Saudi Journal of Kidney Diseases and Transplantation

LETTER TO THE EDITOR
Year
: 2011  |  Volume : 22  |  Issue : 4  |  Page : 810--811

Hypophosphatemia in peritoneal dialysis patients


Mohammadreza Ardalan1, Nazli Azabdaftari2, Hamid Noshad1, Mohammadali Mohajel Shoja3,  
1 Department of Nephrology, Tabriz University of Medical Sciences, Tabriz, Iran
2 Department of Nutrition, Diabetes Research Center, Jondishapour University of Medical Sciences, Ahvaz, Iran
3 Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

Correspondence Address:
Mohammadreza Ardalan
Department of Nephrology, Tabriz University of Medical Sciences, Tabriz
Iran




How to cite this article:
Ardalan M, Azabdaftari N, Noshad H, Shoja MM. Hypophosphatemia in peritoneal dialysis patients.Saudi J Kidney Dis Transpl 2011;22:810-811


How to cite this URL:
Ardalan M, Azabdaftari N, Noshad H, Shoja MM. Hypophosphatemia in peritoneal dialysis patients. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2020 Jul 14 ];22:810-811
Available from: http://www.sjkdt.org/text.asp?2011/22/4/810/82721


Full Text

To the Editor,

Hypophosphatemia is unusual in uremic patients. [1] Phosphate binder therapy, nutritional status, parathyroidectomy (hungry bone syndrome), and intracellular shifting are the major causes of hypophosphatemia among uremic patients. [2]

Severe hypophosphatemia has been reported in a few patients on peritoneal dialysis (PD) and hemodialysis who received total parental nutrition. [3] There is a report of severe hypophosphatemia in a PD patient without concomitant parenteral nutrition. [4]

Hypophosphatemia affects cellular-energy pathways, and by reducing erythrocyte 2,3-diphosphoglycerate produces tissue hypoxia. Rhabdomyolysis, impaired diaphragmatic contractility, seizures, heart failure and hemolysis could be the severe consequences of hypophosphatemia. [2]

We retrospectively studied all PD patients who had one recorded episode of hypophosphatemia (serum phosphate <2.5 mg/dL) to determine the presumptive risk factors [Table 1]. During a 7-year period and from the total 248 PD patients (M/F 130/118, age 2-87 years), 11 patients developed hypophosphatemia (<2.5 mg/ dL), eight (73%) patients developed hypophosphatemia after peritonitis, and three developed the same in the early period of PD. Death occurred in three elderly diabetic women with severe hypophosphatemia. High concentrated glucose of dialysis solutions during peritonitis episodes, high insulin release, high dosage of insulin administration and catabolic status could be the major risk factors of hypophosphatemia.{Table 1}

The results of our study showed that hypophosphatemia could occur in a substantial number of PD patients that could be fatal in some situations. The majority of hypophosphatemic patients were elderly diabetic women.

Hypophosphatemia generally occurs due to three basic mechanisms: low intestinal absorption, renal loss, and cellular shifting. [2] Intravenous glucose, insulin therapy, catecholamine release, and recovery from starvation are the major causes of cellular shifting of phosphorus. [5] In those with protein-calorie malnutrition, particularly when re-feeding is started with a carbohydrate diet, phosphorus shifting toward the intracellular space occurs. [6] Cellular shifting of phosphate and hypophosphatemia develop within a very short time and despite high initial phosphate levels. [3]

Intra-peritoneal carbohydrate load, nutritional recovery, low-protein and a high-carbohydrate diet and low phosphate intake are the predisposing factors for the development of hypophosphatemia at the start of PD. [7] Increased transporter state of peritoneal membrane, highly concentrated solutions and infection-induced catabolic state could be the predisposing factors for the development of hypophosphatemia after peritonitis episodes. Diabetes mellitus and insulin therapy could be the additional risk factors. We could not explain why majority of hypophosphatemic cases were elderly females.

We conclude that hypophosphatemia is easily overlooked and could be fatal in uremic patients. There are combinations of risk factors for the development of hypophosphatemia in some special situations in PD patients.

References

1Tejeda A, Saffarian N, Uday K. Hypophosphatemia in end stage renal disease. Nephron 1996;73:674-8.
2Brunelli SM, Goldfarb S. Hypophosphatemia: Clinical consequences and management. J Am Soc Nephrol 2005;16:520-8.
3Lin KK, Lee JJ, Chen HC. Severe refeeding hypophosphatemia in a CAPD patient: a case report. Ren Fail 2006;28:515-7.
4Ardalan MR, Pourafkari L, Tubbs RS, Shoja MM. Hypophosphatemic encephalopathy in a CAPD patient. Am J Med Sci 2008;335:492-4.
5Georges B, Thissen JP, Lsmbert M. Severe hypophosphatemia in a patient with anorexia nervosa during enteral refeeding. Acta Clin Belg 2004;59:361-4.
6Marinella MA. Refeeding Syndrome and Hypophosphatemia. J Intensive Care Med 2005;20: 155-9.
7Korbonits M, Blaine D, Elia M, Powell-Tuck J. Metabolic and hormonal changes during the refeeding period of prolonged fasting. Eur J Endocr 2007;157:157-66.