letter to the editor
7. Cupisti A, Comar F, Benini O et al. Effect of boiling on dietary phosphate and nitrogen intake. J Renal Nutr 2006; 16: 36–40. 8. Shimamura S, Tamura Y, Mizota T et al. Low-phosphorus whey protein manufacturing method thereof, low-phosphorus purified whey hydrolysate and manufacturing method thereof. US Patent Publication 428,129. Publication data: 9 June 1995. 9. Levin S, Winkelstein JA. Diet and infrequent peritoneal dialysis in chronic anuric uremia. N Engl J Med 1967; 277: 619–624.
John T. Daugirdas1
1 Renal Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA and 2Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA Correspondence: Myles Wolf, Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, 1120 NW 14th Street, Miami, Florida 33136, USA. E-mail:
[email protected]
Kidney International (2010) 77, 930; doi:10.1038/ki.2010.53
1
Department of Medicine, University of Illinois College of Medicine, Chicago, Illinois, USA Correspondence: John T. Daugirdas, Department of Medicine, University of Illinois College of Medicine, Chicago, Illinois 60612, USA. E-mail:
[email protected] Kidney International (2010) 77, 929–930; doi:10.1038/ki.2010.52
The Authors Reply: We thank Daugirdas for his comments in ‘Proposed controlled trials of phosphate reduction in CKD: which whey should we go?’1 We agree that reducing dietary phosphorus intake is an important strategy to control phosphorus balance in renal failure that is worthy of testing in randomized trials. Daugirdas’s interesting approach would effectively dissociate phosphorus restriction from undesirable protein restriction through the use of whey supplements and through avoidance of foods with high phosphorus-to-protein ratios, such as processed foods. In support of this proposal, the feasibility of dietary counseling to reduce serum phosphate levels in dialysis patients has been established by a recent randomized trial.2 It is likely, however, that several factors could limit the effectiveness and sustainability of dietary phosphorus restriction alone. First, the lack of accurate labeling of phosphorus content in food additives and its inconsistency across specific manufacturers3 complicates dietary counseling. Second, while the cost of whey may be low, effective ongoing dietary counseling requires dedicated and relatively costly nutritionists. Perhaps most importantly, kidney disease is largely a disease of poverty, which, under the strain of the recession, is deepening in the United States. Impoverished dialysis patients, even those most successfully counseled, will likely forgo healthy food choices in favor of cheap prepared foods that are phosphorus-laden and widely available. To benefit the majority of patients, we would therefore suggest a multipronged approach to reduce phosphate levels in dialysis patients, involving both pharmaceutical and dietary interventions as suggested by Daugirdas. 1. Daugirdas JT. Proposed controlled trials of phosphate reduction in CKD: which whey should we go? Kidney Int 2010; 77: 929–930. 2. Sullivan C, Sayre SS, Leon JB et al. Effect of food additives on hyperphosphatemia among patients with end-stage renal disease: a randomized controlled trial. JAMA 2009; 301: 629–635. 3. Sherman RA, Mehta O. Dietary phosphorus restriction in dialysis patients: potential impact of processed meat, poultry, and fish products as protein sources. Am J Kidney Dis 2009; 54: 18–23.
Non-infected hemodialysis catheters are associated with increased inflammation compared with arteriovenous fistulas To the Editor: We read with great interest the article by Goldstein et al.,1 reporting that catheters may cause inflammation independent of infection as compared with arteriovenous (AV) fistula use. The authors showed greater levels of serum C-reactive protein (CRP) in patients dialyzed with central catheters in contrast to AV fistulas. We wish to highlight a few important points. First, the authors did not give any information about comorbidity status, underlying primary renal disease, level of uremia, glycemic control of diabetic patients, echocardiographic data, anthropometric measures, or prealbumin and cholesterol concentrations showing nutritional status and residual renal function (RRF) at the start of hemodialysis. It is known that CRP is affected not only by infection but also by many variables, such as RRF, coronary heart disease, peripheral arterial disease, malnutrition, and metabolic syndrome.2,3 Thus, it is very difficult to attribute high CRP levels solely to the presence of a catheter unless these variables are appropriately controlled for. Second, the authors measured only serum CRP concentrations, did not include other inflammation markers, and took measurements just twice in a 6-month period. CRP levels, especially in the hemodialysis population, may fluctuate; thus, obtaining single CRP measurements may be misleading.4 Third, the catheter group involved desperate patients in whom fistula attempt had failed. Thus, there was no option other than catheter use, of course after trying the fistula at a more proximal site and vascular grafts. The advantages of the ‘fistula first’ slogan have long been established for naive patients. Hence, a call for fistula first for patients with failed fistulas seems inappropriate. 1.
2. 3. 4.
