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1. Having Multiple Renal Cysts in a Young Adult is Not Always a Sign of Polycystic Kidney Disease

Author

Kaynar K, Kayıpmaz S, Çebi AH, and Hüseynova Ş

Subjects
ciliopathies, cranioectodermal dysplasia (ced), cystic, kidney diseases, syndrome, Genetics, QH426-470
Abstract

Multiple renal cysts in adult patients could have asymptomatic, benign and a nonprogressive course. However, these cysts could be renal features of a very rare hereditary, progressive syndrome defined as cranioectodermal dysplasia (CED or Sensenbrenner syndrome). Affected patients show dysmorphic features such as craniosynostosis, nail dystrophy, cutaneous dyshydrosis, dry or scaly palmar skin, trichodysplasia, deafness, pectus excavatum, telecanthus, hypertelorism, low set ears, everted lower lip, anteverted nares, short neck and height, joint laxity, inguinal hernia, widely spaced teeth, microdontia, hypodontia in addition to nephronophthisis. We report a 22-year-old male hypertensive patient with multiple renal cysts and dental malformations listed as malocclusion, screwdriver shaped crowns, widely spaced front teeth, microdontia and hyperdontia. Molecular analysis reported missense p.(Ala875Thr) and p.(Lys969Asn) variants in the WDR35 gene. The 1-year follow-up of this case provided the knowledge that angiotensin II receptor blocker drug (olmesartan) reduced the microalbuminuria to normal levels and preserved the renal functions. We suggest interdisciplinary studies, especially intraoral and genetic evaluations for patients with cystic renal diseases. For the first time we report that hyperdontia could be found as a dental feature of CED.

Published
2022
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3. A case report of antineutrophil cytoplasmic antibody-associated vasculitis and glomerular immune depositions

Author

Kaynar, K, Güvercin, B, Demir, S, Mungan, S, and Çifçi, ET

Subjects
Case Report
Abstract

Background: Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic disease leading to renal complications of pauci-immune focal and segmental necrotizing crescentic glomerulonephritis (PI-NCGN). Case description: We present a 57-year-old female patient with rapidly progressive glomerulonephritis, multiple systemic infections [candidiasis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)], severe weight loss, arthralgia, positive myeloperoxidase ANCA, acute deterioration of cardiac function and NCGN with heavy deposition of immunoglobulin (Ig) A and complement 3 (C3) in kidney biopsy. After two months of follow-up and appropriate treatments [methylprednisolone (60 mg/day), cyclophosphamide (15 mg/kg)], our patient recovered from multiple life-threatening infections, including candidiasis treated by fluconazole and SARS-CoV-2 treated by methylprednisolone and acute cardiac failure. In addition, she was saved from dialysis despite all poor prognostic factors. Conclusion: AAV might lead to immune complex deposition in kidneys due to different pathogenetic mechanisms like complement activation and immune complex formation, apart from losing tolerance to neutrophil proteins. HIPPOKRATIA 2022, 26 (2):86-88.

Published
2022

5. To screen or not to screen renal cell cancer in a kidney transplant patient.

Author

Kaynar, K., Alizade, L., Uyar, Ö., Mungan, S., and Rashidzade, K.

Subjects
*RENAL cell carcinoma, *KIDNEY transplantation, *RENAL cancer, *MEDICAL screening, *HOMOGRAFTS
Abstract

Background: The prevalence of malignancies is higher among kidney transplant recipients (KTR) than general population. Although the incidence of renal cell cancer (RCC) after KTR was reported as 0.6 % with a high mortality rate of 13.9 %, none of the guidelines except the European Best Practice Guideline (EBPG) recommends RCC screening based on cost-effectiveness and lack of solid evidence. The EBPG recommends RCC screening in native kidneys (not the allograft) by ultrasonography (USG) every 1-3 years. Case description: A 55-year-old male patient who had a kidney transplant from a living donor 14 years before, presented with sudden onset uncontrolled hypertension (180/110 mmHg) and rapid deterioration in graft functions (increase in serum creatinine to two-times baseline). Evaluations revealed RCC in the allograft. Abdominal pain, hematuria, fever, weight loss, flu-like syndrome, recurrent urinary tract infections, weakness, hypertension, and allograft dysfunction are reported as the main complaints and signs of RCC in KTR patients. Our patient's findings were hypertension and allograft dysfunction. Conclusion: It is essential to follow EBPG for KTR and not to forget the annual USG for screening of RCC both in native kidneys and allograft. [ABSTRACT FROM AUTHOR]

