{"status":"ok","message-type":"work-list","message-version":"1.0.0","message":{"facets":{},"total-results":15,"items":[{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T14:10:35Z","timestamp":1753884635197,"version":"3.41.2"},"reference-count":25,"publisher":"Open Access Pub","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNA"],"abstract":"<jats:p>Introduction\nHypertension is a major cardiovascular risk factor. There is a strong relationship between blood pressure (BP) elevation and stroke, myocardial infarction, heart failure and mortality due to kidney disease. It is known that the loss of the dipping pattern in hypertension is associated with increased target organ damage. In our study, we aimed to investigate the prevalence of dipper hypertension (DHT) and nondipper hypertension (NDHT) and related factors in patients with stage 1 and 2 chronic kidney disease (CKD).\n\nMaterials and Methods\nA total of 158 patients diagnosed with stage 1 or stage 2 CKD were included in the study. Demographic characteristics, anthropometric measurements, physical examination findings and laboratory results of the patients were recorded. Ambulatory BP monitoring was performed in all patients.\n\nResults\nOf the 158 patients (female n: 98), 78 (49%) were in the stage 1 CKD group and 80 (51%) were in the stage 2 CKD group. No significant difference was observed in the prevalence of DHT or NDHT between hypertensive patients in the stage 1 and 2 CKD groups. The rate of NDHT was 59.5% (94\/158 patients). Female patients had more DHT in the general population and in the stage 1 group than male patients (p=0.05, p=0.01, respectively).\n\nConclusion\nNo significant difference was observed in the prevalence of DHT or NDHT between hypertensive patients in the stage 1 and 2 CKD groups. The prevalence of DHT in female patients was significantly higher in both groups than in men in both groups, but especially in the stage 1 CKD group.<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-19-3008","type":"journal-article","created":{"date-parts":[[2019,9,24]],"date-time":"2019-09-24T07:03:25Z","timestamp":1569308605000},"page":"15-23","source":"Crossref","is-referenced-by-count":0,"title":["Comparison of Dipper and Non-Dipper Hypertension Patterns According to Chronic Kidney Disease Stage"],"prefix":"10.14302","volume":"1","author":[{"given":"Esra Turan","family":"Erkek","sequence":"first","affiliation":[{"name":"University of Health Sciences, Dr Lutfi Kirdar Training and Research Hospital, Department of Internal Medicine, Istanbul, Turkey."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seydahmet","family":"Akin","sequence":"additional","affiliation":[{"name":"University of Health Sciences, Dr Lutfi Kirdar Training and Research Hospital, Department of Internal Medicine, Istanbul, Turkey."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasemin","family":"Ozgur","sequence":"additional","affiliation":[{"name":"University of Health Sciences, Dr Lutfi Kirdar Training and Research Hospital, Department of Internal Medicine, Istanbul, Turkey."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zeki","family":"Aydin","sequence":"additional","affiliation":[{"name":"Darica Training and Research Hospital. Department of Nephrology, Kocaeli, Turkey."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zerrin","family":"Bicik","sequence":"additional","affiliation":[{"name":"University of Health Sciences, Dr Lutfi Kirdar Training and Research Hospital, Department of Nephrology, Istanbul, Turkey."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2019,9,24]]},"reference":[{"key":"ref0","unstructured":"1.KilickapM BarcinC, GoksulukH KaraaslanD, Ozer N. (2018) Data on prevalence of hypertension and blood pressurein Turkey: Systematic review, metaanalysis and metaregression of epidemiological studies on cardiovascular risk factors. doi: 10.5543\/tkda.2018.15679.TurkKardiyolDern Ars. 46(7), 525-545."},{"key":"ref1","doi-asserted-by":"publisher","unstructured":"2.SonmezA HaymanaC, Bayram F, Salman S, Dizdar O S.(2018)TEMD Study Group. Turkish nationwide survEy of glycemic and other Metabolic parameters of patients with Diabetes mellitus (TEMD study). doi: 10.1016\/j.diabres.2018.09.010..Diabetes Res ClinPract. 146, 138-147.","DOI":"10.1016\/j.atherosclerosis.2018.06.156"},{"key":"ref2","doi-asserted-by":"publisher","unstructured":"3.Altun B, Suleymanlar G, Utas C, Arinsoy T, Ates K et al. (2012) . Prevalence, Awareness, Treatment and Control of Hypertension in Adults with Chronic Kidney Disease in Turkey: Results from the CREDIT Study. doi: 10.1159\/000339025. Kidney Blood Press Res 36, 36-46.","DOI":"10.1159\/000339025"},{"key":"ref3","doi-asserted-by":"publisher","unstructured":"4.Neal B, MacMahon S, Chapman N. (2000) Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs. , Lancet 356, 1955-1964.","DOI":"10.1016\/s0140-6736(00)03307-9"},{"key":"ref4","doi-asserted-by":"publisher","unstructured":"5.Montalescot Gilles, Collet Jean-Philippe. (2005) Preserving cardiac function in the hypertensive patient: why renal parameters hold the key, doi: https:\/\/doi.org\/10.1093\/eurheartj\/ehi414. , European Heart Journal 26, 2616-2622.","DOI":"10.1093\/eurheartj\/ehi414"},{"key":"ref5","doi-asserted-by":"publisher","unstructured":"6.Wenzel R R. (2005) Renal Protection in Hypertensive Patients: Selection of Antihypertensive Therapy. , Drugs 2(2), 29-39.","DOI":"10.2165\/00003495-200565002-00005"},{"key":"ref6","doi-asserted-by":"crossref","unstructured":"7.Lewis J B. (2003) Treatment of diabetic nephropathy with angiotensin II receptor antagonist. doi:https:\/\/doi.org\/10.1007\/s101570300000. Clin Exp Nephrol 7, 1-8.","DOI":"10.1007\/s101570300000"},{"key":"ref7","doi-asserted-by":"publisher","unstructured":"8.Weiner D E, Tighiouart H, Stark P C, Amin M G, MacLeod B. (2004) Chronic Kidney Disease as a Risk Factor for Cardiovascular Disease and All-Cause Mortality: A Pooled Analysis of Community-Based Studies. doi: 10.1097\/01.ASN.0000123691.46138.E2. Am J Kidney Dis.15: 1307-1315.","DOI":"10.1097\/01.asn.0000123691.46138.e2"},{"key":"ref8","doi-asserted-by":"publisher","unstructured":"9.Lin L, Zhang H, Yang J, Zhang J, Li K. (2016) . Nocturnal and Circadian Rhythm of Blood Pressure Is Associated with Renal Structure Damage and Function in Patients with IgAN. doi: 10.1016\/j.arcmed.2016.01.001.Arch Med Res 47, 25-32.","DOI":"10.1016\/j.arcmed.2016.01.001"},{"key":"ref9","doi-asserted-by":"publisher","unstructured":"10.Hermida R C, Ayala D E, Fern\u00e1ndez J R, Moj\u00f3n A. (2013) Sleep-time blood pressure: prognostic value and relevance as a therapeutic target for cardiovascular risk reduction. doi: 10.3109\/07420528.2012.702581. , Chronobiol Int 30, 68-86.","DOI":"10.3109\/07420528.2012.702581"},{"key":"ref10","doi-asserted-by":"publisher","unstructured":"11.Kim B K, Lim Y H, Lee H T, Lee J U, Kim K S. (2011) . Non-Dipper Pattern is a Determinant of the Inappropriateness of Left Ventricular Mass in Essential Hypertensive Patients. doi: 10.4070\/kcj.2011.41.4.191. Korean Circ J 41, 191-7.","DOI":"10.4070\/kcj.2011.41.4.191"},{"key":"ref11","doi-asserted-by":"publisher","unstructured":"12.Disease Kidney. (2012) Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO. , Kidney Int Suppl 3, 1-150.","DOI":"10.1016\/j.kisu.2017.10.001"},{"key":"ref12","doi-asserted-by":"publisher","unstructured":"13.Seo W S, Oh H S. (2002) The circadian rhythms of blood pressure and heart rate in the hypertensive subjects: dippers and non-dippers. doi: 10.3349\/ymj.2002.43.3.320. , Yonsei Med J 43, 320-328.","DOI":"10.3349\/ymj.2002.43.3.320"},{"key":"ref13","doi-asserted-by":"publisher","unstructured":"14.Pierdomenico S D, Costantini F, Bucci A, D, Bucciarelli T. (1999) Blunted nocturnal fall in blood pressure and oxidative stress in men and women with essential hypertension. , Am J Hypertens 12, 356-363.","DOI":"10.1016\/s0895-7061(00)86961-7"},{"key":"ref14","unstructured":"15.Verdecchia P, Schillaci G, Porcellati C. (1991) Dippers versus non-dippers. , J Hypertens Suppl 9, 42-44."