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Published ahead of print on February 6, 2009
Clin J Am Soc Nephrol 4: 309-315, 2009
© 2009 American Society of Nephrology
doi: 10.2215/CJN.02740608

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Clinical Nephrology

More on Renal Salt Wasting Without Cerebral Disease: Response to Saline Infusion

Solomon Bitew*, Louis Imbriano*,{dagger}, Nobuyuki Miyawaki*,{dagger}, Steven Fishbane*,{dagger}, and John K. Maesaka*,{dagger}

* Division of Nephrology and Hypertension and Department of Medicine, Winthrop-University Hospital, Mineola, New York; and {dagger} State University of New York Stony Brook Medical School, Stony Brook, New York

Correspondence: Dr. John K. Maesaka, 200 Old Country Road, Suite 135, Mineola, NY 11501. Phone: 516-663-2169; Fax: 516-663-2179; E-mail: jmaesaka{at}winthrop.org

Background and objectives: The existence and prevalence of cerebral salt wasting (CSW) or the preferred term, renal salt wasting (RSW), and its differentiation from syndrome of inappropriate antidiuretic hormone (SIADH) have been controversial. This controversy stems from overlapping clinical and laboratory findings and an inability to assess the volume status of these patients. The authors report another case of RSW without clinical cerebral disease and contrast it to SIADH.

Design, setting, participants, & measurements: Three patients with hyponatremia, hypouricemia, increased fractional excretion (FE) of urate, urine sodium >20 mmol/L, and concentrated urines were infused with isotonic saline after collection of baseline data.

Results: One patient with RSW had pneumonia without cerebral disease and showed increased plasma aldosterone and FEphosphate, and two patients with SIADH had increased blood volume, low plasma renin and aldosterone, and normal FEphosphate. The patient with RSW responded to isotonic saline by excretion of dilute urines, prompt correction of hyponatremia, and normal water loading test after volume repletion. Hypouricemia and increased FEurate persisted after correction of hyponatremia. Two patients with SIADH failed to dilute their urines and remained hyponatremic during 48 and 110 h of saline infusion.

Conclusions: The authors demonstrate appropriate stimulation of ADH in RSW. Differences in plasma renin and aldosterone levels and FEphosphate can differentiate RSW from SIADH, as will persistent hypouricemia and increased FEurate after correction of hyponatremia in RSW. FEphosphate was the only contrasting variable at baseline. The authors suggest an approach to treat the hyponatremic patient meeting criteria for SIADH and RSW and changing CSW to the more appropriate term, RSW.







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