Int Urol Nephrol (2014) 46:2239–2241 DOI 10.1007/s11255-014-0817-8
NEPHROLOGY - LETTER TO THE EDITOR
Asymptomatic hyponatremia in peritoneal dialysis patients: an algorithmic approach Carlos G. Musso · Joanne M. Bargman
Received: 26 July 2014 / Accepted: 5 August 2014 / Published online: 22 August 2014 © Springer Science+Business Media Dordrecht 2014
Editor, Hyponatremia is a serious electrolyte problem, with significant prevalence (around 15 %) and unique pathophysiological characteristics in peritoneal dialysis patients [1–4]. We have designed an algorithm for guiding assessment and therapeutic approach to the asymptomatic form of this disorder. Low serum sodium concentration in peritoneal dialysis can be induced by one or more of the following mechanisms: • water and salt excess due to high oral intake (water in excess of sodium) and/or low water excretion (insufficient ultrafiltration). This situation occurs with an increase in body weight, as well as clinical signs of volume overload (edema, venous congestion, and hypertension) (5) • extracellular fluid sodium deficit due to a low intake (low sodium diet) and/or excess sodium loss (excessive ultrafiltration). Clinical clues include a reduction in body weight, signs of volume contraction (hypotension, orthostatic hypotension, and axillary dryness), and low total body water documented by bioelectrical impedance analysis (BIA) [5–7]. • potassium deficit due to low oral intake (low potassium diet) and/or excess potassium loss (such as with diarrhea). Intracellular potassium depletion induces sodium to shift from the extracellular compartment to the intracellular one, in order to keep body compartments elec-
trically neutral. The flux of sodium from the extracellular fluid to the intracellular compartment, leads to extracellular volume contraction. This scenario presents with a reduction in body weight and there may be clinical signs of hypovolemia, but not always hypokalemia [1, 8]. • intracellular phosphate/potassium deficit due to malnutrition. This phenomenon leads to intracellular hypoosmolarity and consequently to water redistribution to extracellular compartment. This mechanism of dilutional hyponatremia presents with reduced body weight (lean mass reduction) but without signs of volume contraction [6, 8]. • free water excess due to an inadequate vasopressin suppression secondary to drugs (opioids, psychotropic medications), endocrinopathies (hypothyroidism, hypoaldosteronism), and other diseases: neurologic, pulmonary, or paraneoplastic ones) in a setting of significant residual renal function (RRF): GFR: 15–20 ml/ min/1.73 m2, such as those patients who start peritoneal dialysis “earlier” due to refractory hyperkalemia or concomitant cardiac failure [9]. • change in the set point for serum sodium tonicity: osmostat reset. This is a hypothesis and should be a diagnosis of exclusion (1)
C. G. Musso (*) Nephrology Division, Hospital Italiano de Buenos Aires, 14 de Julio 246, 1834 Temperley, Province of Buenos Aires, Argentina e-mail: [email protected]
The last two clinical settings mentioned above (free water excess and reset osmostat) typically present without edema or body weight change. Then, based on the above data, we delineated the following algorithm for evaluating asymptomatic hyponatremia in peritoneal dialysis patients
J. M. Bargman The Home Peritoneal Dialysis Unit, University Health Network, University of Toronto, Toronto, Canada
• First step Rule out pseudohyponatremia (severe paraproteinemia, dyslipidemia) (Fig. 1).
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Int Urol Nephrol (2014) 46:2239–2241
serum potassium & nutritional status Asymptomatic Hyponatremia
hypokalemia: potassium supply malnutrition: nourish with caution
* serum glucose & icodextrin use
hyperglycemia: insulin
*First, rule out pseudohyponatremia
Fig. 1 Initial evaluation of asymptomatic hyponatremia. *First, rule out pseudohyponatremia
• Second step Evaluate hyperosmotic hyponatremia (hyperglycemia, icodextrin use) (Fig. 1). • Third step Evaluate the serum potassium level and nutritional status. If the patient presents with hypokalemia, or intracellular potassium depletion is strongly suspected (e.g., in diuretic-induced hyponatremia), potassium should be administered cautiously and with close monitoring of the serum potassium level. If the patient is malnourished, adequate nourishment should be provided, but first assuring normal serum
Fig. 2 Extracellular volume evaluation. RRF renal residual function, Na sodium, ADH antidiuretic hormone, ECV extracellular volume
potassium and phosphorus levels, as well as monitoring them during this process in order to avoid re-feeding syndrome. After that serum sodium should be re-evaluated (Fig. 2). • Fourth step Evaluate extracellular volume (ECV). If ECV is high, negative volume balance should be induced. For this purpose, dextrose-based solutions (removal through aquaporins by osmosis) may be better than icodextrin (removal through small pores by colloid osmosis) since they remove water in excess of sodium, particularly with exchanges of shorter duration (1). If ECV is low, salt supply should be delivered (orally or intravenously, depending on the acuity of the situation); and if ECV is normal with significant residual renal function (RRF), consideration should be given to vasopressin—driven renal water retention; in those without significant RRF, it could be interpreted as an osmostat reset (Fig. 2). In conclusion, we consider that this simple algorithm, with the limitations of any scheme, can help those looking after peritoneal dialysis patients to a systematic approach to asymptomatic hyponatremia.