Published
2023

7. Is C1q nephropathy associated with a WDR19 gene mutation? A case report

Author

Kaynar, K, Güvercin, B, Güler, Ö, Mungan, S, and Çağlayan, E

Subjects
Case Report
Abstract

Background: Even though complement 1q nephropathy (C1qN) was first introduced in 1985, this entity is still unknown and recognized by clinicians due to its rare prevalence (0.2 – 2.5 %) and insufficient emphasis. Description of the case: A 50-year-old woman was incidentally found to have non-nephrotic proteinuria with a normal glomerular filtration rate. Renal biopsy revealed C1qN with severe fibrosis. The presence of consanguinity and kidney diseases in family members of the patient led to genetic research, and homogenous mutation of c.991G>T (p.G331C) in the WD-repeat domain 19 (WDR19) gene was found. The same homozygous and heterozygous mutations in the WDR gene were found in the relatives of our patient with kidney diseases. One year of follow-up with methylprednisolone and mycophenolate mofetil treatment resulted in partial remission of the kidney disease. Conclusion: Renal biopsy for patients with non-nephrotic proteinuria without delay is suggested as it might be a surrogate marker of severe injury. Genetic mutations in the WDR19 gene should be searched for C1qN pathogenesis. This is the first adult case report on C1qN from Turkey.HIPPOKRATIA 2021, 25 (2):87-90.

Published
2021

8. Comparison of mental health, quality of sleep and life among patients with different stages of chronic kidney disease and undergoing different renal replacement therapies

Author

Küçük, O, Kaynar, K, Arslan, FC, Ulusoy, Ş, Gül, HK, Çelik, A, and Çan, G

Subjects
Research Article
Abstract

Background: The present study aimed to investigate and compare mental health, health-related quality of life, and sleep levels of patients with various stages of chronic kidney disease (CKD) and undergoing different renal replacement therapies and analyze the factors affecting these parameters. Methods: Overall, 140 patients with a mean age of 43 ± 14 years were recruited into this study. Study groups [controls and patients with CKD undergoing predialysis, hemodialysis (HD), peritoneal dialysis, kidney transplantation (KT)] were evaluated using Short Form Health Survey-36 (SF-36), Kidney Disease Quality of Life-36 (KDQoL-36), Pittsburgh Sleep Quality Index (PSQI), and General Health Questionnaire-12 (GHQ-12). Results: The KT group had the highest scores in physical and mental components of the subscales of SF-36 and KDQoL-36 but the lowest scores in PSQI and GHQ-12, indicating the best results in terms of mental health and quality of life, and sleep. Serum albumin and hemoglobin levels were positively correlated with several subscales of quality of life. Significant negative correlations were observed among PSQI, GHQ-12, and subscale scores of SF-36 and KDQoL-36. The HD group showed significantly lower scores in the subscales of symptoms and burden of kidney disease of KDQoL-36. Conclusion: KDQoL was worse in the HD group and better in the KT group than in other groups. Serum albumin and hemoglobin levels, and Kt/V (dialyzer clearance of urea multiplied by dialysis time and normalized for urea distribution volume ) values of patients with CKD exerted a linear and significant effect on the quality of life, which showed a significant positive correlation with the quality of sleep and mental health. In contrast, serum calcium x phosphorus levels showed an inverse correlation with the subscale scores of KDQoL. HIPPOKRATIA 2020, 24(2): 51-58.

Published
2020

9. In the presence of hypokalemia and hypomagnesemia; remember Gitelman syndrome

Author

Güvercin, B, Kaynar, K, Güler, Ö, and Kalyoncu, M

Subjects
Case Report
Abstract

Background: Hypokalemia and hypomagnesemia caused due to renal losses with chloride-resistant metabolic alkalosis in normotensive patients should remind clinicians of the rare inherited tubulopathy, Gitelman syndrome. Its diagnosis is further strengthened by the presence of consanguinity and the absence of kaliuretic medications. A definitive diagnosis should be based on genetic testing. Case report: We present the cases of three asymptomatic adult patients who were genetically (mutation in the SCL12A3 gene) diagnosed with Gitelman syndrome of different severity and response to therapy in terms of hypokalemia, hypomagnesemia, and metabolic alkalosis. Conclusion: This lifelong disease could cause life-threatening conditions due to the cardiac complications of hypokalemia in some of the affected patients. Therefore, it is necessary to be aware of the appropriate diagnosis and treatment for patients admitted to the clinic with hypokalemia, hypomagnesemia, hypocalciuria, and hyperreninemia. HIPPOKRATIA 2019, 23(4): 175-178.