},{"key":"ref15","doi-asserted-by":"publisher","unstructured":"16.O\u2019Brien E, Sheridan J, O\u2019Malley K. (1988) Dippers and non-dippers. , Doi:https:\/\/doi.org\/10.1016\/S0140-6736(88)92867-X. Lancet 2, 397.","DOI":"10.1016\/s0140-6736(88)92867-x"},{"key":"ref16","unstructured":"17.Ersoylu Z D, Tugcu A, Yildirimturk O, Aytekin V, Aytekin S. (2008) Comparison of the incidences of left ventricular hypertrophy, left ventricular diastolic dysfunction, and arrhythmia between patients with dipper and non-dipper hypertension.Turk Kardiyol Dern Ars. 36, 310-317."},{"key":"ref17","doi-asserted-by":"publisher","unstructured":"18.Redon J, Plancha E, Swift P A, Pons S, Mu\u00f1oz J. (2010) Nocturnal blood pressure and progression to end-stage renal disease or death in nondiabetic chronic kidney disease stages 3 and 4. doi: 10.1097\/HJH.0b013e328333fe4d. , J Hypertens 28, 602-607.","DOI":"10.1097\/hjh.0b013e328333fe4d"},{"key":"ref18","doi-asserted-by":"publisher","unstructured":"19.Agarwal R, Anderson M J. (2006) Prognostic importance of ambulator blood pressure recordings in patients with chronic kidney disease. doi: 10.1038\/sj.ki.5000247. , Kidney Int 69, 1175-1180.","DOI":"10.1038\/sj.ki.5000247"},{"key":"ref19","doi-asserted-by":"publisher","unstructured":"20.Kobrin I, Oigman W, Kumar A, Ventura H O, Messerli F H. (1984) Diurnal variation of blood pressure in elderly patients with essential hypertension. , J Am Geriatr Soc 2, 896-899.","DOI":"10.1111\/j.1532-5415.1984.tb00890.x"},{"key":"ref20","doi-asserted-by":"publisher","unstructured":"21.Minutolo R, Agarwal R, Borrelli S, Chiodini P, Bellizzi V. (2011) . Prognostic Role of Ambulatory Blood Pressure Measurement in Patients With Nondialysis Chronic Kidney Disease. doi: 10.1001\/archinternmed.2011.230. Arch Intern Med 171, 1090-1098.","DOI":"10.1001\/archinternmed.2011.230"},{"key":"ref21","doi-asserted-by":"publisher","unstructured":"22.Cuspidi C, Meani S, Valerio C, Sala C, Fusi V. (2007) Reproducibility of dipping\/nondipping pattern in untreated essential hypertensive patients: impact of sex and age. doi: 10.1097\/MBP.0b013e32809efa51. Blood Press Monit. 12, 101-106.","DOI":"10.1097\/mbp.0b013e32809efa51"},{"key":"ref22","doi-asserted-by":"publisher","unstructured":"23.CuspidiC MeaniS, Valerio C, Negri F, Sala C. (2008) Body mass index, nocturnal fall in blood pressure and organ damage in untreated essential hypertensive patients. doi: 10.1097\/MBP.0b013e32830d4bf8.Blood PressMonit. 13(6), 318-24.","DOI":"10.1097\/mbp.0b013e32830d4bf8"},{"key":"ref23","doi-asserted-by":"publisher","unstructured":"24.An H R, Park S, Yoo T H, Kang S W, Ryu J H. (2011) Non-dipper status and left ventricular hypertrophy as predictors of incident chronic kidney disease. doi: 10.3346\/jkms.2011.26.9.1185. , J Korean Med Sci 26, 1185-1190.","DOI":"10.3346\/jkms.2011.26.9.1185"},{"key":"ref24","doi-asserted-by":"crossref","unstructured":"25.Tonelli M, Wiebe N, Culleton B, House A, RabbatC. (2006) Chronic kidney disease and mortality risk: a systematic review.J Am SocNephrol. 17, 2034-2047.","DOI":"10.1681\/ASN.2005101085"}],"container-title":["Journal of Nephrology Advances"],"link":[{"URL":"https:\/\/openaccesspub.org\/jna\/article\/1170","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,24]],"date-time":"2019-09-24T07:03:36Z","timestamp":1569308616000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/openaccesspub.org\/jna\/article\/1170"}},"editor":[{"given":"Elbaih","family":"Zico","sequence":"additional","affiliation":[{"name":"Suez Canal University, Ismailia, Egypt."}],"role":[{"role":"editor","vocabulary":"crossref"}]}],"issued":{"date-parts":[[2019,9,24]]},"references-count":25,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2016,10,12]]}},"URL":"https:\/\/doi.org\/10.14302\/issn.2574-4488.jna-19-3008","ISSN":["2574-4488"],"issn-type":[{"type":"electronic","value":"2574-4488"}],"published":{"date-parts":[[2019,9,24]]},"article-number":"1170"},{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T20:31:39Z","timestamp":1777494699018,"version":"3.51.4"},"reference-count":17,"publisher":"Open Access Pub","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNA"],"abstract":"<jats:p>Introduction\nIncreased oxidative stress and blunted anti-oxidant mechanisms are important problems in hemodialysis (HD) patients. Reactive oxygen species (ROS) act directly on proteins, leading to the formation of oxidized amino acids. Advanced oxidation protein products (AOPP) are among these substances. Many oxidant substances increase the level of AOPP. Iron is an element with strong oxidant capacity, especially when used intravenously. It is thought that iron treatment further increases the oxidative stress in HD patients. We aimed to investigate the relationship between AOPP and inflammatory status in HD patients.\n\nMaterials and Methods\nPatients who were on maintenance HD program without additional co-morbidities and no history of use of intravenous iron within the last two weeks were recruited in the study. The blood samples taken just before the dialysis session were analyzed for AOPP, serum iron, total iron binding capacity (TIBC), ferritin, C-reactive protein (CRP), \u00df2-microglobulin, fibrinogen, interleukin (IL)-1, IL-6 and tumor necrosis factor-\u03b1 levels besides routine biochemical measurements and complete blood count.\n\nResults\nThe number of patients included in the study was 102 (n: 53 female, %52.0) and the mean age was 47.6\u00b113.9 years. The mean transferrin saturation was 25.4%. AOPP levels, iron use in patients was higher compared to patients who do not use (respectively 2.58\u00b10.19 mmol\/l and 2.50 \u00b10.16mmol\/l, p = 0.046). We did not detect statistically significant correlation of AOPP levels with iron parameters and other inflammatory markers.\n\nConclusion\nThe present study showed that intravenous iron therapy does not increase oxidative stress. Although serum AOPP level was higher in patients on intravenous iron treatment, it was not correlated with iron indices and inflammatory markers. So, intravenous iron may exert its oxidant effect free from serum iron indices.<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-19-3112","type":"journal-article","created":{"date-parts":[[2019,12,26]],"date-time":"2019-12-26T10:20:17Z","timestamp":1577355617000},"page":"24-30","source":"Crossref","is-referenced-by-count":3,"title":["Evaluation of the Relationship Between Advanced Oxidation end Products and Inflammatory Markers in Maintenance Hemodialysis Patients"],"prefix":"10.14302","volume":"1","author":[{"given":"Zeki","family":"Aydin","sequence":"first","affiliation":[{"name":"Darica Farabi Training and Research Hospital, Department of Nephrology, Kocaeli, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Serhat","family":"Karadag","sequence":"additional","affiliation":[{"name":"Haseki Training and Research Hospital, Department of Nephrology, Istanbul, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Savas","family":"Ozturk","sequence":"additional","affiliation":[{"name":"Haseki Training and Research Hospital, Department of Nephrology, Istanbul, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Meltem","family":"Gursu","sequence":"additional","affiliation":[{"name":"Bezmialem Vakif University Hospital, Department of Nephrology, Istanbul, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sami","family":"Uzun","sequence":"additional","affiliation":[{"name":"Haseki Training and Research Hospital, Department of Nephrology, Istanbul, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Egemen","family":"Cebeci","sequence":"additional","affiliation":[{"name":"Haseki Training and Research Hospital, Department of Nephrology, Istanbul, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Abdullah","family":"Sumnu","sequence":"additional","affiliation":[{"name":"Haseki Training and Research Hospital, Department of Nephrology, Istanbul, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rumeyza","family":"Kazancioglu","sequence":"additional","affiliation":[{"name":"Bezmialem Vakif University Hospital, Department of