Reviewer response for version 1
This paper reports a patient with small cell cancer and recurrent episodes of hyponatremia. 
The first episode was entirely consistent with SIADH and responded to water restriction and demeclocycline. 
The second episode of hyponatremia occurred with a nadir Na of 118 and an “inappropriately” concentrated urine of 563 and a high urine Na of 128 mm/l. 
The measured ADH level was low and his aldosterone level was also low. 
The patient seemed to be euvolemic on exam.
Clearly this patient had inappropriate urine concentration with a high urine osmolality, clinical euvolemia, and a urine Na of 128. 
The question is why. 
The single serum ADH level was low but is it correct? 
If it is truly low (and a level of 1.7 may still be too high for a plasma Na of 125) then something else is driving urine concentration.
My understanding of ANP is in agreement with the author’s figure 3: it increases renal blood flow, GFR, and causes natiuresis. 
But it does not directly generate a concentrated urine. 
If ANP causes too much natiuresis (ie an “inappropriate ANP” syndrome) then the urine will become concentrated as a result of ECF volume contraction and high ADH levels. 
If the authors are proposing that “inappropriate ANP” syndrome can generate hyponatremia independent of elevated ADH levels this would be a new physiologic principal and I need a lot more evidence that this can occur than what is presented in this manuscript.
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