Extracellular Volume Status evaluation by clinical exam & bioimpedance
HIGH: reduce water supply and increase ultrafiltration re-evaluate If persists despite ECV correction
13
NORMAL: - inadequate suppresion of ADH in high RRF - reset osmostat
LOW: increase Na supply re-evaluate If persists despite ECV correction
Int Urol Nephrol (2014) 46:2239–2241 Conflict of interest The authors declare that they have received no financial support for this original report and that they have no conflicts of interests.
References 1. Dimitriadis C, Sekercioglu N, Pipili C, Oreopoulos D, Bargman J (2013) Hyponatremia in peritoneal dialysis: epidemiology in a single center and correlation with clinical and biochemical parameters. Perit Dial Int 34:260–270 2. Halperin M, Hyponatremia Goldstein M (1999) In: Halperin M, Goldstein M (eds) Fluid, electrolyte, and acid-base physiology. W.B. Saunders, Philadelphia, pp 283–328 3. Port F, Young E (1996) Fluid, electrolyte disorders in dialysis. In: Kokko J, Tannen R (eds) Fluids and electrolytes. W.B. Saunders, Philadelphia, pp 533–560
2241 4. Cherney DZ, Zevallos G, Oreopoulos D, Halperin ML (2001) A physiological analysis of hyponatremia: implications for patients on peritoneal dialysis. Perit Dial Int 21(1):7–13 5. Kang S, Cho K, Park J, Yoon K, Do J (2013) Characteristics and clinical outcomes of hyponatraemia in peritoneal dialysis patients. Nephrology 18:132–137 6. Uribarri IJ, Prabhakar S, Kahn T (2004) Hyponatremia in peritoneal dialysis patients. Clin Nephrol 61:54–58 7. Musso CG, Capotondo M, Duarte G, Núñez HR, Núñez JFM (2013) Hyponatremia secondary to a sodium deficit in patients on continuous out-patient peritoneal dialysis. Electron J Biomed 1:1–2 8. Zevallos G, Oreopoulos DG, Halperin ML (2001) Hyponatremia in patients undergoing CAPD: role of water gain and/or malnutrition. Perit Dial Int 21(1):72–76 9. Sterns R, Spital A, Clark E (1996) Disorders of water balance. In: Kokko J, Tannen R (eds) Fluids and electrolytes. W.B. Saunders, Philadelphia, pp 63–109
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NEPHROLOGY - LETTER TO THE EDITOR
Asymptomatic hyponatremia in peritoneal dialysis patients: an algorithmic approach Carlos G. Musso · Joanne M. Bargman
Received: 26 July 2014 / Accepted: 5 August 2014 / Published online: 22 August 2014 © Springer Science+Business Media Dordrecht 2014
Editor, Hyponatremia is a serious electrolyte problem, with significant prevalence (around 15 %) and unique pathophysiological characteristics in peritoneal dialysis patients [1–4]. We have designed an algorithm for guiding assessment and therapeutic approach to the asymptomatic form of this disorder. Low serum sodium concentration in peritoneal dialysis can be induced by one or more of the following mechanisms: • water and salt excess due to high oral intake (water in excess of sodium) and/or low water excretion (insufficient ultrafiltration). This situation occurs with an increase in body weight, as well as clinical signs of volume overload (edema, venous congestion, and hypertension) (5) • extracellular fluid sodium deficit due to a low intake (low sodium diet) and/or excess sodium loss (excessive ultrafiltration). Clinical clues include a reduction in body weight, signs of volume contraction (hypotension, orthostatic hypotension, and axillary dryness), and low total body water documented by bioelectrical impedance analysis (BIA) [5–7]. • potassium deficit due to low oral intake (low potassium diet) and/or excess potassium loss (such as with diarrhea). Intracellular potassium depletion induces sodium to shift from the extracellular compartment to the intracellular one, in order to keep body compartments elec-
trically neutral. The flux of sodium from the extracellular fluid to the intracellular compartment, leads to extracellular volume contraction. This scenario presents with a reduction in body weight and there may be clinical signs of hypovolemia, but not always hypokalemia [1, 8]. • intracellular phosphate/potassium deficit due to malnutrition. This phenomenon leads to intracellular hypoosmolarity and consequently to water redistribution to extracellular compartment. This mechanism of dilutional hyponatremia presents with reduced body weight (lean mass reduction) but without signs of volume contraction [6, 8]. • free water excess due to an inadequate vasopressin suppression secondary to drugs (opioids, psychotropic medications), endocrinopathies (hypothyroidism, hypoaldosteronism), and other diseases: neurologic, pulmonary, or paraneoplastic ones) in a setting of significant residual renal function (RRF): GFR: 15–20 ml/ min/1.73 m2, such as those patients who start peritoneal dialysis “earlier” due to refractory hyperkalemia or concomitant cardiac failure [9]. • change in the set point for serum sodium tonicity: osmostat reset. This is a hypothesis and should be a diagnosis of exclusion (1)
C. G. Musso (*) Nephrology Division, Hospital Italiano de Buenos Aires, 14 de Julio 246, 1834 Temperley, Province of Buenos Aires, Argentina e-mail: [email protected]
The last two clinical settings mentioned above (free water excess and reset osmostat) typically present without edema or body weight change. Then, based on the above data, we delineated the following algorithm for evaluating asymptomatic hyponatremia in peritoneal dialysis patients
J. M. Bargman The Home Peritoneal Dialysis Unit, University Health Network, University of Toronto, Toronto, Canada
• First step Rule out pseudohyponatremia (severe paraproteinemia, dyslipidemia) (Fig. 1).
