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|Year : 2007 | Volume
| Issue : 1 | Page : 20--22
Hyponatremia and hypokalemia in a continuous ambulatory peritoneal dialysis patient
CH Ramakrishna, K Sunil Kumar, S Padmnabhan, V Siva Kumar
Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati - 517501, Andhra Pradesh, India
V Siva Kumar
Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati - 517 501, Andhra Pradesh
Patients on dialysis cannot independently regulate salt and water removal. Although hypokalemia has been reported to occur in 10-36% of peritoneal dialysis patients, hyponatremia is uncommon. We describe a rare case in whom hyponatremia and hypokalemia developed while on continuous ambulatory peritoneal dialysis and discuss the management.
|How to cite this article:|
Ramakrishna C H, Sunil Kumar K, Padmnabhan S, Siva Kumar V. Hyponatremia and hypokalemia in a continuous ambulatory peritoneal dialysis patient.Indian J Nephrol 2007;17:20-22
|How to cite this URL:|
Ramakrishna C H, Sunil Kumar K, Padmnabhan S, Siva Kumar V. Hyponatremia and hypokalemia in a continuous ambulatory peritoneal dialysis patient. Indian J Nephrol [serial online] 2007 [cited 2023 Feb 8 ];17:20-22
Available from: https://www.indianjnephrol.org/text.asp?2007/17/1/20/35017
The kidneys have an inherent capacity to independently regulate sodium and water excretion. In normal persons, despite wide variations in sodium and water intake, serum sodium is maintained within the normal range. Dialysis patients, especially when they are anuric, cannot independently regulate salt and water removal since water removal during dialysis is necessarily associated with sodium removal. Even then hyponatremia is uncommon in peritoneal dialysis (PD) and is reported to occur in only around 2.4% of such patients.  Hypokalemia has been reported to occur in 10-36% of PD patients and is attributed to the ongoing potassium losses in the dialysate, coupled with poor intake of potassium.  In the current report, we discuss the management of hyponatremia and hypokalemia in a continuous ambulatory peritoneal dialysis (CAPD) patient.
A 56-year-old postmenopausal woman with chronic kidney disease stage V, presumed to be due to chronic interstitial nephritis and hypertension, was started on CAPD in March 2004. She was on three exchanges (1.5%, 2.5%, and 2.5% dextrose; 2 l each) per day; the ultrafiltrate being 1000 to 1200 ml. She was a low-average transporter. She was not a diabetic. Her dry weight was 47.5 kg. Her medications included amlodipine 10 mg/day, calcium acetate 667 mg thrice daily, and inj. erythropoietin 2000 units SC twice a week. She was admitted to our emergency ward on 16-07-2004 with lethargy, fatigue, nausea, and persistent vomiting of 10 days' duration. She had also had two episodes of generalized tonic-clonic seizures a day prior to admission.
On examination she was in fluid overload with a weight gain of 9.5 kg. She was drowsy without any lateralizing signs. Evaluation revealed severe hyponatremia (112 mEq/l), hypokalemia (3.2 mEq/l), and severe hyperglycemia (550 mg/dl). She was stabilized with corrective measures for the hyponatremia and hypokalemia, and with dialysis, insulin, and phenytoin. She was discharged on insulin. Her weight at the time of discharge was 48 kg. She was on regular follow-up and her serum sodium and potassium were always low, ranging between 120-125 mEq/l and 2.6-3.2 mEq/l, respectively. She did not need antidiabetic medication after October 2004. She was readmitted in July 2005 for evaluation of complaints of weakness, nausea, and fatigue. Her weight was 47 kg. Serum sodium, potassium, and fasting and postprandial blood sugars were 124 mEq/l, 3.2 mEq/l, 110 mg% and 130 mg%, respectively.
We did a 24-h PD fluid effluent analysis for assessment of sodium and potassium losses; this was as follows: she had received three exchanges of 2 l each, 1.5%, 2.5%, and 2.5% dextrose containing potassium-free PD fluid (6 l in all, with total sodium of 792 mEq/l, as the sodium content of the PD fluid was 132 mEq/l); she had an ultrafiltrate of 1000 ml (the total volume drained was 7 l). The total 24-h PD fluid sodium and potassium were found to be 910 mEq and 17 mEq, respectively, when her serum sodium and potassium levels were 128 mEq/l and 2.8 mEq/l. Therefore, with a daily ultrafiltrate of 1000-1200 ml, she was losing around 130-156 mEq/day of sodium and 17-20 mEq/day of potassium. Her symptoms improved with oral and parenteral sodium supplementation and oral potassium chloride.