Published
2019

10. The relationship between dermatological findings and serum interleukin 31 and serum uridine diphosphate glucose ceramide glucosyltransferase levels among patients with chronic kidney disease

Author

Güvercin, B, Kaynar, K, Arıca, DA, Kural, BV, Ulusoy, Ş, Cansız, M, Selçuk, LB, Akyüz, A, and Kolaylı, CC

Subjects
skin and connective tissue diseases, Research Article
Abstract

Background: Cutaneous diseases are observed with increasing duration and severity of renal disease in patients with chronic kidney disease (CKD). This study aimed to elucidate dermatological manifestations at different stages of CKD and determine their relationship with interleukin 31 (IL-31), a T-cell cytokine that induces severe pruritus, and uridine diphosphate (UDP)-glucose ceramide glucosyltransferase (UGCG), an enzyme that metabolizes ceramide, which plays an important role in moisturizing epidermis. Methods: In this retrospective cohort study 145 patients with a mean age of 46 ± 17 years were categorized into hemodialysis (group 1), peritoneal dialysis (group 2), kidney transplant (group 3), CKD (group 4), and healthy control (group 5) groups. Serum IL-31 and UGCG levels were measured using enzyme-linked immunosorbent assay, and clinical dermatologists evaluated dermatological manifestations. Results: In the overall cohort, pruritus was significantly and inversely correlated with glomerular filtration rate and serum hemoglobin and albumin levels (p

Published
2019

11. Is C1q nephropathy associated with a WDR19 gene mutation? A case report.

Author

Kaynar, K., Güvercin, B., Güler, Ö., Mungan, S., and Çağlayan, E.

Subjects
*GENETIC mutation, *KIDNEY diseases, *RENAL biopsy, *GLOMERULAR filtration rate, *DISEASE remission, *BIOMARKERS
Abstract

Background: Even though complement 1q nephropathy (C1qN) was first introduced in 1985, this entity is still unknown and recognized by clinicians due to its rare prevalence (0.2 - 2.5 %) and insufficient emphasis. Description of the case: A 50-year-old woman was incidentally found to have non-nephrotic proteinuria with a normal glomerular filtration rate. Renal biopsy revealed C1qN with severe fibrosis. The presence of consanguinity and kidney diseases in family members of the patient led to genetic research, and homogenous mutation of c.991G>T (p.G331C) in the WD-repeat domain 19 (WDR19) gene was found. The same homozygous and heterozygous mutations in the WDR gene were found in the relatives of our patient with kidney diseases. One year of follow-up with methylprednisolone and mycophenolate mofetil treatment resulted in partial remission of the kidney disease. Conclusion: Renal biopsy for patients with non-nephrotic proteinuria without delay is suggested as it might be a surrogate marker of severe injury. Genetic mutations in the WDR19 gene should be searched for C1qN pathogenesis. This is the first adult case report on C1qN from Turkey. [ABSTRACT FROM AUTHOR]

Published
2021

12. Comparison of mental health, quality of sleep and life among patients with different stages of chronic kidney disease and undergoing different renal replacement therapies.

Author

Küçük, O., Kaynar, K., Arslan, F. C., Ulusoy, Ş., Gül, HK., Çelik, A., and Çan, G.

Subjects
*QUALITY of life, *CHRONIC kidney failure, *MENTAL health, *SERUM albumin, *KIDNEY transplantation, *PERITONEAL dialysis, *HEMODIAFILTRATION
Abstract

