Nephrogenic diabetes insipidus is a disorder of water balance. The body normally balances fluid intake with the excretion of fluid in urine. However, people with nephrogenic diabetes insipidus produce too much urine (polyuria), which causes them to be excessively thirsty (polydipsia). Affected individuals can quickly become dehydrated if they do not drink enough water, especially in hot weather or when they are sick.
{"title":"[Nephrogenic diabetes insipidus].","authors":"Y. Kondo","doi":"10.32388/jhhu9s","DOIUrl":"https://doi.org/10.32388/jhhu9s","url":null,"abstract":"Nephrogenic diabetes insipidus is a disorder of water balance. The body normally balances fluid intake with the excretion of fluid in urine. However, people with nephrogenic diabetes insipidus produce too much urine (polyuria), which causes them to be excessively thirsty (polydipsia). Affected individuals can quickly become dehydrated if they do not drink enough water, especially in hot weather or when they are sick.","PeriodicalId":19721,"journal":{"name":"Nihon Jinzo Gakkai shi","volume":"196 1","pages":"177-80"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89295390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-01DOI: 10.1093/med/9780198784081.003.0006
Y. Yuzawa, M. Hasegawa, K. Nabeshima
Membranous nephropathy (MN) is a glomerular disease that is the leading cause of nephrotic syndrome in non-diabetic Caucasian adults. MN is most often primary (idiopathic) and the remaining is secondary to systemic disease or exposure to infection or drugs. The majority of patients with MN have circulating antibodies to the podocyte antigens phospholipase A 2 receptor (PLA2R) (70%) and thrombospondin type-1 domain-containing 7A (THSD7A) (3–5%). Immunologic remission (depletion of PLA2R antibodies) often precedes and may predict clinical remission. Untreated, about one-third of patients undergo spontaneous remission, one-third have persistent proteinuria but maintain kidney function and the remaining one-third will develop end stage kidney failure. All patients with idiopathic MN should be treated with conservative care from the time of diagnosis to minimise proteinuria. Immunosuppressive therapy is traditionally reserved for patients who have persistent nephrotic-range proteinuria despite conservative care. Immunosuppressive agents for primary MN include combination of corticosteroids/ alkylating agent or calcineurin inhibitors and rituximab. This chapter will review the epidemiology, diagnosis and treatment of MN, particularly focusing on idiopathic MN.
{"title":"[Membranous nephropathy].","authors":"Y. Yuzawa, M. Hasegawa, K. Nabeshima","doi":"10.1093/med/9780198784081.003.0006","DOIUrl":"https://doi.org/10.1093/med/9780198784081.003.0006","url":null,"abstract":"Membranous nephropathy (MN) is a glomerular disease that is the leading cause of nephrotic syndrome in non-diabetic Caucasian adults. MN is most often primary (idiopathic) and the remaining is secondary to systemic disease or exposure to infection or drugs. The majority of patients with MN have circulating antibodies to the podocyte antigens phospholipase A 2 receptor (PLA2R) (70%) and thrombospondin type-1 domain-containing 7A (THSD7A) (3–5%). Immunologic remission (depletion of PLA2R antibodies) often precedes and may predict clinical remission. Untreated, about one-third of patients undergo spontaneous remission, one-third have persistent proteinuria but maintain kidney function and the remaining one-third will develop end stage kidney failure. All patients with idiopathic MN should be treated with conservative care from the time of diagnosis to minimise proteinuria. Immunosuppressive therapy is traditionally reserved for patients who have persistent nephrotic-range proteinuria despite conservative care. Immunosuppressive agents for primary MN include combination of corticosteroids/ alkylating agent or calcineurin inhibitors and rituximab. This chapter will review the epidemiology, diagnosis and treatment of MN, particularly focusing on idiopathic MN.","PeriodicalId":19721,"journal":{"name":"Nihon Jinzo Gakkai shi","volume":"60 1","pages":"894-8"},"PeriodicalIF":0.0,"publicationDate":"2019-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77212176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-01DOI: 10.1093/NDT/GFX163.MP123
Shogo Kimura, Yuka Sekiya-Soga, Y. Kato, M. Mizutani, H. Ohashi