The serum sodium concentration is determined by the body's sodium, potassium, and total body water content. Hyponatremia, defined as serum sodium concentration less than 130 mEq/l, can therefore occur by an increase in electrolyte-free water, a decrease in body solutes (either Na + or K + ), or any combination of both. In most cases, more than one of these mechanisms operate. 
When hyponatremia occurs in hospitalized patients, it is usually due to a disorder of water balance. However patients on PD are unique in that they cannot undergo a water diuresis when given a water load; water removal in PD is necessarily associated with sodium removal.  In stable CAPD patients, the average daily water removal was 1220 ml with a sodium concentration of 132 mmol/l, indicating that a sodium intake of 160 mmol/day would be required to maintain sodium balance in these patients. Thus, in the dialysis setting, increased water intake will always result in hyponatremia unless the increased water intake is accompanied by an increase in sodium intake. 
During PD, in the early part of the dwell sodium removal is primarily by ultrafiltration despite the interplay of the sodium sieving effect. In the later part of the dwell it is mainly by diffusion.  This phenomenon highlights the importance of ultrafiltration in sodium handling, suggesting that there is higher sodium removal as the concentration of the hypertonic dextrose in the peritoneal dialysate increases. Dialysate sodium loss is primarily influenced by the net volume of dialysate removed. Serum sodium concentration is much less important than dialysate water removal in influencing sodium loss.
In a 4-h dwell of 1.5% dextrose, the sodium removal is about 5 mEq, whereas in a 4-h dwell of 4.25% dextrose the sodium removal is about 70 mEq; This indicates the important effect of hypertonic dextrose in the dialysate on sodium removal. This knowledge helps in making prescription adjustments in problematic hyponatremic PD patients. Keeping this variability in sodium removal in mind, we measured the sodium content in 24-h PD effluent and found that the sodium loss was 130-156 mmol with a prescription of one exchange of 1.5% dextrose and two exchanges of 2.5% dextrose, with an ultrafiltrate of 1000 to 1200 ml daily.
In CAPD patients, hyponatremia has been described in three different situations. Occurrence of hyponatremia with weight gain implies that a positive balance of electrolyte-free water is the basis for the hyponatremia. In some situations hyponatremia may be observed in the absence of weight gain; in these cases, the sodium deficit is because of reduced intake or excessive dialytic sodium removal. It may be associated with extracellular fluid (ECF) volume concentration. Sometimes, in malnutrition or catabolic states, loss of potassium and inorganic phosphates from the intracellular compartment is the cause of the hyponatremia. It is associated with expansion of ECF volume, with or without weight loss. 
In our patient, at the first admission in July 2004, hyponatremia was associated with a fluid overload and a weight gain of 9.5 kg. The electrolyte-free water gain was considered to be responsible for the hyponatremia. With energetic dialysis support and fluid removal, her weight was reduced and the serum sodium improved to 134 mEq/l. During the second admission in July 2005, though she was hyponatremic, there was no change in her body weight. Hyponatremia was secondary to the sodium loss associated with dialytic water removal and also because of inadequate intake as, despite our dietary advice, the patient and her attendants revealed that they had restricted sodium intake through the diet. Hyponatremia was corrected with oral and IV saline.
Hypokalemia is reported to occur in 10-36% of CAPD patients as a result of potassium loss through the dialysate, inadequate intake, bowel losses, and cellular uptake.  In our patient, association of hypokalemia with hyponatremia was attributed to the potassium loss through the dialysate, inadequate intake, and obligatory losses through the bowel. The hypokalemia was corrected with potassium supplementation.
The treatment of hyponatremia in dialysis patients is guided by the understanding of the mechanisms of its causation. If hyponatremia is due to gain in electrolyte-free water, the aim should be to remove free water and to restrict water intake. If the fall in serum sodium is greater than can be explained by the weight gain, there is bound to be sodium depletion. An increase in serum sodium can be achieved by giving sodium either orally or parenterally. If the hyponatremia is due to malnutrition or a catabolic state, the aim should be to restore intracellular fluid composition (i.e., to correct malnutrition). Persistent hypokalemia needs correction with potassium supplementation.
In conclusion, hyponatremia and hypokalemia are uncommon in PD patients. Our case report highlights the fact that to maintain normal serum sodium and potassium concentrations, salt and potassium intake must be proportional to the water loss by dialysis, because dialytic water removal is necessarily associated with their removal.
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