Background: The present study aimed to investigate and compare mental health, health-related quality of life, and sleep levels of patients with various stages of chronic kidney disease (CKD) and undergoing different renal replacement therapies and analyze the factors affecting these parameters. Methods: Overall, 140 patients with a mean age of 43 ± 14 years were recruited into this study. Study groups [controls and patients with CKD undergoing predialysis, hemodialysis (HD), peritoneal dialysis, kidney transplantation (KT)] were evaluated using Short Form Health Survey-36 (SF-36), Kidney Disease Quality of Life-36 (KDQoL-36), Pittsburgh Sleep Quality Index (PSQI), and General Health Questionnaire-12 (GHQ-12). Results: The KT group had the highest scores in physical and mental components of the subscales of SF-36 and KDQoL-36 but the lowest scores in PSQI and GHQ-12, indicating the best results in terms of mental health and quality of life, and sleep. Serum albumin and hemoglobin levels were positively correlated with several subscales of quality of life. Significant negative correlations were observed among PSQI, GHQ-12, and subscale scores of SF-36 and KDQoL-36. The HD group showed significantly lower scores in the subscales of symptoms and burden of kidney disease of KDQoL-36. Conclusion: KDQoL was worse in the HD group and better in the KT group than in other groups. Serum albumin and hemoglobin levels, and Kt/V (dialyzer clearance of urea multiplied by dialysis time and normalized for urea distribution volume) values of patients with CKD exerted a linear and significant effect on the quality of life, which showed a significant positive correlation with the quality of sleep and mental health. In contrast, serum calcium x phosphorus levels showed an inverse correlation with the subscale scores of KDQoL. HIPPOKRATIA 2020, 24(2): 51-58. [ABSTRACT FROM AUTHOR]

Published
2020

13. Evaluation of nutritional parameters of hemodialysis patients

Author

Kaynar, K., Tat, Songul T., Ulusoy, S., Cansiz, M., Ozkan, G., Gul, S., and Bektas, O.

Subjects
carbohydrates (lipids), parasitic diseases, food and beverages, Original Article
Abstract

This study was performed to investigate nutritional parameters of hemodialysis patients by using anthropometric and biochemical measurements.Data from the last 6 months of 22 adult hemodialysis patients with a mean age of 61 ± 14 years were analyzed retrospectively. Dialysis vintage, normalized protein catabolic rate (nPCR), serum biochemical parameters, mid arm muscle circumference (MAMC) were determined as mean and standard deviation. Correlations between the variables were computed by coefficient p of Pearson.We found significant positive correlations: age of patients versus C-reactive protein, MAMC versus LDL-Cholesterol, MAMC versus body mass index, albumin versus hemoglobin. There were also significant negative correlations: age versus serum creatinine, age versus albumin, age versus intact parathyroid hormone (iPTH), dialysis vintage versus MAMC.In conclusion, age seem to be negatively associated with iPTH and albumin. As dialysis vintage increases, muscle mass seems to decrease.

Published
2012

14. Esansiyel Hipertansiyonda Nifedipinin Serum, İdrar Elektrolitlerine ve Renin/Na+ İndeksine Tesiri

Author

SAĞKAN, O., TANYERİ, F., KAYNAR, K., KIPICI, S., AYKAN, F., BAYSAL, P., ALVUR, M., and İLİÇİN, G.

Abstract

Serum and urine electrolytes (Na+, K+, Ca+ +,) and serum Rennin/Na + index are measured before and 2 and 4 hours after nifedipine administration.Both systolic and diastolic blood pressures decreased after the drug administration, being maximum from 1.5 to 2.5 hours (p < 0.05), and remained at low levels up to the end of the traatment.No statistically important difference is found between serum and urine renin/Ma"1" indexes and electrolytes before and after the edminist ratior of nifedipine. But serum Ca+ + , blood and urine Na+ levels tend to increase while K+ levels and urine Ca++ levels tend to decrease after nifedipine administration.Bu çalışma ağızdan 10 nıgr nifedipin (Adalat) verilen esensiyel hipertansiyona 22 hastada yapıldı.Hastaların nifedipin verilmeden önce ve verildikten ilk 2 ve 4'cü saatler arasında kan basıncı, kan ve idrar elektrolitleri (Na, K, Ca) serum Re-nin/Na-i- indeksi değerleri araştırıldı.Gerek sistoük gerek diyastolik kan basınçlarının en fazla ilk 1,5 ilâ 2,5 saatte anlamlı düşüş (p

Published
2010

15. Hipertansiyonda Sistolik Pik Basıncının / Sistol Sonu Çapa Oranının Sol Ventrikül Sistolik Fonksiyonunu Değerlendirmedeki Önemi

Author

KAYNAR, K., SAĞKAN, O., and İLİÇİN, G.