Nephrology, Istanbul, Turkey"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2019,12,25]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"1.Cavdar C, Camsari T, Semin I, Gonen S, Ac\u0131kgoz O. (1997) Lipid peroxidation and antioxidant activity in chronic haemodialysis patients treated with recombinant human erythropoietin. , Scand J Urol Nephrol 31, 371-75.","DOI":"10.3109\/00365599709030622"},{"key":"ref1","doi-asserted-by":"publisher","unstructured":"2.Herbelin A, Nguyen A T, Zingraff J, Urena P, Descamps-Latscha B. (1990) Influence of uremia and hemodialysis on circulation interleukin-1 and tumor necrosis factor alpha. , Kidney Int 37, 116-25.","DOI":"10.1038\/ki.1990.16"},{"key":"ref2","doi-asserted-by":"crossref","unstructured":"3.Lander H. (1997) An essentiol role for free radicals and derived species in signal transduction. , FASEB J 11, 118-24.","DOI":"10.1096\/fasebj.11.2.9039953"},{"key":"ref3","doi-asserted-by":"publisher","unstructured":"4.Gil-del Valle L, L de la C Milian, Toledo A, Vilar\u00f3 N, T\u00e1panes R et al. (2005) Altered redox status in patients with Diabetes Mellitus Type 1. , Pharmacological Research 51, 375-80.","DOI":"10.1016\/j.phrs.2004.10.012"},{"key":"ref4","doi-asserted-by":"publisher","unstructured":"5.Witko-Sarsat V, Friedlander M, Capeillere-Blandin C, Nguyen-Khoa T, Nguyen A T et al. (1996) Advanced oxidation protein products as a novel marker of oxidative stres in uremia. , Kidney Int 49, 1304-13.","DOI":"10.1038\/ki.1996.186"},{"key":"ref5","doi-asserted-by":"publisher","unstructured":"6.Lim P S, Wei Y H, Yu Y L, Kho B. (1999) Enhanced oxidative stress in haemodialysis patients receiving intravenous iron therapy. , Nephrol Dial Transplant 14, 2680-87.","DOI":"10.1093\/ndt\/14.11.2680"},{"key":"ref6","doi-asserted-by":"publisher","unstructured":"7.Kumbasar A, Gursu M, Kaya C, Ozturk S, Ergen A et al. (2012) effect of different doses and types of intravenous iron on oxidative stress and inflammation in hemodialysis patients.J. , Nephrol 25, 825-32.","DOI":"10.5301\/jn.5000072"},{"key":"ref7","doi-asserted-by":"publisher","unstructured":"8.Delmas-Beauvieux M C, Combe C, Peuchant E, Carbonneau M A, Dubourg L et al. (1995) Evaluation of red blood cell lipoperoxidation in hemodialysis patients during erythropoietin therapy supplemented or not with iron. , Nephron 69, 404-10.","DOI":"10.1159\/000188510"},{"key":"ref8","doi-asserted-by":"publisher","unstructured":"9.Stenvinkel P, Heimburger O, Lindholm B, Kaysen G A, Bergstr\u00f6m J. (2000) Are there two types of malnutrition in chronic renal failure? Evidence for relationships between malnutrition, inflammation and atherosclerosis (MIA syndrome). , Nephrol Dial Transplant 15, 953-60.","DOI":"10.1093\/ndt\/15.7.953"},{"key":"ref9","doi-asserted-by":"publisher","unstructured":"10.Richard M, Arnaud J, Jurkovitz C, Hachache T, Meftahi H et al. (1991) Trace elements and lipid perokxidation abnormalities in patiets with chronic renal failure. , Nephron 57, 10-15.","DOI":"10.1159\/000186208"},{"key":"ref10","doi-asserted-by":"publisher","unstructured":"11.Matkovics B, Laszlo A, Varga S I, Gal G, Solymosi T. (1998) Changes and correlations of antioxidant enzymes, lipid peroxidation and serum neutral lipids due to hemodialysis treatment in chronic ureamic patients. , Int Urol Nephrol 20, 559-64.","DOI":"10.1007\/bf02550619"},{"key":"ref11","doi-asserted-by":"crossref","unstructured":"12.Coskun C, Kural A, Doventas Y, Koldas M, Ozturk H et al. (2007) and protein oxidation products.Ann. , N Y Acad Sci 1100, 404-08.","DOI":"10.1196\/annals.1395.045"},{"key":"ref12","doi-asserted-by":"publisher","unstructured":"13.Colombo G, Reggiani F, Astori E, Altomare A, Finazzi S et al. (2019) Advanced oxidation protein products in nondiabetic end stage renal disease patients on maintenance haemodialysis. Free Radic Res. 22, 1-11.","DOI":"10.1080\/10715762.2019.1690651"},{"key":"ref13","doi-asserted-by":"publisher","unstructured":"14.Xu H, Cabezas-Rodriguez I, Qureshi A R, Heimburger O, Barany P et al. (2015) Increased Levels of Modified Advanced Oxidation Protein Products Are Associated with Central and Peripheral Blood Pressure in Peritoneal Dialysis Patients. Perit Dial Int. 35(4), 460-70.","DOI":"10.3747\/pdi.2013.00064"},{"key":"ref14","doi-asserted-by":"publisher","unstructured":"15.Dr\u00fceke T, Witko-Sarsat V, Massy Z, Descamps-Latscha B, Guerin A P et al. (2002) therapy, advanced oxidation protein products, and carotid artery intima-media thickness in end-stage renal disease.Circulation. 106, 2212-17.","DOI":"10.1161\/01.cir.0000035250.66458.67"},{"key":"ref15","doi-asserted-by":"publisher","unstructured":"16.Heimburger O, Qureshi A R, Blaner W S, Berglund L, Stenvinkel P. (2000) Hand-grip muscle strength, lean body mass, and plasma proteins as marker of nutritional status in patients with chronic renal failure close to start to dialysis therapy. , Am J Kidney Dis 6, 1213-25.","DOI":"10.1053\/ajkd.2000.19837"},{"key":"ref16","doi-asserted-by":"crossref","unstructured":"17.Stenvinkel P. (2001) The role of inflammation in the anaemia of endstage renal disease. , Nephrol Dial Transplant 1, 36-40.","DOI":"10.1093\/ndt\/16.suppl_7.36"}],"container-title":["Journal of Nephrology Advances"],"link":[{"URL":"https:\/\/openaccesspub.org\/jna\/article\/1229","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,12,26]],"date-time":"2019-12-26T10:20:36Z","timestamp":1577355636000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/openaccesspub.org\/jna\/article\/1229"}},"editor":[{"given":"Syed Arshad","family":"Hussain","sequence":"additional","affiliation":[{"name":"Tripura Universit, India."}],"role":[{"role":"editor","vocabulary":"crossref"}]}],"issued":{"date-parts":[[2019,12,25]]},"references-count":17,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2016,10,12]]}},"URL":"https:\/\/doi.org\/10.14302\/issn.2574-4488.jna-19-3112","ISSN":["2574-4488"],"issn-type":[{"value":"2574-4488","type":"electronic"}],"published":{"date-parts":[[2019,12,25]]},"article-number":"1229"},{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T14:11:14Z","timestamp":1753884674329,"version":"3.41.2"},"reference-count":15,"publisher":"Open Access Pub","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNA"],"abstract":"<jats:p>Primary membranous nephropathy (MN) is due to autoantibodies to phospholipase A2 receptor (PLA2R Ab). It is unclear whether COVID-19 vaccines can trigger flares of glomerular diseases such as primary MN. There have been increasing reports of glomerular diseases presenting or flaring after receipt of COVID-19 vaccines. We present a patient with primary MN who developed nephrotic syndrome after receiving her second mRNA-1273 COVID-19 vaccine with positive PLA2R Ab. Renal biopsy confirmed primary MN. She was treated for her primary MN flare with rituximab in a manner similar to non-vaccine-associated MN, which led to significant reduction in both PLA2R Ab level and proteinuria. This case adds to the growing literature on MN flares after receipt of mRNA COVID-19 vaccines. Close follow-up of patients with primary MN and other glomerular diseases after COVID-19 vaccination is warranted. Further research is needed to determine the pathophysiology behind vaccine-induced MN flares and whether there is a potential association between exposure to SARS-CoV-2 antigens and loss of tolerance to the PLA2R antigen.