Phosphate Homeostasis in Chronic Kidney Disease with Emphasis in Peritoneal Dialysis

Round 1

Reviewer 1 Report

Comments and Suggestions for Authors

In this article, the authors provide an overview of phosphate homeostasis in dialysis patients. It is right that this should be an important aspect of clinical care for peritoneal dialysis patients.

Remarks:

• the title of the article does not correlate very well with the content of the article: only the introduction and sub-section 10 (Clinical approach...) talk about PD.
• phosphate homeostasis is described in general, not with a focus on PD. 
• there is a lack of mention the importance of phosphate as a uremic toxin
• uremic state and duration of PD cause peritoneal deterioration – thus, pathophysiological mechanisms of phosphate importance from this aspect can also be included. Homeostasis changes over time in PD patients, resulting in an ultrafiltration disorder - what causes this? And, are there changes in the clinical approach?

Author Response

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Author Response File: Author Response.pdf

Reviewer 2 Report

Comments and Suggestions for Authors

The aim of the review is to explain the main aspects of body phosphate homeostasis in healthy subject and in dialysis patients, which is important for a more rational approach to manage serum phosphate in ESRD patients and especially in those on peritoneal dialysis. With that aim, the author first clearly explained the phosphate balance in healthy subjects and patients on CAPD followed by logical chapters on absorption, hormonal regulation and other links in the chain of maintenance of phosphate homeostasis. The text is clear and I only have a couple of suggestions.

1. No references are cited in subchapter 5 and 6 (Exchange of Phosphate Between Extra-and Intracellular Fluids and Exchange of Phosphate with Bone) and I think they are needed.
2. The part about the hormonal regulation of phosphate should be described in a little more detail. The author cites the work of Jacquillet G & Unwin RJ, but there are several other papers that provide data on the role of all hormones in phosphate regulation, especially FGF23 and Klotho. That's why I suggest that that part of the paper be expanded a little.

Author Response

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Author Response File: Author Response.pdf

Reviewer 3 Report

Comments and Suggestions for Authors

I was given to the opportunity to review the manuscript on Phosphat homeostasis in PD.

The review is written in a very clear and informative way, and I enjoyed reading it. The topic is narrated with quantitative aspects that illustrate the problem of the prevailing hyperphosphatemia in PD patients and the possibility to mitigate it.

I have the following suggestions:

-in the legend of Figure 1: it is stated that 900 mg must be divided by 11 l. However, the patient has filling volumes of 4 x 2 l + 1 l UF, yielding 9 l. Please clarify.

-line 43 / 165: please always give the concentration in mM as well

-please consider to discuss and cite the following publication: PMID 28531904

-line 92: it should read H2PO4 - and H2PO4 2-

-line 164: duplication of the term “348 mg of Ca added”

-line 252: a vascular tree in a PD patient is shown here https://turkjnephrol.org/Content/files/sayilar/431/22-TJN_20220375_nlm_new_indd.pdf

Please cite.

-please give an estimate of intracellular phosphorus concentration which I recall to be around 30 mM. This is in vast excess over extracellular P.

-I suggest to mention the idea of premature aging caused by high P: PMID 20197072

Author Response

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Author Response File: Author Response.pdf

Round 2

Reviewer 1 Report

Comments and Suggestions for Authors

Now the title sounds better. The text has been adequately supplemented.

Since serum phosphate measured in clinical laboratories is only inorganic, Pi should be used as the abbreviation, not P. This should be consistent throughout the article.