Abstract

SUMMARYThe role of the ratio of the systolic peak pressor to the end of the systolicdiameter on the determination of the left ventricular fonction in the hyper¬tensive parents.Left ventricular systolic functions (EF, Vcf and LVESD ratio) inves¬tigated non-invansively in 27 hypertensive and 10 normal adults EF and Vcf were found normal in a group of patients and as decreased in others. LVSPP/LVESD ratio was increased in all hypertensive patients (% 96.29). The mean values of EF, Vcf, LVSPP/LVESD and LVESD were compared in normal and adults patient group Vcf were singificantly decreased (p

Published
2009

16. AKI - Experimental

Author

Kaynar, K., primary, Kaynar, K., additional, Ersoz, S., additional, Aliyazioglu, R., additional, Uzun, A., additional, Ulusoy, S., additional, Al, S., additional, Ozkan, G., additional, Cansiz, M., additional, Bertocchio, J.-P., additional, Lancon, J., additional, El Moghrabi, S., additional, Galmiche, G., additional, Duong Van Huyen, J.-P., additional, Rieu, P., additional, Jaisser, F., additional, Albertoni, G., additional, Andrade, S., additional, Barreto, J. A., additional, Borges, F., additional, Schor, N., additional, Ho, W.-Y., additional, Chen, S.-H., additional, Tseng, C.-J., additional, Bienholz, A., additional, Feldkamp, T., additional, Weinberg, J. M., additional, Suller Garcia, J., additional, Naves, M., additional, Aparecida Reis, L., additional, Simoes, M. d. J., additional, S Almeida, W., additional, Moreau Longo, V., additional, Segreto, H. R. C., additional, Ghoneim, A., additional, Elkholy, A., additional, Medhat Abbas, T., additional, El Hadeedy, M., additional, Elhusseini, F., additional, Elessawey, B., additional, Eltanaihy, E., additional, Lotfy, A., additional, Eldesoky, S., additional, Sheashaa, H., additional, Sobh, M., additional, Minning, D. M., additional, Warnock, D., additional, Mohamed, A. S., additional, Wirthlin, J. B., additional, Chintalacharuvu, S. R., additional, Boone, L., additional, Brenner, R. M., additional, Santina Christo, J., additional, Dos Santos Passos, C., additional, Rene de Alencar, D., additional, De Braganca, A. C., additional, Canale, D., additional, Goncalves, J. G., additional, Brandao, T. P. B., additional, Shimizu, M. H. M., additional, Volpini, R. A., additional, Seguro, A. C., additional, Andrade, L., additional, Lee, J.-W., additional, Kim, H. K., additional, Cho, W. Y., additional, Jo, S.-K., additional, Cho, E., additional, Hocherl, K., additional, Schmidt, C., additional, Mulay, S. R., additional, Kulkarni, O. P., additional, Rupanagudi, K. V., additional, Migliorini, A., additional, Liapis, H., additional, Anders, H.-J., additional, Pevzner, I., additional, Chupyrkina, A., additional, Plotnikov, E., additional, Zorov, D., additional, Lopez-Novoa, J.-M., additional, Eleno, N., additional, Perez-Barriocanal, F., additional, Arevalo, M., additional, Docherty, N., additional, Castellano, G., additional, Divella, C., additional, Loverre, A., additional, Stasi, A., additional, Curci, C., additional, Rossini, M., additional, Ditonno, P., additional, Battaglia, M., additional, Daha, M. R., additional, Van Kooten, C., additional, Gesualdo, L., additional, Schena, F. P., additional, Grandaliano, G., additional, Tsuda, H., additional, Kawada, N., additional, Iwatani, H., additional, Moriyama, T., additional, Takahara, S., additional, Rakugi, H., additional, Isaka, Y., additional, Schley, G., additional, Kalucka, J., additional, Klanke, B., additional, Jantsch, J., additional, Olbrich, S., additional, Baumgartl, J., additional, Amann, K., additional, Eckardt, K.