<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-24-5219","type":"journal-article","created":{"date-parts":[[2024,10,7]],"date-time":"2024-10-07T09:40:37Z","timestamp":1728294037000},"page":"12-18","source":"Crossref","is-referenced-by-count":0,"title":["Primary Membranous Nephropathy Flare After COVID-19 Vaccination"],"prefix":"10.14302","volume":"1","author":[{"given":"Kelly","family":"V. Liang","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Nephrology and Hypertension, Jared Grantham Kidney Institute, University of Kansas Medical Center, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Syeda","family":"B. Ahmad","sequence":"additional","affiliation":[{"name":"Department of Medicine, Renal-Electrolyte Division, University of Pittsburgh Medical Center, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elizabeth","family":"C. Kurtz","sequence":"additional","affiliation":[{"name":"Department of Medicine, Renal-Electrolyte Division, University of Pittsburgh Medical Center, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew","family":"Pittappilly","sequence":"additional","affiliation":[{"name":"Department of Medicine, Renal-Electrolyte Division, University of Pittsburgh Medical Center, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marta","family":"I. Minervini","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Pittsburgh Medical Center, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2024,9,5]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"1.Kutlucan A, Gonen I, Yildizhan E. (2012) Can influenza H1N1 vaccination lead to the membranous glomerulonephritis?. , Indian Journal of Pathology & Microbiology 55(2), 239-241.","DOI":"10.4103\/0377-4929.97893"},{"key":"ref1","doi-asserted-by":"publisher","unstructured":"2.Patel C, Shah H H. (2015) Membranous nephropathy and severe acute kidney injury following influenza vaccination. , Saudi Journal of Kidney Diseases 26-6.","DOI":"10.4103\/1319-2442.168676"},{"key":"ref2","unstructured":"3.Palevsky P M, Radhakrishnan J, Townsend R R. (2022) COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension. UpToDate."},{"key":"ref3","doi-asserted-by":"publisher","unstructured":"4.Klomjit N, Alexander M P, Fervenza F C. (2021) COVID-19 Vaccination and Glomerulonephritis. Kidney Int Rep. 6(12), 2969-2978.","DOI":"10.1016\/j.ekir.2021.09.008"},{"key":"ref4","doi-asserted-by":"publisher","unstructured":"5.HHL Wu, Kalra P A, Chinnadurai R. (2021) New-Onset and Relapsed Kidney Histopathology Following COVID-19 Vaccination: A Systematic Review. Vaccines (Basel). , Oct29; 9(11), 1252.","DOI":"10.3390\/vaccines9111252"},{"key":"ref5","doi-asserted-by":"publisher","unstructured":"6.Izzedine H, Bonilla M, Jhaveri K D. (2021) Nephrotic syndrome and vasculitis following SARS-CoV-2 Vaccine: True association or circumstantial? Nephrol Dial Transplant. 10, 215.","DOI":"10.1093\/ndt\/gfab215"},{"key":"ref6","doi-asserted-by":"publisher","unstructured":"7.Anderegg M A, Liu M, Saganas C.et al.(2021).De novo vasculitis after mRNA-1273 (Moderna)vaccination. Kidney Int.100:. 474.","DOI":"10.1016\/j.kint.2021.05.016"},{"key":"ref7","doi-asserted-by":"publisher","unstructured":"8.Sekar A, Campbell R, Tabbara J. (2021) . ANCA Glomerulonephritis post Moderna COVID-19 vaccination. Kidney Int 100(2), 473-474.","DOI":"10.1016\/j.kint.2021.05.017"},{"key":"ref8","doi-asserted-by":"publisher","unstructured":"9.Shakoor M T, Birkenbach M P, Lynch M. (2021) ANCA-associated vasculitis following Pfizer-BioNTech COVID-19 vaccine. Am J Kidney Dis. 78, 611-613.","DOI":"10.1053\/j.ajkd.2021.06.016"},{"key":"ref9","doi-asserted-by":"publisher","unstructured":"10.Weijers J, Alvarez C, MMH Hermans. (2021) Post-vaccinal minimal change disease. Kidney Int. 100(2), 459-461.","DOI":"10.1016\/j.kint.2021.06.004"},{"key":"ref10","doi-asserted-by":"publisher","unstructured":"11.Da Y, Goh G H, Khatri P. (2021) A case of membranous nephropathy following Pfizer-BioNTech mRNA vaccination against COVID-19. Kidney Int. 100(4), 938-939.","DOI":"10.1016\/j.kint.2021.07.016"},{"key":"ref11","doi-asserted-by":"publisher","unstructured":"12.Gueguen L, Loheac C, Saidani N. (2021) Membranous nephropathy following anti-COVID-19 mRNA vaccination. Kidney Int. 100(5), 1140-1141.","DOI":"10.1016\/j.kint.2021.08.006"},{"key":"ref12","doi-asserted-by":"publisher","unstructured":"13.Ayd\u0131n M F, Y\u0131ld\u0131z A, Oru\u00e7 A. (2021) Relapse of primary membranous nephropathy after inactivated SARS-CoV-2 virus vaccination. Kidney Int. 100(2), 464-465.","DOI":"10.1016\/j.kint.2021.05.001"},{"key":"ref13","doi-asserted-by":"publisher","unstructured":"14.Li N L, Coates P T, Rovin B H. (2021) COVID-9 vaccination followed by activation of glomerular diseases: does association equal causation? Kidney Int. 100-959.","DOI":"10.1016\/j.kint.2021.09.002"},{"key":"ref14","doi-asserted-by":"publisher","unstructured":"15.Bomback A S, Kudose S.D&apos;Agati VD.(2021).De Novo and Relapsing Glomerular Diseases After COVID-19 Vaccination: What Do We Know So Far?. , Am J Kidney Dis.78: 477.","DOI":"10.1053\/j.ajkd.2021.06.004"}],"container-title":["Journal of Nephrology Advances"],"link":[{"URL":"https:\/\/openaccesspub.org\/jna\/article\/2165","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,10,7]],"date-time":"2024-10-07T09:40:43Z","timestamp":1728294043000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/openaccesspub.org\/jna\/article\/2165"}},"issued":{"date-parts":[[2024,9,5]]},"references-count":15,"journal-issue":{"issue":"4","published-online":{"date-parts":[[2023,5,15]]}},"URL":"https:\/\/doi.org\/10.14302\/issn.2574-4488.jna-24-5219","ISSN":["2574-4488"],"issn-type":[{"type":"electronic","value":"2574-4488"}],"published":{"date-parts":[[2024,9,5]]},"article-number":"2165"},{"indexed":{"date-parts":[[2024,10,8]],"date-time":"2024-10-08T04:11:32Z","timestamp":1728360692358},"reference-count":0,"publisher":"Open Access Pub","content-domain":{"domain":[],"crossmark-restriction":false},"DOI":"10.14302\/issn.2574-4488","type":"journal","created":{"date-parts":[[2017,9,10]],"date-time":"2017-09-10T06:21:28Z","timestamp":1505024488000},"source":"Crossref","is-referenced-by-count":1,"title":["Journal of Nephrology Advances"],"prefix":"10.14302","member":"5410","deposited":{"date-parts":[[2024,10,7]],"date-time":"2024-10-07T09:40:38Z","timestamp":1728294038000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/openaccesspub.org\/journal\/jna"}},"short-title":["JNA"],"issued":{"date-parts":[[null]]},"references-count":0,"URL":"https:\/\/doi.org\/10.14302\/issn.2574-4488","ISSN":["2574-4488"],"issn-type":[{"type":"electronic","value":"2574-4488"}]},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T07:28:07Z","timestamp":1649143687817},"reference-count":39,"publisher":"Open Access Pub","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNA"],"abstract":"<jats:p>The aim of this study was to evaluate the impact of Biofield Energy Treated\/Blessed Proprietary Test Formulation and Biofield Energy Treatment\/Blessing per se on kidney biomarkers on L-NAME and high fat diet (HFD)-induced cardiovascular disorders in Sprague Dawley rats. In this experiment, the functional kidney biomarkers such as epinephrine\/adrenaline, inducible nitric oxide synthase (iNOS), angiotensin-II, C-reactive protein (CRP), and renin were measured using ELISA assay. A test formulation was formulated including minerals (magnesium, zinc, copper, calcium, selenium, and iron), vitamins (vitamin C, vitamin B6, vitamin B12, vitamin B9, and vitamin D3), cannabidiol (CBD) isolate, Panax ginseng extract, and \u03b2-carotene. The components of the test item were divided into two; one section was defined as the untreated test formulation, while the other part and three group of animals received Mr. Mahendra Kumar Trivedi\u2019s Biofield Energy healing\/Blessing remotely for about 3 minutes. The results showed that the level of adrenaline was reduced by 31.62%, 19.58%, 34.32%, 37.07%, and 29.87% in the G5 (L-NAME + HFD + the Biofield Energy Treated test formulation), G6 (L-NAME + HFD + Biofield Energy Treatment per se to animals from day -15), G7 (L-NAME + HFD + the Biofield Energy Treated test formulation from day-15), and G8 (L-NAME + HFD + Biofield Energy Treatment per se plus the Biofield Energy Treated test formulation from day-15), and G9 (L-NAME + HFD + Biofield Energy Treatment per se animals plus the untreated test formulation) groups, respectively as compared to the disease control group (G2). Moreover, the level of iNOS was reduced by 56.76%, 49.51%, 61.79%, 57.63%, and 62.44% in the G5, G6, G7, G8, and G9 groups, respectively, as compared to the disease control group (G2). Additionally, the level of angiotensin-II was decreased by 41.09%, 34.92%, 60.65%, 53.28%, and 60.09% in the G5, G6, G7, G8, and G9 groups, respectively, as compared to the G2 group. The level of CRP was decreased by 47.21%, 38.89%, 59.81%, 55.52%, and 64.02% in the G5, G6, G7, G8, and G9 groups, respectively as compared to the G2 group. Besides, the level of renin was decreased by 20.27%, 20.13%, 12.99%, and 25.73% in the G5, G7, G8, and G9 groups, respectively as compared to the G2 group. Overall, the data suggested significance improvement of vital functional kidney biomarkers of the Biofield Energy Treated\/Blessed test formulation and Biofield Energy Treatment per se along with preventive measure on the animal with respect to various pathological conditions that might be beneficial various types of cardiovascular disorders. Therefore, the results showed the significant slowdown the inflammation-related cardiovascular disease progression and its complications\/symptoms in the preventive Biofield Energy Treatment group per se and\/or Biofield Energy Treated\/Blessed Test formulation groups (viz. G6, G7, G8, and G9).