Kidney Res Clin Pract > Volume 33(2); 2014 > Article
Prime determinants of serum phosphorus level in hemodialysis patients
To the Editor,
The concept that hyperphosphatemia in hemodialysis (HD) patients is a risk factor for various outcomes has now been widely accepted. Many patients on maintenance HD with a high serum phosphorus level are linked to the development of aspects of chronic kidney disease-mineral and bone disorder; they are thus recommended to maintain serum phosphorus level within a normal range [1]. In order to control this, we have options such as dietary restriction and the use of phosphate binders. However, more than half of patients did not reach the target range in the United States, Europe, and Japan [2], and the proportion of patients with hyperphosphatemia may be similar in Korea because the mean serum phosphorus level was reported to be 5.14±1.64 mg/dL [3].
Rhee et al [4] reported that the factors associated with phosphate control were different depending on the residual renal function status in Korean patients on maintenance HD. They also emphasized the preservation of residual renal function for the optimal phosphorus control in non-anuric patients. Although I totally agree with the findings of the study, it could not be overlooked that we have only a couple of ways to preserve residual renal function in HD patients, including the use of ultrapure dialysate, biocompatible membranes, avoiding nephrotoxic drugs, decreasing dialysis frequency, and/or avoidance of aggressive water removal [5]. Therefore, I would like to point out that dietary phosphate restriction with appropriate protein intake could be the first strategy for controlling serum phosphorus levels in HD patients. In this regard, as the authors mentioned in the limitations of the study [4], controlling the amount of dietary phosphate may not only be important in designing clinical research, but could also be crucial in the treatment of HD patients with hyperphosphatemia.
Conflicts of interest
None.
Dong-Ryeol Ryu
Division of Nephrology, Department of Internal Medicine,School of Medicine, Ewha Womans University, Seoul, Korea
E-mail address: drryu@ewha.ac.kr
References
[1] Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl 113:S1-S130, 2009
[2] Young EW, Albert JM, Satayathum S, Goodkin DA, Pisoni RL, Akiba T, Akizawa T, Kurokawa K, Bommer J, Piera L, Port FK: Predictors and consequences of altered mineral metabolism: the Dialysis Outcomes and Practice Patterns Study. Kidney Int 67:1179-1187, 2005
[3] Jin DC, Han JS: Renal replacement therapy in Korea, 2012. Kidney Res Clin Pract 33:9-18, 2014
[4] Rhee H, Yang JY, Jung WJ, Shin MJ, Yang BY, Song SH, Kwak IS, Seong EY: Significance of residual renal function for phosphate control in chronic hemodialysis patients. Kidney Res Clin Pract 33:58-64, 2014
[5] Liu S, Diao Z, Zhang D, Zhang D, Ding J, Cui W, Liu W: Preservation of residual renal function by not removing water in new hemodialysis patients: a randomized, controlled study. Int Urol Nephrol 46:83-90, 2014
In Reply:
We appreciate your interest in our recent article entitled “Significance of residual renal function for phosphate control in chronic hemodialysis patients”. Phosphate is the key regulator in the chronic kidney disease-mineral bone disease, which is deeply associated with the cardiovascular outcome in chronic hemodialysis patients. In the normal physiologic state, increasing serum phosphate concentration induces secretion of parathyroid hormone and fibroblast growth factor 23 (FGF-23). These two phosphaturic hormones reduce expression of sodium-dependent phosphate co-transporters in the proximal tubules, thereby diminishing phosphate reabsorption and increasing urinary phosphate excretion [1]. However, in end stage renal disease state, phosphaturia is significantly diminished because of failure in glomerular filtration, even though the amount of increase of parathyroid hormone or FGF-23 is considerable. Thus, as our study [2] pointed out, residual renal function must be the prime determinant of serum phosphate control in end stage renal disease patients [3].
However, as you pointed out, the key element in the management of elevated serum phosphate is still dietary phosphate restriction along with oral phosphate binder even in chronic hemodialysis patient, and the current Kidney Disease Improving Global Outcomes guidelines recommended limiting dietary phosphate intakes as a first line therapy for the treatment of hyperphosphatemia [4]. Also, in several previous studies [5,6], restricting dietary phosphate alone successfully decreased serum FGF-23 levels in patients with chronic kidney disease. However considering that phosphate-rich foods tend to be good sources of dietary protein, long-term restriction of phosphate might lead to protein-energy malnutrition. In fact, in the study by Lynch et al [7], prescribed dietary phosphate restriction is not associated with improved survival among prevalent hemodialysis patients, and increased level of restriction may be associated with greater mortality in some subgroups. Thus, we believe that, balancing between phosphate restriction and sufficient protein-energy supplement is the most important aspect in the management of chronic hemodialysis patients.
Conflicts of interest
The authors declare no conflicts of interest.
Harin Rhee and Eun Young Seong
Division of Nephrology, Department of Internal Medicine,
Pusan National University Hospital, Busan, Korea
E-mail address: sey-0220@hanmail.net
References
[1] Farrow EG, White KE: Recent advances in renal phosphate handling. Nat Rev Nephrol 6:207-217, 2010
[2] Rhee H, Yang JY, Jung WJ, Shin MJ, Yang BY, Song SH, Kwak IS, Seong EY: Significance of residual renal function for phosphate control in chronic hemodialysis patients. Kidney Res Clin Pract 33:58-64, 2014
[3] Iwasawa H, Nakao T, Matsumoto H, Okada T, Nagaoka Y and Wada T: Phosphate handling by end-stage kidneys and benefits of residual renal function on phosphate removal in patients on haemodialysis. Nephrology 18:285-291, 2013
[4] Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group: KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int 76 (Suppl 113):S1-S130, 2009
[5] Sigrist M, Tang M, Beaulieu M, Espino-Hernandez G, Er L, Djurdjev O, Levin A: Responsiveness of FGF-23 and mineral metabolism to altered dietary phosphate intake in chronic kidney disease (CKD): Results of a randomized trial. Nephrol Dial Transplant 28:161-169,2013
[6] Ichikawa S, Austin AM, Gray AK, Allen MR, EconsMJ: Dietary phosphate restriction normalizes biochemical and skeletal abnormalities in a murine model of tumoralcalcinosis. Endocrinology 152:4504-4513,2011
[7] Lynch KE, Lynch R, Curhan GC, Brunelli SM: Prescribed dietary phosphate restriction and survival among hemodialysis patients. Clin J Am Soc Nephrol 6:620-629, 2011


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