4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Dietary phosphorus and renal disease in cats: where are we?

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Practical relevance:

          Phosphorus is an essential nutrient required for the normal function of every cell in the body and a deficiency in dietary phosphorus may lead to adverse effects. Conversely, high dietary phosphorus may cause kidney damage in otherwise healthy adult cats, particularly when provided in highly bioavailable forms and when the calcium-to-phosphorus ratio is low. For cats that have chronic kidney disease (CKD), phosphorus is the most important mineral in its pathogenesis and morbidity. As the disease progresses, elevated phosphorus may increase the risk of complications such as soft tissue mineralization, which can lead to a further decrease in renal function. Additionally, the hormones secreted in response to increased circulating phosphorus have harmful effects, such as bone resorption, and can cause cardiovascular pathology. Very low phosphorus diets can also be problematic in cats with early CKD, potentially leading to hypercalcemia.

          Clinical challenges:

          There is currently a lack of maximum safety limits for dietary phosphorus in accepted nutritional guidelines in North American and Europe, which makes it difficult to assess the safety of some higher phosphorus cat foods. Additionally, information regarding phosphorus bioavailability is unknown for many diets and there are no commercially available tests. Similarly, there is no consensus regarding phosphorus requirement and recommended intake in cats with International Renal Interest Society stage 1-4 CKD despite there being targets for serum phosphorus.

          Aims:

          This review evaluates dietary phosphorus in healthy cats and cats with renal disease, and describes how newer research is informing evolving clinical approaches in feline nutrition.

          Audience:

          The article is aimed at general practitioners, internal medicine specialists and veterinary nutritionists.

          Evidence base:

          Information provided in this article is drawn from the published literature.

          Related collections

          Most cited references26

          • Record: found
          • Abstract: found
          • Article: not found

          Renal control of calcium, phosphate, and magnesium homeostasis.

          Calcium, phosphate, and magnesium are multivalent cations that are important for many biologic and cellular functions. The kidneys play a central role in the homeostasis of these ions. Gastrointestinal absorption is balanced by renal excretion. When body stores of these ions decline significantly, gastrointestinal absorption, bone resorption, and renal tubular reabsorption increase to normalize their levels. Renal regulation of these ions occurs through glomerular filtration and tubular reabsorption and/or secretion and is therefore an important determinant of plasma ion concentration. Under physiologic conditions, the whole body balance of calcium, phosphate, and magnesium is maintained by fine adjustments of urinary excretion to equal the net intake. This review discusses how calcium, phosphate, and magnesium are handled by the kidneys.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Parathyroid hormone metabolism and signaling in health and chronic kidney disease

            Circulating parathyroid hormone (PTH) shows a complex relationship with hard outcomes in subjects with chronic kidney disease (CKD). Moreover, intervention studies directly targeting PTH failed to yield unequivocal results. Disturbed PTH metabolism, posttranslational modifications of PTH, and end-organ hyporesponsiveness to PTH may explain the poor performance of PTH as an outcome biomarker and precise target of therapy in the setting of CKD, at least in the gray middle target zone. PTH fragments accumulate in CKD patients and may exert effects that are distinct from, if not opposite to biointact (1-84)PTH. Posttranslational modification of PTH and especially oxidation may alter the interaction of PTH with its receptor. Its clinical relevance, however, remains a matter of ongoing debate. Less controversial is the issue of end-organ hyporesponsiveness to PTH. This phenomenon, formally referred to as PTH resistance, has long been recognized in CKD, but factors and mechanisms contributing to it remain poorly defined. Subsequent evidence identified downregulation of the PTH receptor and competing downstream signals as underlying pathophysiologic mechanisms. End-organ hyporesponsiveness to PTH in CKD, along with important analytical and biological variability, renders defining the PTH target range in CKD challenging. Although this may still be accomplished at the population level, it may prove to be very difficult at the individual level. This is a disillusioning thought in an era of personalized medicine. Parallel to the search of a functional and readily available assay quantifying PTH signaling tone or sensitivity, additional biomarkers (or a panel of biomarkers) should be formally evaluated.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Phosphate homeostasis and the renal-gastrointestinal axis.

              Transport of phosphate across intestinal and renal epithelia is essential for normal phosphate balance, yet we know less about the mechanisms and regulation of intestinal phosphate absorption than we do about phosphate handling by the kidney. Recent studies have provided strong evidence that the sodium-phosphate cotransporter NaPi-IIb is responsible for sodium-dependent phosphate absorption by the small intestine, and it might be that this protein can link changes in dietary phosphate to altered renal phosphate excretion to maintain phosphate balance. Evidence is also emerging that specific regions of the small intestine adapt differently to acute or chronic changes in dietary phosphate load and that phosphatonins inhibit both renal and intestinal phosphate transport. This review summarizes our current understanding of the mechanisms and control of intestinal phosphate absorption and how it may be related to renal phosphate reabsorption; it also considers the ways in which the gut could be targeted to prevent, or limit, hyperphosphatemia in chronic and end-stage renal failure.
                Bookmark

                Author and article information

                Contributors
                Journal
                J Feline Med Surg
                J Feline Med Surg
                JFM
                spjfm
                Journal of Feline Medicine and Surgery
                SAGE Publications (Sage UK: London, England )
                1098-612X
                1532-2750
                8 October 2024
                October 2024
                : 26
                : 10
                : 1098612X241283355
                Affiliations
                [1-1098612X241283355]Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Long Island University, New York, USA
                Author notes
                Author information
                https://orcid.org/0000-0002-0236-0128
                Article
                10.1177_1098612X241283355
                10.1177/1098612X241283355
                11529143
                39376053
                6aa97da7-28c8-47e9-a8e9-bd68d89cc54f
                © The Author(s) 2024

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Funding
                Funded by: Journal of Feline Medicine and Surgery, ;
                Categories
                Review
                Custom metadata
                October 2024
                ts1

                Surgery
                phosphorus,calcium,kidney,renal,diet,parathyroid hormone,fibroblast growth factor-23
                Surgery
                phosphorus, calcium, kidney, renal, diet, parathyroid hormone, fibroblast growth factor-23

                Comments

                Comment on this article