<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-21-3847","type":"journal-article","created":{"date-parts":[[2021,7,31]],"date-time":"2021-07-31T10:12:35Z","timestamp":1627726355000},"page":"12-22","source":"Crossref","is-referenced-by-count":0,"title":["Evaluation of Renal and Cardioprotective Potential of the Biofield Energy Treated Proprietary Test Formulation on L-NAME and High Fat Diet-Induced Cardiovascular Disorders in Sprague Dawley Rats"],"prefix":"10.14302","volume":"1","author":[{"given":"Mahendra Kumar","family":"Trivedi","sequence":"first","affiliation":[{"name":"Trivedi Global, Inc., Henderson, Nevada, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alice","family":"Branton","sequence":"additional","affiliation":[{"name":"Trivedi Global, Inc., Henderson, Nevada, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dahryn","family":"Trivedi","sequence":"additional","affiliation":[{"name":"Trivedi Global, Inc., Henderson, Nevada, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Snehasis","family":"Jana","sequence":"additional","affiliation":[{"name":"Trivedi Science Research Laboratory Pvt. Ltd., Thane (W), Maharashtra, India."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2021,6,26]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"1.Clifton W Callaway. (2013) Epinephrine for cardiac arrest. , Current Opinion in Cardiology 28(1), 36-42.","DOI":"10.1097\/hco.0b013e32835b0979"},{"key":"ref1","doi-asserted-by":"publisher","unstructured":"2.Tsutsui M, Shimokawa H, Otsuji Y, Ueta Y, Sasaguri Y et al. (2009) Nitric oxide synthases and cardiovascular diseases: Insights from genetically modified mice. , Circ J 73(6), 986-993.","DOI":"10.1253\/circj.cj-09-0208"},{"key":"ref2","doi-asserted-by":"crossref","unstructured":"3.Besedina A. (2016) NO-synthase activity in patients with coronary heart disease associated with hypertension of different age groups. , J Med Biochem 35(1), 43-49.","DOI":"10.1515\/jomb-2015-0008"},{"key":"ref3","doi-asserted-by":"publisher","unstructured":"4.Ferrario C M. 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Macedonia, WHO CC and Ga2len CC."}],"role":[{"role":"editor","vocabulary":"crossref"}]}],"issued":{"date-parts":[[2021,6,26]]},"references-count":39,"journal-issue":{"issue":"3","published-online":{"date-parts":[[2020,12,16]]}},"URL":"https:\/\/doi.org\/10.14302\/issn.2574-4488.jna-21-3847","ISSN":["2574-4488"],"issn-type":[{"value":"2574-4488","type":"electronic"}],"published":{"date-parts":[[2021,6,26]]}},{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T14:12:47Z","timestamp":1753884767374,"version":"3.41.2"},"reference-count":22,"publisher":"Open Access Pub","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNA"],"abstract":"<jats:p>Polycystic kidney disease is an inherited disease that can lead to high blood pressure and kidney failure. In Mexico, 4.5% of patients with kidney failure are carriers of this disease; the liver is another of the organs affected by this disease that can manifest as abdominal pain and a mass effect in the abdominal cavity; we present 2 cases of polycystic kidney and liver disease (mother and child), in addition to describing the clinical manifestations, two different stages of the disease are shown, being a hereditary disease it is suggested that once a case is identified, an abdominal ultrasound is performed to first-degree relatives in search of cystic lesions to indicate preventive measures that help us preserve the overall well-being of the patient.<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-21-3887","type":"journal-article","created":{"date-parts":[[2021,7,26]],"date-time":"2021-07-26T09:42:13Z","timestamp":1627292533000},"page":"23-30","source":"Crossref","is-referenced-by-count":0,"title":["Hepatic Cysts as a Manifestation of Polycystic Kidney Disease (Polycystic Liver Report of 2 Mother-Son Cases)"],"prefix":"10.14302","volume":"1","author":[{"given":"Osnaya-Romero","family":"N","sequence":"first","affiliation":[{"name":"Unidad de investigaci\u00f3n cl\u00ednica Instituto Nacional de Pediatr\u00eda."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Conrado","family":"S","sequence":"additional","affiliation":[{"name":"Endocrinologia Hospital 1\u00b0 de octubre Hospital del ISSTE"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dautt","family":"P","sequence":"additional","affiliation":[{"name":"Radiologia Hospital ABC."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2021,7,21]]},"reference":[{"doi-asserted-by":"publisher","unstructured":"1. Panozo Borda SV, Heredia Moy K, Oviedo Gamboa I, Villarroel Arze T, Zegara Santiesteban W, Ricalder Mu\u00f1oz R. Estudio imagenologico de poliquistosis   renal autos\u00f3mica dominante, reporte de un caso y revisi\u00f3n de la literatura.Gac.Med. Bol. 2012; 35(1):31-34","key":"ref0","DOI":"10.14201\/gredos.22489"},{"doi-asserted-by":"publisher","unstructured":"2. Ars E, Bernis C, Fraga G, Martinez V, Martins J, Ortiz A, Rodriguez-Perez J C, Sans Laia, Torra R. Gu\u00edas Cl\u00ednicas Espa\u00f1olas de Poliquistosis renal Autos\u00f3mica               Dominante 2015. https:\/\/escolasaude.sergas.es\/Docs\/EGSPC\/pilula\/Poliquistosis\/resources\/doc02.pdf","key":"ref1","DOI":"10.14201\/gredos.22489"},{"doi-asserted-by":"publisher","unstructured":"3. M\u00e9ndez-Dur\u00e1n A, M\u00e9ndez-Bueno J F, Tapia-Y\u00e1\u00f1ez T,  Mu\u00f1oz Montes A,  Aguilar-S\u00e1nchez L. (2010). Epidemiolog\u00eda de la insuficiencia renal cr\u00f3nica en M\u00e9xico.Dial-Trasp. 31(1): 7-11","key":"ref2","DOI":"10.1016\/s1886-2845(10)70004-7"},{"doi-asserted-by":"crossref","unstructured":"4. Harris P C, Torres V E. Polycystic kidney disease.        Annu Rev Med. 2009; 60:321-37.","key":"ref3","DOI":"10.1146\/annurev.med.60.101707.125712"},{"doi-asserted-by":"publisher","unstructured":"5. Gradzik M, Niemczyk M, Golebiowski M, Paczek L. Diagnostic Imaging of Autosomal Dominant               Polycystic Kidney Disease. Pol J Radiol. 2016; 81:            441-53.","key":"ref4","DOI":"10.12659\/pjr.894482"},{"doi-asserted-by":"publisher","unstructured":"6. Ravine D, Gibson RN, Walker RG, Sheffield LJ,               Kincaid-Smith P, Danks DM. (1994). Evaluation of                    ultrasonographic diagnostic criteria for autosomal dominant polycystic kidney disease 1. Lancet. 343: 824-7","key":"ref5","DOI":"10.1016\/s0140-6736(94)92026-5"},{"doi-asserted-by":"publisher","unstructured":"7. Pei Y, Obaji J, Dupuis A, Paterson AD, Magistroni R, Dicks E, et al. Unified criteria for ultrasonographic diagnosis of ADPKD. Journal of the American Society of Nephrology. JASN. 2009; 20(1):205-12.","key":"ref6","DOI":"10.1681\/asn.2008050507"},{"unstructured":"8. Tobal D. Noboa O. Poliquistosis renal autos\u00f3mica     dominante. Necesidad de diagn\u00f3stico y tratamiento oportuno. Rev med Urug. 2014; 30(3):184-192.","key":"ref7"},{"doi-asserted-by":"publisher","unstructured":"9. Pirson Y, Chauveau D, Torres V. (2002). Management of        cerebral aneurysms in autosomal dominant                 polycystic kidney disease. J Am Soc Nephrol. 