Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins
Abstract This study aimed to investigate whether phosphate contributes to the pathogenesis of chronic kidney disease (CKD) in dolphins. Renal necropsy tissue of an aged captive dolphin was analyzed and in vitro experiments using cultured immortalized dolphin proximal tubular (DolKT-1) cells were per...
| Main Authors: | , , , , , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2023-03-01
|
| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-023-32399-6 |
| _version_ | 1797853826886139904 |
|---|---|
| author | Nourin Jahan Hiroyuki Ohsaki Kiyoko Kaneko Asadur Rahman Takeshi Nishiyama Makoto Koizumi Shuichiro Yamanaka Kento Kitada Yuki Sugiura Kenji Matsui Takashi Yokoo Takayuki Hamano Makoto Kuro-o Takuya Itou Miwa Suzuki Keiichi Ueda Akira Nishiyama |
| author_facet | Nourin Jahan Hiroyuki Ohsaki Kiyoko Kaneko Asadur Rahman Takeshi Nishiyama Makoto Koizumi Shuichiro Yamanaka Kento Kitada Yuki Sugiura Kenji Matsui Takashi Yokoo Takayuki Hamano Makoto Kuro-o Takuya Itou Miwa Suzuki Keiichi Ueda Akira Nishiyama |
| author_sort | Nourin Jahan |
| collection | DOAJ |
| description | Abstract This study aimed to investigate whether phosphate contributes to the pathogenesis of chronic kidney disease (CKD) in dolphins. Renal necropsy tissue of an aged captive dolphin was analyzed and in vitro experiments using cultured immortalized dolphin proximal tubular (DolKT-1) cells were performed. An older dolphin in captivity died of myocarditis, but its renal function was within the normal range until shortly before death. In renal necropsy tissue, obvious glomerular and tubulointerstitial changes were not observed except for renal infarction resulting from myocarditis. However, a computed tomography scan showed medullary calcification in reniculi. Micro area X-ray diffractometry and infrared absorption spectrometry showed that the calcified areas were primarily composed of hydroxyapatite. In vitro experiments showed that treatment with both phosphate and calciprotein particles (CPPs) resulted in cell viability loss and lactate dehydrogenase release in DolKT-1 cells. However, treatment with magnesium markedly attenuated this cellular injury induced by phosphate, but not by CPPs. Magnesium dose-dependently decreased CPP formation. These data support the hypothesis that continuous exposure to high phosphate contributes to the progression of CKD in captive-aged dolphins. Our data also suggest that phosphate-induced renal injury is mediated by CPP formation in dolphins, and it is attenuated by magnesium administration. |
| first_indexed | 2024-04-09T19:57:05Z |
| format | Article |
| id | doaj.art-012b64be875745bba67c6ca815f50a15 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-04-09T19:57:05Z |
| publishDate | 2023-03-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-012b64be875745bba67c6ca815f50a152023-04-03T05:24:38ZengNature PortfolioScientific Reports2045-23222023-03-0113111310.1038/s41598-023-32399-6Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphinsNourin Jahan0Hiroyuki Ohsaki1Kiyoko Kaneko2Asadur Rahman3Takeshi Nishiyama4Makoto Koizumi5Shuichiro Yamanaka6Kento Kitada7Yuki Sugiura8Kenji Matsui9Takashi Yokoo10Takayuki Hamano11Makoto Kuro-o12Takuya Itou13Miwa Suzuki14Keiichi Ueda15Akira Nishiyama16Department of Pharmacology, Faculty of Medicine, Kagawa UniversityDepartment of Medical Biophysics, Kobe University Graduate School of Health ScienceFaculty of Pharmaceutical Sciences, Teikyo Heisei UniversityDepartment of Pharmacology, Faculty of Medicine, Kagawa UniversityPrime Hospital TamashimaLaboratory Animal Facility, Research Center for Medical Sciences, Jikei University School of MedicineDivision of Nephrology and Hypertension, Department of Internal Medicine, The Jikei University School of MedicineDepartment of Pharmacology, Faculty of Medicine, Kagawa UniversityMultiomics Platform, Center for Cancer Immunotherapy and Immunobiology, Kyoto University Graduate School of MedicineDivision of Nephrology and Hypertension, Department of Internal Medicine, The Jikei University School of MedicineDivision of Nephrology and Hypertension, Department of Internal Medicine, The Jikei University School of MedicineDepartment of Nephrology, Nagoya City University Graduate School of Medical SciencesDivision of Anti-Aging Medicine, Center for Molecular Medicine, Jichi Medical UniversityNihon University Veterinary Research Center, Nihon UniversityDepartment of Marine Science and Resources, College of Bioresource Sciences, Nihon UniversityOkinawa Churashima FoundationDepartment of Pharmacology, Faculty of Medicine, Kagawa UniversityAbstract This study aimed to investigate whether phosphate contributes to the pathogenesis of chronic kidney disease (CKD) in dolphins. Renal necropsy tissue of an aged captive dolphin was analyzed and in vitro experiments using cultured immortalized dolphin proximal tubular (DolKT-1) cells were performed. An older dolphin in captivity died of myocarditis, but its renal function was within the normal range until shortly before death. In renal necropsy tissue, obvious glomerular and tubulointerstitial changes were not observed except for renal infarction resulting from myocarditis. However, a computed tomography scan showed medullary calcification in reniculi. Micro area X-ray diffractometry and infrared absorption spectrometry showed that the calcified areas were primarily composed of hydroxyapatite. In vitro experiments showed that treatment with both phosphate and calciprotein particles (CPPs) resulted in cell viability loss and lactate dehydrogenase release in DolKT-1 cells. However, treatment with magnesium markedly attenuated this cellular injury induced by phosphate, but not by CPPs. Magnesium dose-dependently decreased CPP formation. These data support the hypothesis that continuous exposure to high phosphate contributes to the progression of CKD in captive-aged dolphins. Our data also suggest that phosphate-induced renal injury is mediated by CPP formation in dolphins, and it is attenuated by magnesium administration.https://doi.org/10.1038/s41598-023-32399-6 |
| spellingShingle | Nourin Jahan Hiroyuki Ohsaki Kiyoko Kaneko Asadur Rahman Takeshi Nishiyama Makoto Koizumi Shuichiro Yamanaka Kento Kitada Yuki Sugiura Kenji Matsui Takashi Yokoo Takayuki Hamano Makoto Kuro-o Takuya Itou Miwa Suzuki Keiichi Ueda Akira Nishiyama Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins Scientific Reports |
| title | Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins |
| title_full | Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins |
| title_fullStr | Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins |
| title_full_unstemmed | Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins |
| title_short | Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins |
| title_sort | possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins |
| url | https://doi.org/10.1038/s41598-023-32399-6 |
| work_keys_str_mv | AT nourinjahan possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT hiroyukiohsaki possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT kiyokokaneko possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT asadurrahman possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT takeshinishiyama possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT makotokoizumi possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT shuichiroyamanaka possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT kentokitada possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT yukisugiura possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT kenjimatsui possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT takashiyokoo possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT takayukihamano possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT makotokuroo possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT takuyaitou possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT miwasuzuki possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT keiichiueda possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins AT akiranishiyama possiblecontributionofphosphatetothepathogenesisofchronickidneydiseaseindolphins |