PURPOSE We examined the effect of the angiotensin II receptor antagonist (ARB), irbesartan (Irb), on urinary markers in hypertensive patients. SUBJECTS AND METHODS We evaluated 87 patients in a 12-month prospective study: Group 1) 33 patients who were newly administered Irb (100 mg); Group 2) 33 patients who were switched to Irb ; and Group 3) 21 patients who did not undergo change to pre-existing Irb administration. Height, weight, systolic and diastolic blood pressure, clinical parameters, urine protein : creatinine ratio (UPC), and urinary markers (liver-type fatty acid binding protein (L-FABP), N-acetyl-β-d-glucosaminidase, α1-microglobulin, and β2-microglobulin) were measured at the baseline and at 12, 24, and 48 weeks. We examined changes in the clinical parameters, UPC, and urinary markers from the baseline. RESULTS A tendency toward hypotension was observed in all groups (group newly administered Irb, group switched to Irb, and group without changes to Irb), but the difference was not statistically significant. Urinary L-FABP concentration (μg/g x Cr) decreased from 13.2 --> 8.9 and13.2 --> 10.2 at 24 and 48 weeks, respectively, after administration (p < 0.01) in the group newly administered Irb, from 19.5 --> 10.1 at 48 weeks after administration (p < 0.01) in the switched group, and from 9.6 --> 8.3, 8.1, and 6.2 (p < 0.01) in the group without changes to Irb. Changes in the Irb-administered groups were readily apparent. UPC decreased in the Irb-administered groups (p < 0.05), but there were no significant differences in the other urinary markers. Changes in urinary L-FABP and UPC were positively correlated in all cases of the Irb-administered groups (r = 0.25-0.57, p < 0.05), but were not positively correlated in the group without changes to Irb administration. The change in UPC was positively correlated with changes in systolic and diastolic blood pressure in all cases (r = 0.23-0.57, p < 0.05). CONCLUSION It was concluded that the urinary L-FABP level, blood pressure, and UPC of hypertensive patients should be managed in daily practice using an ARB, including Irb.
{"title":"[Effect of the angiotensin II receptor antagonist (ARB), Irbesartan, on urinary markers in hypertensive patients].","authors":"Shogo Kimura, Yuka Sekiya-Soga, Y. Kato, M. Mizutani, H. Ohashi","doi":"10.1093/NDT/GFX163.MP123","DOIUrl":"https://doi.org/10.1093/NDT/GFX163.MP123","url":null,"abstract":"PURPOSE\u0000We examined the effect of the angiotensin II receptor antagonist (ARB), irbesartan (Irb), on urinary markers in hypertensive patients.\u0000\u0000\u0000SUBJECTS AND METHODS\u0000We evaluated 87 patients in a 12-month prospective study: Group 1) 33 patients who were newly administered Irb (100 mg); Group 2) 33 patients who were switched to Irb ; and Group 3) 21 patients who did not undergo change to pre-existing Irb administration. Height, weight, systolic and diastolic blood pressure, clinical parameters, urine protein : creatinine ratio (UPC), and urinary markers (liver-type fatty acid binding protein (L-FABP), N-acetyl-β-d-glucosaminidase, α1-microglobulin, and β2-microglobulin) were measured at the baseline and at 12, 24, and 48 weeks. We examined changes in the clinical parameters, UPC, and urinary markers from the baseline.\u0000\u0000\u0000RESULTS\u0000A tendency toward hypotension was observed in all groups (group newly administered Irb, group switched to Irb, and group without changes to Irb), but the difference was not statistically significant. Urinary L-FABP concentration (μg/g x Cr) decreased from 13.2 --> 8.9 and13.2 --> 10.2 at 24 and 48 weeks, respectively, after administration (p < 0.01) in the group newly administered Irb, from 19.5 --> 10.1 at 48 weeks after administration (p < 0.01) in the switched group, and from 9.6 --> 8.3, 8.1, and 6.2 (p < 0.01) in the group without changes to Irb. Changes in the Irb-administered groups were readily apparent. UPC decreased in the Irb-administered groups (p < 0.05), but there were no significant differences in the other urinary markers. Changes in urinary L-FABP and UPC were positively correlated in all cases of the Irb-administered groups (r = 0.25-0.57, p < 0.05), but were not positively correlated in the group without changes to Irb administration. The change in UPC was positively correlated with changes in systolic and diastolic blood pressure in all cases (r = 0.23-0.57, p < 0.05).\u0000\u0000\u0000CONCLUSION\u0000It was concluded that the urinary L-FABP level, blood pressure, and UPC of hypertensive patients should be managed in daily practice using an ARB, including Irb.","PeriodicalId":19721,"journal":{"name":"Nihon Jinzo Gakkai shi","volume":"1053 1","pages":"104-13"},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85659693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[The possibility of a kidney-gut axis based on dysregulation of the mucosal immune response].","authors":"Toshiki Kano, Hitoshi Suzuki, Yusuke Suzuki","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":19721,"journal":{"name":"Nihon Jinzo Gakkai shi","volume":"59 4","pages":"552-556"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36833861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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