13(1): 269-76.","key":"ref8","DOI":"10.1681\/asn.v131269"},{"doi-asserted-by":"publisher","unstructured":"10. Torres M J, Rodr\u00edguez P\u00e9rez J.C, Hern\u00e1ndez Socorro C.R, Anabitarte Caballero A, V\u00e1zquez C,                          Fern\u00e1ndez-Burriel M, P\u00e9rez \u2013Borges P. Palop L.       Diagn\u00f3stico molecular de la poliquistosis renal           autos\u00f3mica dominante en la comunidad aut\u00f3noma  de canarias. Nefrolog\u00eda. 2006; 26(1): 666-672","key":"ref9","DOI":"10.14201\/gredos.22489"},{"doi-asserted-by":"publisher","unstructured":"11. Akoh JA. (2015). Current management of autosomal dominant polycystic kidney disease. World J Nephrol. 4(4):468-79","key":"ref10","DOI":"10.5527\/wjn.v4.i4.468"},{"doi-asserted-by":"publisher","unstructured":"12. Igarashi P, Somlo S. (2002). Genetics and pathogenesis of      polycystic kidney disease. Journal of the American Society of Nephrology . 13(9):2384-98","key":"ref11","DOI":"10.1097\/01.asn.0000028643.17901.42"},{"doi-asserted-by":"publisher","unstructured":"13. Torres VE, Harris PC, Pirson Y. (2007). Autosomal dominant polycystic kidney disease. The Lancet. 369: 1287-381","key":"ref12","DOI":"10.1016\/s0140-6736(07)60601-1"},{"doi-asserted-by":"publisher","unstructured":"14.  Mart\u00ednez Morcillo A, Esteban de la Rosa MA, De Diego Fern\u00e1ndez P, Garc\u00eda Gonz\u00e1lez M, Fern\u00e1ndez Castillo M, Arg\u00fcelles Toledo I et al. Panor\u00e1mica de la                poliquistosis renal autos\u00f3mica dominante en una      regi\u00f3n del sur de Espa\u00f1a. Nefro 2018; 38(2): 190-196.","key":"ref13","DOI":"10.1016\/j.nefro.2017.07.002"},{"doi-asserted-by":"publisher","unstructured":"15. Hateboer N,  Dijk MA, Bogdanova N, Coto E,                 Saggar-Malik AK, San Millan JL, et al. Comparison of phenotypes of polycystic kidney disease types 1 and 2. European PKD1-PKD2 Study Group. Lancet. 1999;353(9147):103-107","key":"ref14","DOI":"10.1016\/s0140-6736(98)03495-3"},{"unstructured":"16. Fraile G\u00f3mez P, Corral Moro E, Garc\u00eda-Cosmes P,      Gonzalez Sarmiento R, Tabernero Romo JM. Genetic analysis (PKD2) of autosomal dominant poliycystic kidney disease. Nefrolog\u00eda. 2009; 29 (6):562-568","key":"ref15"},{"unstructured":"17. Garc\u00eda-Garces M, S\u00e1nchez Zavala J, Mckinney Novelo I, Corrales Rosas B, Zavala Garc\u00eda C, Brisuela Alc\u00e1ntara D, Herrera Bello H, Albores Saavedra J, Gonz\u00e1lez Chon O. Enfermedad poliqu\u00edstica hep\u00e1tica asociada a         enfermedad poliq\u00edstica renal autos\u00f3mica dominante. Rev Invest Med Sur. 2011; 18(3): 132-135.","key":"ref16"},{"unstructured":"18. Irazabal M.V, Torres V.E. Poliquistosis renal                 autos\u00f3mica dominante .Nefrolog\u00eda suplemento                 extraordinario.  2011; 2(1) :1-33","key":"ref17"},{"doi-asserted-by":"publisher","unstructured":"19. Martinez-Perez, Alberola Soler A, Domingo del Pozo C, Permartin-Comella B, Martinez -Lopez E, Vazquez Tarragon A. Laparoscopic surgery and polycistic liver disease: Clinicopathological features and new trend in management. J Min Access Surg .2016; 12: 265-70.","key":"ref18","DOI":"10.4103\/0972-9941.169976"},{"doi-asserted-by":"publisher","unstructured":"20. van Aerts RMM, van de Laarschot LFM, Banales JM, Drenth JPH. Clinical management of polycystic liver disease. J Hepatol. 2018 Apr;68(4):827-837.","key":"ref19","DOI":"10.1016\/j.jhep.2017.11.024"},{"doi-asserted-by":"publisher","unstructured":"21. Ryu H, Kim H, Park HC, et al. (2017). Total kidney and liver volume is a major risk factor for malnutrition in                 ambulatory patients with autosomal dominant               polycystic kidney disease. BMC Nephrol. 18(1):22.","key":"ref20","DOI":"10.1186\/s12882-016-0434-0"},{"doi-asserted-by":"publisher","unstructured":"22. Rahbari-Oskoui F, Williams Olubunmi, Ch A.                        Mechanisms and management of hypertension in       autosomal dominant polycystic kidney disease.      Nephrol Dial Transplant. 2014; Dec; 29(12):2194-2201.","key":"ref21","DOI":"10.1093\/ndt\/gft513"}],"container-title":["Journal of Nephrology Advances"],"link":[{"URL":"https:\/\/openaccesspub.org\/jna\/article\/1665","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,26]],"date-time":"2021-07-26T09:42:19Z","timestamp":1627292539000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/openaccesspub.org\/jna\/article\/1665"}},"editor":[{"given":"Sasho","family":"Stoleski","sequence":"additional","affiliation":[{"name":"Institute of Occupational Health of R. 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Seibert E Levin N W Kuhlmann M K Zhu F Bioimpedance, dry weight and blood pressure control: new methods and consequences. Curr Opin Nephrol Hypertens 2005 14 6 543 549","DOI":"10.1097\/01.mnh.0000185983.48319.00"},{"key":"ref002","doi-asserted-by":"crossref","unstructured":"2. Ozkahya M Ok E Toz H Asci G Duman S Basci A Kose T DorhoutMees E J Long-term survival rates in haemodialysis patients treated with strict volume control.Nephrol Dial Transplant 2006 21 12 3506 3513","DOI":"10.1093\/ndt\/gfl487"},{"key":"ref003","doi-asserted-by":"crossref","unstructured":"3. Parfrey P S Foley R N Harnett J D Kent G M Murray D C Barre P E Outcome and risk factors for left ventricular disorders in chronic uraemia. Nephrol Dial Transplant 1996 11 1277 1285","DOI":"10.1093\/oxfordjournals.ndt.a027540"},{"key":"ref004","doi-asserted-by":"crossref","unstructured":"4. Zoccali C Benedetto F A Mallamaci F Prognostic value of echocardiographic indicators of left ventricular systolic function in asymptomatic dialysis patients 2004 J Am Soc Nephrol 15 1029 37","DOI":"10.1097\/01.ASN.0000117977.14912.91"},{"key":"ref005","doi-asserted-by":"crossref","unstructured":"5. Picano E Frassi F Agricola E Gligorova S Gargani L Mottola G Ultrasound lung comets: a clinically useful sign of extravascular lung water 2006 J Am Soc Echocardiogr 19 356 363","DOI":"10.1016\/j.echo.2005.05.019"},{"key":"ref006","doi-asserted-by":"crossref","unstructured":"6. Lichtenstein D M\u00e9zi\u00e8re G Biderman P The comet-tail artifact. An ultrasound sign of alveolar-interstitial syndrome 1997 Am J Respir Crit Care Med 156 5 1640 1646","DOI":"10.1164\/ajrccm.156.5.96-07096"},{"key":"ref007","doi-asserted-by":"crossref","unstructured":"7. Dexheimer L Dalcin P Teixeira C Beltrami F Lung ultrasound in critically ill patients: a new diagnostic tool 2012 J Bras Pneumol 38 246 56","DOI":"10.1590\/S1806-37132012000200015"},{"key":"ref008","doi-asserted-by":"crossref","unstructured":"8. Picano E Gargani L Gheorghiade M Why when, and how to assess pulmonary congestion in heart failure: pathophysiological, clinical, and methodological implications. Heart Fail Rev 2010 15 63 72","DOI":"10.1007\/s10741-009-9148-8"},{"key":"ref009","doi-asserted-by":"crossref","unstructured":"9. Frassi F Gargani L Tesorio P Raciti M Mottola G PicanoE Prognostic value of extravascular lung water assessed with ultrasound lung comets by chest sonography in patients with dyspnea and\/or chest pain.JCardFail 2007 13 10 830 835","DOI":"10.1016\/j.cardfail.2007.07.003"},{"key":"ref010","doi-asserted-by":"crossref","unstructured":"10. Mallamaci F Benedetto F A Tripepi R Rastelli S Castellino P Tripepi G Picano E Zoccali C Detection of pulmonary congestion by chest ultrasound in dialysis patients. JACC Cardiovasc Imaging 2010 3 6 586 594","DOI":"10.1016\/j.jcmg.2010.02.005"},{"key":"ref011","doi-asserted-by":"crossref","unstructured":"11. Machek P Jirka T Moissl U Chamney P Wabel P Guided optimization of fluid status in haemodialysis patients 2010 Nephrol Dial Transplant 25 2 538 544","DOI":"10.1093\/ndt\/gfp487"},{"key":"ref012","doi-asserted-by":"crossref","unstructured":"12. Brennan J M Ronan A Goonewardena S Blair J E Hammes M Shah D Vasaiwala S Kirkpatrick J N Spencer K T Handcarried ultrasound measurement of the inferior vena cava for assessment of intravascular volume status in the outpatient hemodialysis clinic. Clin J Am SocNephrol 2006 1 4 749 753","DOI":"10.2215\/CJN.00310106"},{"key":"ref013","doi-asserted-by":"crossref","unstructured":"13. Volpicelli G Mussa A Garofalo G Cardinale L Casoli G Perotto F Fava