- sate had only marginal effects on blood glucose and insulin levels. 2,3 However, with the use of hyper- tonic glucose solutions, the tendency toward the development of hyperglycemia and hyperinsulin- emia is more pronounced. Wideroe et al 4 reported increased plasma C-peptide levels along with an increased ratio of C-peptide to insulin levels in PD From the Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China. Received September 21, 2006; accepted in revised form January 16, 2007. Originally published online as doi:10.1053/j.ajkd.2007.01.018 on March 1, 2007. Support: CUHK research account 6901031. Potential conflicts of interest: None. Address reprint requests to Cheuk-Chun Szeto, MD, FRCP(Edin), Department of Medicine & Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China. E-mail: ccszeto@cuhk.edu.hk © 2007 by the National Kidney Foundation, Inc. 0272-6386/07/4904-0004$32.00/0 doi:10.1053/j.ajkd.2007.01.018 American Journal of Kidney Diseases, Vol 49, No 4 (April), 2007: pp 524-532 524