13
2240
Int Urol Nephrol (2014) 46:2239–2241
serum potassium & nutritional status Asymptomatic Hyponatremia
hypokalemia: potassium supply malnutrition: nourish with caution
* serum glucose & icodextrin use
hyperglycemia: insulin
*First, rule out pseudohyponatremia
Fig. 1 Initial evaluation of asymptomatic hyponatremia. *First, rule out pseudohyponatremia
• Second step Evaluate hyperosmotic hyponatremia (hyperglycemia, icodextrin use) (Fig. 1). • Third step Evaluate the serum potassium level and nutritional status. If the patient presents with hypokalemia, or intracellular potassium depletion is strongly suspected (e.g., in diuretic-induced hyponatremia), potassium should be administered cautiously and with close monitoring of the serum potassium level. If the patient is malnourished, adequate nourishment should be provided, but first assuring normal serum
Fig. 2 Extracellular volume evaluation. RRF renal residual function, Na sodium, ADH antidiuretic hormone, ECV extracellular volume
potassium and phosphorus levels, as well as monitoring them during this process in order to avoid re-feeding syndrome. After that serum sodium should be re-evaluated (Fig. 2). • Fourth step Evaluate extracellular volume (ECV). If ECV is high, negative volume balance should be induced. For this purpose, dextrose-based solutions (removal through aquaporins by osmosis) may be better than icodextrin (removal through small pores by colloid osmosis) since they remove water in excess of sodium, particularly with exchanges of shorter duration (1). If ECV is low, salt supply should be delivered (orally or intravenously, depending on the acuity of the situation); and if ECV is normal with significant residual renal function (RRF), consideration should be given to vasopressin—driven renal water retention; in those without significant RRF, it could be interpreted as an osmostat reset (Fig. 2). In conclusion, we consider that this simple algorithm, with the limitations of any scheme, can help those looking after peritoneal dialysis patients to a systematic approach to asymptomatic hyponatremia.
Extracellular Volume Status evaluation by clinical exam & bioimpedance
HIGH: reduce water supply and increase ultrafiltration re-evaluate If persists despite ECV correction
13
NORMAL: - inadequate suppresion of ADH in high RRF - reset osmostat
LOW: increase Na supply re-evaluate If persists despite ECV correction
Int Urol Nephrol (2014) 46:2239–2241 Conflict of interest The authors declare that they have received no financial support for this original report and that they have no conflicts of interests.
References 1. Dimitriadis C, Sekercioglu N, Pipili C, Oreopoulos D, Bargman J (2013) Hyponatremia in peritoneal dialysis: epidemiology in a single center and correlation with clinical and biochemical parameters. Perit Dial Int 34:260–270 2. Halperin M, Hyponatremia Goldstein M (1999) In: Halperin M, Goldstein M (eds) Fluid, electrolyte, and acid-base physiology. W.B. Saunders, Philadelphia, pp 283–328 3. Port F, Young E (1996) Fluid, electrolyte disorders in dialysis. In: Kokko J, Tannen R (eds) Fluids and electrolytes. W.B. Saunders, Philadelphia, pp 533–560
2241 4. Cherney DZ, Zevallos G, Oreopoulos D, Halperin ML (2001) A physiological analysis of hyponatremia: implications for patients on peritoneal dialysis. Perit Dial Int 21(1):7–13 5. Kang S, Cho K, Park J, Yoon K, Do J (2013) Characteristics and clinical outcomes of hyponatraemia in peritoneal dialysis patients. Nephrology 18:132–137 6. Uribarri IJ, Prabhakar S, Kahn T (2004) Hyponatremia in peritoneal dialysis patients. Clin Nephrol 61:54–58 7. Musso CG, Capotondo M, Duarte G, Núñez HR, Núñez JFM (2013) Hyponatremia secondary to a sodium deficit in patients on continuous out-patient peritoneal dialysis. Electron J Biomed 1:1–2 8. Zevallos G, Oreopoulos DG, Halperin ML (2001) Hyponatremia in patients undergoing CAPD: role of water gain and/or malnutrition. Perit Dial Int 21(1):72–76 9. Sterns R, Spital A, Clark E (1996) Disorders of water balance. In: Kokko J, Tannen R (eds) Fluids and electrolytes. W.B. Saunders, Philadelphia, pp 63–109
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