C Frascisco M Bedside lung ultrasound in the assessment of alveolar-interstitial syndrome 2006 Am J Emerg Med 24 6 689 696","DOI":"10.1016\/j.ajem.2006.02.013"},{"key":"ref014","doi-asserted-by":"crossref","unstructured":"14. Basso F Milan Manani S Cruz D N Teixeira C Brendolan A Nalesso F Zanella M Ronco C Comparison and Reproducibility of Techniques for Fluid Status Assessment in Chronic Hemodialysis Patients. Cardiorenal Med 2013 3 2 104 112","DOI":"10.1159\/000351008"},{"key":"ref015","doi-asserted-by":"crossref","unstructured":"15. Peacock W F Soto K M Current techniques of fluid status assessment 2010 ContribNephrol 164 128 142","DOI":"10.1159\/000313726"},{"key":"ref016","doi-asserted-by":"crossref","unstructured":"16. Di Iorio BR Scalfi L Terracciano V Bellizzi V A systematic evaluation of bioelectrical impedance measurement after hemodialysis session. Kidney Int 2004 65 6 2435 2440","DOI":"10.1111\/j.1523-1755.2004.00660.x"},{"key":"ref017","doi-asserted-by":"crossref","unstructured":"17. Agarwal R Bouldin J M Light R P Garg A Inferior vena cavadiameter and left atrial diameter measure volume but not dry weight 2011 Clin J Am SocNephrol 6 5 1066 1072","DOI":"10.2215\/CJN.09321010"},{"key":"ref018","doi-asserted-by":"crossref","unstructured":"18. Trezzi M Torzillo D Ceriani E Costantino G Caruso S Damavandi P T Genderini A Cicardi M Montano N Cogliati C Lung ultrasonography for the assessment of rapid extravascular water variation: evidence from hemodialysis patients 2013 Intern Emerg Med 8 5 409 415","DOI":"10.1007\/s11739-011-0625-4"},{"key":"ref019","doi-asserted-by":"crossref","unstructured":"19. N Dugo M Vitturi M Simoni F Soattin L Zagatti R Maresca Maresca M C Lung ultrasound during hemodialysis: the role in the assessment of volume status. Int Urol Nephrol 2014 46 169 174","DOI":"10.1007\/s11255-013-0500-5"},{"key":"ref020","doi-asserted-by":"crossref","unstructured":"20. Noble V E Murray A F Capp R Sylvia-Reardon M H Steele D J Liteplo A Ultrasound assessment for extravascular lung water in patients undergoing hemodialysis. Time course for resolution 2009 Chest 135 1433 1439","DOI":"10.1378\/chest.08-1811"},{"key":"ref021","doi-asserted-by":"crossref","unstructured":"21. Kalantar-Zadeh K Regidor D L Kovesdy C P D Van Wyck Bunnapradist S Horwich T B Fluid retention is associated with cardiovascular mortality in patients undergoing long-term hemodialysis 2009 Circulation 119 671 679","DOI":"10.1161\/CIRCULATIONAHA.108.807362"}],"container-title":["Journal Of Nephrology 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progressive process affecting kidneys in chronic kidney disease (CKD), regardless of cause. Although no effective targeted therapy yet existed to retard renal fibrosis, a number of important recent advances have highlighted the cellular and molecular mechanisms underlying the renal fibrosis. The advances including TGF-\u03b2\/Smad pathway, oxidative stress and inflammation, hypoxia and gut microbiota-derived from uremic solutes were highlighted that could provide therapeutic targets. New therapeutic targets and strategies that are particularly promising for development of new treatments for patients with CKD were also highlighted.<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-18-2443","type":"journal-article","created":{"date-parts":[[2018,11,13]],"date-time":"2018-11-13T06:47:28Z","timestamp":1542091648000},"page":"4-14","source":"Crossref","is-referenced-by-count":15,"title":["Action Mechanisms and Therapeutic Targets of Renal Fibrosis"],"prefix":"10.14302","volume":"1","author":[{"given":"Shi-Xing","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Nephrology, Baoji Central Hospital, No. 8 Jiangtan Road, Baoji, Shaanxi 721008, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"You-Quan","family":"Shang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Baoji Central Hospital, No. 8 Jiangtan Road, Baoji, Shaanxi 721008, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huan-Qiao","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Baoji Central Hospital, No. 8 Jiangtan Road, Baoji, Shaanxi 721008, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Baoji Central Hospital, No. 8 Jiangtan Road, Baoji, Shaanxi 721008, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2018,11,12]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"1.Webster A C, Nagler E V, Morton R L, Masson P. 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Cell-free microRNA-148a is associated with renal allograft dysfunction: Implication for biomarker discovery. , Journal of Cellular Biochemistry 0.","DOI":"10.1002\/jcb.27860"},{"key":"ref111","doi-asserted-by":"publisher","unstructured":"112.Ma Y, Shi J, Wang F. (2018) MiR-130b increases fibrosis of HMC cells by regulating the TGF-\u03b21 pathway in diabetic nephropathy. , Journal of Cellular Biochemistry 0.","DOI":"10.1002\/jcb.27688"}],"container-title":["Journal of Nephrology Advances"],"link":[{"URL":"https:\/\/openaccesspub.org\/jna\/article\/895","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,11,1]],"date-time":"2019-11-01T20:49:44Z","timestamp":1572641384000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/openaccesspub.org\/jna\/article\/895"}},"editor":[{"given":"Ying-Yong","family":"Zhao","sequence":"additional","affiliation":[{"name":"Northwest University, China."}],"role":[{"role":"editor","vocabulary":"crossref"}]}],"issued":{"date-parts":[[2018,11,12]]},"references-count":112,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2016,10,12]]}},"URL":"https:\/\/doi.org\/10.14302\/issn.2574-4488.jna-18-2443","ISSN":["2574-4488"],"issn-type":[{"type":"electronic","value":"2574-4488"}],"published":{"date-parts":[[2018,11,12]]},"article-number":"895"},{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T14:11:14Z","timestamp":1753884674319,"version":"3.41.2"},"reference-count":48,"publisher":"Open Access Pub","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNA"],"abstract":"<jats:p>This study aimed to analyze pharmacological actions of phenolic compound luteolin on the renal and cardiac hypertrophy, blood pressure (BP), baroreflex sensitivity (BRS), levels of epoxyeicosatrienoic acids (EETs), prostaglandin E-2 (PGE-2) and endothelin-1 (E1) in plasma in the 2 kidney - 1 clip (2K-1C) model of renovascular hypertension (RVH).\n\nAll animals, were randomized into 2 groups: control (normal) I - sham-operated, II- RVH male Wistar rats, which after 4 weeks of surgical intervention secondly randomized to control II group, treated 0.1% dimethyl sulphoxide (DMSO) and main group - with luteolin in 15 DMSO, 3 mg\/kg body weight, intraperitonially, during 2 weeks. ET-1, EETs and PGE2 levels investigated in carotid artery blood plasma and analyzed using ELISA kits. All data statistically analyzed using the SPSS-10.0 program.\n\nIn RVH rats BP increased by 32%, cardiac and right kidney hypertrophy and reduction in parasympathetic component of BRS by 40% and sympathetic by 39%. The plasma level of total trans-EETs and PGE2 in RVH rats decreased by 44% and 50% respectively, while the level of ET-1 increased by 67%. Two weeks treatment with luteolin lowered BP, improved parasympathetic, without marked changes in sympathetic component of BRS. Deremodeling of cardiac and renal hypertrophy under prolonged treatment with luteolin accompanied with increasing in the level of EETs by 44%, PGE-2 by 50% and markedly reducing of plasma content of ET-1 (by 60%).\n\nInhibition of EET hydrolase using low doses of luteolin provides beneficial cardio and renoprotective action in experimental model of RVH.