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NDT Advance Access originally published online on August 5, 2008
Nephrology Dialysis Transplantation 2008 23(10):3366; doi:10.1093/ndt/gfn414
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Correcting hypervolaemic hypernatraemia

Nephrol Dial Transplant 2008; doi:10.1093/ndt/gfn418

E-mail: tring{at}gvdnet.dk

Sir,

Nguyen and Kurtz [1] have provided a formula to help achieve a negative Na+ + K+ balance and a negative water balance to treat hypervolaemic hypernatraemia by infusing a modelled volume of isotonic glucose (D5W) and furosemide.

The formula, however, is not easy to use. Besides knowing the initial [Na] and deciding on a required endpoint in [Na] and a desired reduction in total body water (VMB), you will have to know the initial total body water (TBW1), and what is more demanding, you will have to know the combined [E]urine = [Na+] + [K+] in urine over the treatment course.

In practice, knowing both TBW1 and [E]urine is not straightforward. In their patient example, the authors happen to know in advance that [E]urine is going to be 80 mmol/l, and from that they compute a volume of D5W infusate of 5.6 l. If instead of assuming that [E]urine is known, we let it vary between, say, 60 mmol/l and 140 mmol/l, we get from the authors’ formula a volume of infusate between 2.4 l and 8.2 l. Even more important, if we keep the volume of infusate at 5.6l and investigate the final [Na+] resulting solely from changing the [E]urine within the range 60– 140 mmol/l, we get a new [Na+] ranging from 123 mmol/l to 146 mmol/l. This uses a new ancillary formula we have devised solely with the intent of avoiding accidents secondary to using the formula given by Nguyen and Kurtz at face value (ignoring, as they do in their example, non-renal outputs and non-infusate inputs):


Formula

The patient's history, which the authors use to illustrate the utility of their formula, is extraordinary. The patient is not stated to be demented, to have diabetes insipidus or osmotic diuresis, or to have been denied access to water, or to have been given hypertonic saline, yet this elderly lady with congestive heart failure develops hypernatraemia that is said to be secondary to furosemide treatment. This is indeed a rare occurrence, and hyponatraemia would be more likely under these circumstances.

Besides that, as previously demonstrated [2], the modelled intercept term 23.8 from Edelman [3] is very uncertain with 99% CI including 0 since all measurements of (exchangeable sodium + exchangeable potassium)/total body water were very far from 0.

Hence, returning to the patient's history, we fully agree with the authors that any formula is dangerous without frequent and comprehensive assessment of the response to treatment. In practice, administering furosemide and D5W (or water per os?) would not be much helped by using a formula with at least two unknown central entries always in need of an update. Rather, the existence of a pseudo-accurate formula might comfort the caretakers unduly into becoming less scrupulous. This pertains in particular to a situation in which the underlying pathophysiology is not well understood, for instance, the absence of the expected increased Na excretion under hypernatraemia [4] as in the patient described.

Conflict of interest statement. None declared.

Troels Ring1 and Christian Overgaard2

1 Department of Nephrology Aalborg Hospital, Hobrovej 18-22 Aalborg 2 Department of Anesthesiology Aarhus University Hospital, Aarhus Denmark

References

  1. Nguyen MK, Kurtz I. Correction of hypervolemic hypernatremia by inducing negative Na+ and K+ balance in excess of negative water balance: a new quantitative approach. Nephrol Dial Transplant (2008) 23:2223–2227.[Abstract/Free Full Text]
  2. Ring T. Response to ‘quantitative analysis of the Dysnatremias’. Kidney Int (2006) 70:1381–1382.[CrossRef]
  3. Edelman IS, Leibman J, O’Meara MP, et al. Interrelationships between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. J Clin Invest (1958) 37:1236–1256.[Web of Science][Medline]
  4. Kamm De, Levinsky NG. Inhibition of renal tubular sodium reabsorption by hypernatremia. J Clin Invest (1965) 44:1144–1150.[CrossRef][Web of Science][Medline]

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This Article
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