-U., additional, Weidemann, A., additional, Dolgolikova, A., additional, Pilotovich, V., additional, Ivanchik, G., additional, Shved, I., additional, Banki, N. F., additional, Antal, Z., additional, Hosszu, A., additional, Koszegi, S., additional, Vannay, A., additional, Wagner, L., additional, Prokai, A., additional, Muller, V., additional, Szabo, A. J., additional, Fekete, A., additional, Farrag, S., additional, Abulasrar, S., additional, Salama, , M., additional, Amin, M., additional, Ali, A., additional, Rubera, I., additional, Duranton, C., additional, Cougnon, M., additional, Melis, N., additional, Tauc, M., additional, Jankauskas, S., additional, Morosanova, M., additional, Pulkina, N., additional, Zorova, L., additional, Shin, Y. T., additional, Kim, S. S., additional, Chang, Y. K., additional, Choi, D. E., additional, Na, K.-R., additional, Lee, K. W., additional, Choi, J.-Y., additional, Jin, D.-C., additional, Cha, J.-H., additional, Schneider, R., additional, Betz, B., additional, Meusel, M., additional, Held, C., additional, Wanner, C., additional, Gekle, M., additional, Sauvant, C., additional, Pisani, A., additional, Rossano, R., additional, Mancini, A., additional, Arfian, N., additional, Yagi, K., additional, Nakayama, K., additional, Ali, H., additional, Mayasari, D. S., additional, Purnomo, E., additional, Emoto, N., additional, Efrati, S., additional, Berman, S., additional, Abu Hamad, R., additional, Weissgarten, J., additional, Scherbaum, C. R., additional, Allam, R., additional, Lichtnekert, J., additional, Darisipudi, M. N., additional, Hagele, H., additional, Hohenstein, B., additional, Hugo, C., additional, Schaefer, L., additional, Corsi, C., additional, Ferramosca, E., additional, Grandi, E., additional, Pisoni, L., additional, Rivolta, I., additional, Dalpozzo, B., additional, Hoxha, E., additional, Severi, S., additional, Santoro, A., additional, Laurent, M., additional, Cedric, R., additional, Dominique, C., additional, Sophie, V., additional, Nochy, D., additional, Loic, G., additional, Patrice, C., additional, Chantal, J., additional, Marie-Christine, V., additional, Alexandre, H., additional, Eric, R., additional, Cantaluppi, V., additional, Medica, D., additional, Quercia, A. D., additional, Figliolini, F., additional, Dellepiane, S., additional, Randone, O., additional, Segoloni, G. P., additional, Camussi, G., additional, Ahn, B.-H., additional, Kim, S. H., additional, Yasue Saito Miyagi, M., additional, Camara, N., additional, Cerqueira Leite Seelaender, M., additional, Maceratesi Enjiu, L., additional, Estler Rocha Guilherme, P., additional, Pisciottano, M., additional, Hiyane, M., additional, Yuri Hayashida, C., additional, De Andrade Oliveira, V., additional, Olsen Saraiva Camara, N., additional, Tami Amano, M., additional, Sancho-Martinez, S. M., additional, Sanchez-Juanes, F., additional, Vicente, L., additional, Gonzalez-Buitrago, J. M., additional, Morales, A. I., additional, Lopez-Novoa, J. M., additional, Lopez-Hernandez, F. J., additional, Chen, J.-S., additional, Chang, L.-C., additional, Chen, C.-C., additional, Park, M. Y., additional, Choi, S. J., additional, Kim, J. G., additional, Hwang, S. D., additional, Vicente-Vicente, L., additional, Ferreira, L., additional, Prieto, M., additional, Garcia-Sanchez, O., additional, Sevilla, M. A., additional, Lopez-Novoa, F. J., additional, Christoph, K., additional, Kuper, C., additional, Maria-Luisa, F., additional, Franz-Xaver, B., additional, Neuhofer, W., additional, Vervaet, B., additional, Le Clef, N., additional, Verhulst, A., additional, D'haese, P., additional, Tanaka, T., additional, Yamaguchi, J., additional, Eto, N., additional, Kojima, I., additional, Fujita, T., additional, Nangaku, M., additional, Wystrychowski, A., additional, Wystrychowski, G., additional, Obuchowicz, E., additional, Grzeszczak, W., additional, Wiecek, A., additional, Esposito, C., additional, Torreggiani, M., additional, Castoldi, F., additional, Migotto, C., additional, Serpieri, N., additional, Grosjean, F., additional, Manini, A., additional, Pertile, E., additional, and Dal Canton, A., additional

Published
2012
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17. Nutrition / inflammation