Tamara Isakova1, Orlando M. Gutie´ rrez2 and Myles Wolf2 930
Goldstein SL, Ikizler TA, Zappitelli M et al. Non-infected hemodialysis catheters are associated with increased inflammation compared to arteriovenous fistulas. Kidney Int 2009; 76: 1063–1069. Devaraj S, Singh U, Jialal I. Human C-reactive protein and the metabolic syndrome. Curr Opin Lipidol 2009; 20: 182–189. Wang AY, Lai KN. The importance of residual renal function in dialysis patients. Kidney Int 2006; 69: 1726–1732. Snaedal S, Heimbu¨rger O, Qureshi AR et al. Comorbidity and acute clinical events as determinants of C-reactive protein variation in hemodialysis patients: implications for patient survival. Am J Kidney Dis 2009; 53: 1024–1033. Kidney International (2010) 77, 928–933
letter to the editor
Yalcin Solak1 and Huseyin Atalay1 1
Nephrology Department, Meram School of Medicine, Selcuk University, Konya, Turkey Correspondence: Yalcin Solak, Nephrology Department, Selcuk Universitesi, Meram Tip Fakultesi, Hemodiyaliz Sekreterligi, Konya, Meram 42080, Turkey. E-mail:
[email protected] Kidney International (2010) 77, 930–931; doi:10.1038/ki.2010.55
The Authors Reply: We thank Drs Solak and Atalay1 for their interest in our work.2 With regard to their first comment, we reported data about diabetes, age, and gender, and adjusted for these factors. More importantly, we adjusted for phosphorus level—a well-known factor for cardiovascular morbidity and mortality in dialysis patients.3 Furthermore, we excluded patients with a failed renal allograft or clotted, arteriovenous graft in place—two well-known causes of inflammation.4,5 Finally, 47 of 50 patients in the fistulacatheter group had urine output less than 200 ml at the initiation of dialysis. With regard to inflammatory markers, C-reactive protein (CRP) is the most commonly assessed marker in dialysis studies; we had other evidence of inflammation (lower hematocrit and albumin, higher Erythropoiesis Resistance Index) in catheter patients. In addition, although CRP can fluctuate, in all cases, the mean (s.d.) CRP levels did not overlap between fistula and catheter patients at any time point, suggesting a strong association between CRP and access. Additional markers, such as IL-6, may provide more specificity, but would not have altered the interpretation of our data. Finally, the last comment is incorrect—all patients had fistula placement as an elective procedure; catheters were never placed as a ‘desperate’ attempt, but were used as vascular access until fistula maturation. Thus, we believe our data support the role of a noninfected dialysis catheter as the sole cause of inflammation.
The CANUSA study and the importance of residual kidney function in dialysis patients To the Editor: I read with much interest the mini-review by Rosansky et al.1 that examined the implications of starting dialysis at a higher glomerular filtration rate (GFR). There were a couple of inaccurate statements that need to be corrected for your readers. The authors describe the Canada – USA Peritoneal Dialysis Study Group study as ‘an observational study that suggested a potential benefit on renal survival of a weekly peritoneal creatinine clearance of 470 l/1.73 m2.’ The benefit of that clearance value was for survival of the patient, not for renal survival. In the same paragraph is the following: ‘In addition, although the Canada – USA Peritoneal Dialysis Study Group study supported a relationship between the level of peritoneal clearance and survival, one can argue that the RKF in these continuous ambulatory peritoneal dialysis patients was primarily responsible for the survival advantage.’ One could indeed argue this, and it was exactly this finding that was reported in the re-analysis of the Canada – USA Peritoneal Dialysis Study Group study.2 In this re-analysis, the small solute clearance parameters were subdivided into the peritoneal and renal contribution. The peritoneal clearance had no predictive power on patient survival, whereas every 5 l/week of residual GFR was associated with a 12% reduction in mortality. Urine volume was an even more powerful predictor of outcome, with every 250 ml/day associated with a 36% reduction in mortality.2 We need to avoid becoming so obsessed with small solute kinetics that we forget about the importance of residual kidney function in our dialysis patients. 1.
1. Solak Y, Atalay H. Non-infected hemodialysis catheters are associated with increased inflammation compared with arteriovenous fistulas. Kidney Int 2010; 77: 930–931. 2. Goldstein SL, Ikizler TA, Zappitelli M et al. Non-infected hemodialysis catheters are associated with increased inflammation compared to arteriovenous fistulas. Kidney Int 2009; 76: 1063–1069. 3. Ayus JC, Mizani MR, Achinger SG et al. Effects of short daily versus conventional hemodialysis on left ventricular hypertrophy and inflammatory markers: a prospective, controlled study. J Am Soc Nephrol 2005; 16: 2778–2788. 4. Ayus JC, Sheikh-Hamad D. Silent infection in clotted hemodialysis access grafts. J Am Soc Nephrol 1998; 9: 1314–1317. 5. Ayus JC, Achinger SG. At the peril of dialysis patients: ignoring the failed transplant. Semin Dial 2005; 18: 180–184.
2.
Rosansky SJ, Clark WF, Eggers P et al. Initiation of dialysis at higher GFRs: is the apparent rising tide of early dialysis harmful or helpful? Kidney Int 2009; 76: 257–261. Bargman JM, Thorpe K, Churchill DN, for the CANUSA Study Group. Relative contribution of residual renal function and peritoneal clearance to adequacy of dialysis: a reanalysis of the CANUSA study. J Am Soc Nephrol 2001; 12: 2158–2162.
Joanne M. Bargman1 1
University Health Network, Toronto General Hospital, Toronto, Canada Correspondence: Joanne M. Bargman, University Health Network, Toronto General Hospital, 200 Elizabeth Street, 8N-840, Toronto, Canada M5G 2C4. E-mail:
[email protected] Kidney International (2010) 77, 931; doi:10.1038/ki.2010.44
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Stuart L. Goldstein and Juan Carlos Ayus
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1 Baylor College of Medicine – Pediatrics, Texas Children’s Hospital, Houston, Texas, USA Correspondence: Stuart L. Goldstein, Baylor College of Medicine – Pediatrics, Texas Children’s Hospital, 6621 Fannin St MC 3-2482, Houston, Texas 77030, USA. E-mail:
[email protected]
Kidney International (2010) 77, 931; doi:10.1038/ki.2010.57 Kidney International (2010) 77, 928–933
The Authors Reply: We strongly agree with Dr Bargman’s1 reference to the importance of residual kidney function in the decision to start dialysis. In fact, the assumptions used to 931