<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-23-4545","type":"journal-article","created":{"date-parts":[[2024,1,13]],"date-time":"2024-01-13T12:29:02Z","timestamp":1705148942000},"page":"1-11","source":"Crossref","is-referenced-by-count":1,"title":["Baroreflex Sensitivity, Cardiac and Kidney Remodeling and Deterioration in Vasoactive Substances Content in Blood in Experimental Model of Renovascular Hypertension. Action of Natural Flavone, Luteolin"],"prefix":"10.14302","volume":"`","author":[{"given":"N.A.","family":"Papiashvili","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical Technology, Tbilisi State Medical University, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.V.","family":"Ghonghadze","sequence":"additional","affiliation":[{"name":"Department of Medical Pharmacology, Tbilisi State Medical University, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N.V.","family":"Sharikadze","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Ilia State University, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. P.","family":"Khutsishvili","sequence":"additional","affiliation":[{"name":"Laboratory of Biochemistry of Meta Clinic, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.A.","family":"Bakuridze","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Technology, Tbilisi State Medical University, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.J.","family":"Bakuridze","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Technology, Tbilisi State Medical University, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G.V.","family":"Sukoyan","sequence":"additional","affiliation":[{"name":"International Scientific Center of introduction of New Biomedical Technology, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N.V.","family":"Gongadze","sequence":"additional","affiliation":[{"name":"Department of Medical Pharmacology, Tbilisi State Medical University, Tbilisi, Georgia."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2023,5,15]]},"reference":[{"unstructured":"1. 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Fatty 64(1), 5-10.","key":"ref42","DOI":"10.1054\/plef.2000.0232"},{"doi-asserted-by":"publisher","unstructured":"44.Li X, Chu G, Zheng Z, Wang X, Zhang G. (2020) Epoxyeicosatrienoic acid prevents maladaptive remodeling in pressure overload by targeting calcineurin \/NFAT and smad-7. Exp Cell Res. 386, 1016.","key":"ref43","DOI":"10.1016\/j.yexcr.2019.111716"},{"doi-asserted-by":"publisher","unstructured":"45.Neckar J, MAH Khan, Gross G, Cyprova M, al Hardicha J at. (2019) Epoxyeicosatrienoic acid analog EET-B attenuates post-myocardial infarction remodeling in SHR. Clein sci. , (Lond) 133, 939-951.","key":"ref44","DOI":"10.1042\/cs20180728"},{"doi-asserted-by":"publisher","unstructured":"46.Ronchi S N, Brasil G A, AMD Nascimento, EMD Lima, Scherer R. (2015) Phytochemical and in vitro and in vivo biological investigation of the antihypertensive activity of mango leaves (Mangifera indica L.) 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The thyroid produces hormones (T3 and T4) that have many actions including metabolism, development, protein synthesis, and the regulation of many other important hormones. There is a lot of interaction between the kidney and thyroid gland during the disease States thyroid hormones have a major role in regulating the glomerular filtration rate through its hormonal actions in normal physiology. But these things are altered in the disease States such as chronic kidney disease. It is a well-known fact that hypothyroidism causes decreased Glomerular filtration rate whereas hyperthyroidism causes increased Glomerular filtration rate leading to renin-angiotensin-aldosterone system activation. In our study we aim to see the prevalence of low T3 syndrome in different stages of CKD which is a state of physiological benefit in preserving the proteins lost through the Kidneys in CKD patients and since CKD is progressed in hyperthyroidism state it is a protective mechanism in restoring the CKD status. Other subclinical hypothyroidism hyperthyroidism. Autoimmune hypothyroidism. Glomerulonephritis are all part of a dynamic endocrine and nephrology sequence. Thorough knowledge of these is required for optimum treatment of thyroid in CKD patients.<\/jats:p>","DOI":"10.14302\/issn.2574-4488.jna-21-4039","type":"journal-article","created":{"date-parts":[[2022,12,10]],"date-time":"2022-12-10T12:27:19Z","timestamp":1670675239000},"page":"31-34","source":"Crossref","is-referenced-by-count":1,"title":["Thyroid Function Abnormalities in Patients with Chronic Kidney Disease"],"prefix":"10.14302","volume":"1","author":[{"given":"A K Al","family":"Miraj","sequence":"first","affiliation":[{"name":"Research Assistant, Department of Vascular surgery Bangabandhu Sheikh Mujib Medical University (BSMMU) Dhaka, Bangladesh"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Magfur","family":"Rahman","sequence":"additional","affiliation":[{"name":"Medical Officer Cardiac Surgery Department, Bangabandhu Sheikh Mujib Medical University (BSMMU) Dhaka, Bangladesh"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anwarul","family":"Hoque Faraji","sequence":"additional","affiliation":[{"name":"Associate professor of Nephrology, Colonel Maleq Medical college Mnikgangue Bangladesh."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Muhammad","family":"Abduz Zaher","sequence":"additional","affiliation":[{"name":"Associate Professor, Institute of Nutrition and Food Science, University of Dhaka Bangladesh."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mohammad","family":"Ata Ullah","sequence":"additional","affiliation":[{"name":"Assistant Professor Department of Cardiac Surgery, Bangabandhu Sheikh Mujib Medical University (BSMMU) Dhaka, Bangladesh."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"5410","published-online":{"date-parts":[[2022,2,3]]},"reference":[{"key":"ref0","unstructured":"1.Joanne M B, Karl S K. 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(2014) Thyroid disorders and chronic kidney disease. International journal of nephrology. 14, 1-6.","DOI":"10.1155\/2014\/520281"},{"key":"ref5","doi-asserted-by":"publisher","unstructured":"6.Levey A S, Coresh J, Balk E, Kausz A T, Levin A et al. (2003) National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Annals of internal medicine. 139(2), 137-47.","DOI":"10.7326\/0003-4819-139-2-200307150-00013"},{"key":"ref6","doi-asserted-by":"publisher","unstructured":"7.Feinstein E I, Kaptein E M, Nicoloff J T, Massry S G. (1982) Thyroid function in patients with nephrotic syndrome and normal renal function. American journal of nephrology. 2(2), 70-6.","DOI":"10.1159\/000166587"},{"key":"ref7","unstructured":"8.Dudani R A. (1981) Thyroid dysfunction in Uremia. , Journal Assoc Physicians India 29, 1037-40."},{"key":"ref8","unstructured":"9.Quionverde H, Kaptein E M, Rodriguez H, Massry S. (1984) Prevalence of thyroid-disease in chronic-renal failure (CRF) and dialysis patients. In KIDNEY INTERNATIONAL350 MAIN ST, MALDEN, MA02148: BLACKWELL SCIENCE INC 25(1), 190-190."},{"key":"ref9","unstructured":"10.Joseph L J, Desai K B, Mehta H J, Mehta M N, Almeida A F et al. (1993) Measurement of serum thyrotropin levels using sensitive immunoradiometric assays in patients with chronic renal failure: alterations suggesting an intact pituitary thyroid axis. Thyroidology. 5(2), 35-9."},{"key":"ref10","unstructured":"11.Karunanidhi A. (1979) Thyroid function in patients with chronic renal failure. , Indian J Med Research 69, 792-7."},{"key":"ref11","doi-asserted-by":"publisher","unstructured":"12.Hardy M J, Ragbeer S S, Nascimento L. (1988) Pituitarythyroid function in chronic renal failure assessed by a highly sensitive thyrotropin assay. , The Journal of Clinical Endocrinology 66(1), 233-6.","DOI":"10.1210\/jcem-66-1-233"},{"key":"ref12","doi-asserted-by":"publisher","unstructured":"13.Heged\u0171s L, Andersen J R, Poulsen L R, Perrild H, Holm B et al.Thyroid gland volume and serum concentrations of thyroid hormones in chronic renal failure. , Nephron 40(2), 171-4.","DOI":"10.1159\/000183455"},{"key":"ref13","doi-asserted-by":"crossref","unstructured":"14.Iglesias P, Diez J J. (2009) Thyroid dysfunction and kidney disease. European journal of endocrinology. 160(4), 503-15.","DOI":"10.1530\/EJE-08-0837"},{"key":"ref14","doi-asserted-by":"publisher","unstructured":"15.Couser W G, Remuzzi G, Mendis S, Tonelli M. (2011) The contribution of chronic kidney disease to the global burden of major noncommunicable diseases. 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