Author

Wong, M. M. Y., primary, Thijssen, S., additional, Usvyat, L. A., additional, Kotanko, P., additional, Maddux, F. W., additional, Speer, T., additional, Rohrer, L., additional, Blyzszuk, P., additional, Krankel, N., additional, Zewinger, S., additional, Martin, T., additional, von Eckardstein, A., additional, Luscher, T., additional, Landmesser, U., additional, Fliser, D., additional, Prats, M., additional, Font, R., additional, Garcia, C., additional, Cabre, C., additional, Jariod, M., additional, Martinez Vea, A., additional, Costa, E., additional, Ribeiro, S., additional, do Sameiro-Faria, M., additional, Rocha-Pereira, P., additional, Kohlova, M., additional, Fernandes, J., additional, Reis, F., additional, Miranda, V., additional, Quintanilha, A., additional, Bronze-da-Rocha, E., additional, Belo, L., additional, Santos-Silva, A., additional, Nascimento, H., additional, Schepers, E., additional, Glorieux, G., additional, Van den Abeele, T., additional, Neirynck, N., additional, Vanholder, R., additional, Boelaert, J., additional, Liabeuf, S., additional, Massy, Z., additional, Kaynar, K., additional, Kural, B. V., additional, Ulusoy, S., additional, Cansiz, M., additional, Akcan, B., additional, Misir, N., additional, Yaman, S., additional, Kaya, N., additional, Dimas, G. G., additional, Iliadis, F. S., additional, Tegos, T. J., additional, Spiroglou, S. G., additional, Pitsalidis, C. G., additional, Karamouzis, I. M., additional, Didaggelos, T. P., additional, Adamidou, A. P., additional, Savopoulos, C. G., additional, Karamouzis, M. I., additional, Orologas, A. G., additional, Hatzitolios, A. I., additional, Grekas, D. M., additional, Flisinski, M., additional, Brymora, A., additional, Stefanska, A., additional, Strozecki, P., additional, Manitius, J., additional, Khalfina, T. N., additional, Maksudova, A. N., additional, Valeeva, I. K., additional, Bantis, C., additional, Kouri, N.-M., additional, Bamichas, G., additional, Stangou, M., additional, Tsantekidou, E., additional, Natse, T., additional, Fazio, M. R., additional, Basile, G., additional, Lucisano, S., additional, Montalto, G., additional, Valeria, C., additional, Donato, V., additional, Lupica, R., additional, Trimboli, D., additional, Aloisi, C., additional, Buemi, M., additional, Henze, A., additional, Raila, J., additional, Scholze, A., additional, Schweigert, F., additional, Tepel, M., additional, Nakamichi, R., additional, Prates, E., additional, Redublo Quinto, B. M., additional, Zanella, M. T., additional, Batista, M. C., additional, Masajtis-Zagajewska, A., additional, Kurnatowska, I., additional, Wajdlich, M., additional, Nowicki, M., additional, Mennini, F., additional, Russo, S., additional, Marcellusi, A., additional, Quintaliani, G., additional, Andrulli, S., additional, Chiavenna, C., additional, Bigi, M. C., additional, Tentori, F., additional, Crepaldi, M., additional, Corti, M. M., additional, Dell'Oro, C., additional, Bacchini, G., additional, Limardo, M., additional, Pontoriero, G., additional, Williams, C., additional, Abbas, S. R., additional, Zhu, F., additional, Flores-Gama, C., additional, Moskowitz, J., additional, Cartagena, C., additional, Carter, M., additional, Levin, N., additional, de Oliveira, R. B., additional, Okazaki, H., additional, Lenglet, A., additional, Desjardins, L., additional, Lemke, H.-D., additional, Valholder, R., additional, Choukroun, G., additional, and Massy, Z. A., additional

Published
2013
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19. Renal histopathology

Author

Saddadi, F., primary, Najafi, I., additional, Hakemi, M., additional, Jahani, M., additional, Ali Moghadam, K., additional, Ghavamzadeh, A., additional, Soleimanian, T., additional, Perkowska-Ptasinska, A., additional, Wagrowska-Danilewicz, M., additional, Danilewicz, M., additional, Halon, A., additional, Komuda, E., additional, Karkoszka, H., additional, Andrzejewska, A., additional, Okon, K., additional, Kurnatowska, I., additional, Krasnicka, M., additional, Hryszko, T., additional, Kusztal, M., additional, Wiechecka-Korenkiewicz, J., additional, Marcinkowska, E., additional, Korenkiewicz, J., additional, Marszalek, A., additional, Sypniewska, G., additional, Manitius, J., additional, Cappuccino, L., additional, Verzola, D., additional, Tosetti, F., additional, Marre, S., additional, Villaggio, B., additional, Salvidio, G., additional, Garibotto, G., additional, Pasquariello, A., additional, Innocenti, M., additional, Pasquariello, G., additional, Mattei, P., additional, Samoni, S., additional, Sami, N., additional, Cupisti, A., additional, Malvar, B., additional, Viana, H., additional, Galvao, M., additional, Carvalho, F., additional, Oksa, A., additional, Demes, M., additional, Danis, D., additional, Hilhorst, M., additional, van Paassen, P., additional, van Breda Vriesman, P., additional, Cohen Tervaert, J. W., additional, Ciszek, M., additional, Urbanowicz, A., additional, Kwiatkowski, A., additional, Durlik, M., additional, Saito, T., additional, Kawano, M., additional, Saeki, T., additional, Nishi, S., additional, Yamaguchi, Y., additional, Hisano, S., additional, Nakashima, H., additional, Yamanaka, N., additional, Oh, S.-W., additional, Chin, H. J., additional, Na, K. Y., additional, Chae, D.-W., additional, Ozkan, G., additional, Ulusoy, S., additional, Ersoz, S., additional, Orem, A., additional, Alkanat, M., additional, Yucesan, F., additional, Kaynar, K., additional, Al, S., additional, Simic Ogrziovic, S., additional, Bojic, S., additional, Basta Jovanovic, G., additional, Kotur Stevuljevic, J., additional, Dosaj, V., additional, Lezaic, V., additional, Yagisawa, T., additional, Kimura, T., additional, Ishikawa, N., additional, and Yashi, M., additional

Published
2011
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20. Acute kidney injury - Experimental models

Author

Nagasaki, Y., primary, Yoshitomi, T., additional, Hirayama, A., additional, Schock-Kusch, D., additional, Xie, Q., additional, Shulhevich, Y., additional, Hesser, J., additional, Stsepankou, S., additional, Koenig, S., additional, Heinrich, R., additional, Pill, J., additional, Gretz, N., additional, Efrati, S., additional, Berman, S., additional, Abu-Hamad, R., additional, Siman-Tov, Y., additional, Weissgarten, J., additional, Kimura, T., additional, Takabatake, Y., additional, Takahashi, A., additional, Kaimori, J.-y., additional, Matsui, I., additional, Namba, T., additional, Kitamura, H., additional, Niimura, F., additional, Matsusaka, T., additional, Rakugi, H., additional, Isaka, Y., additional, Ito, K., additional, Watanabe, M., additional, Nakashima, H., additional, Abe, Y., additional, Ifuku, M., additional, Nishimura, S., additional, Saito, T., additional, Mulay, S. R., additional, Thomasova, D., additional, Ryu, M., additional, Anders, H.-J., additional, Nakayama, Y., additional, Ueda, S., additional, Yamagishi, S.-i., additional, Ando, R., additional, Kaida, Y., additional, Iwatani, R., additional, Fujimi, A., additional, Fukami, K., additional, Okuda, S., additional, Shin, Y. T., additional, Jeong, J. Y., additional, Jang, W. I., additional, Chung, S., additional, Choi, D. E., additional, Na, K. R., additional, Lee, K. W., additional, Mugitani, N., additional, Shimizu, Y., additional, Satake, K., additional, Suzuki, Y., additional, Horikoshi, S., additional, Tomino, Y., additional, Schneider, R., additional, Meusel, M., additional, Betz, B., additional, Wanner, C., additional, Koepsell, H., additional, Sauvant, C., additional, Dursun, B., additional, Abban, G., additional, Kucukatay, V., additional, Tufan, L., additional, Dodurga, Y., additional, Guclu, A., additional, Gok, D., additional, Vicente-Vicente, L., additional, Sanchez-Gonzalez, P. D., additional, Prieto, M., additional, Lopez-Novoa, J. M., additional, Lopez-Hernandez, F. J., additional, Morales, A. I., additional, Torres, A., additional, Dnyanmote, A., additional, Wu, W., additional, Nigam, S., additional, Wystrychowski, A., additional, Wystrychowski, W., additional, Kolodziejczyk, A., additional, Obuchowicz, E., additional, Wiecek, A., additional, Reis, L. A., additional, Borges, F. T., additional, Simoes, M. d. J., additional, Schor, N., additional, Mesnard, L., additional, Rafat, C., additional, Vandermeersch, S., additional, Nochy, D., additional, Garcon, L., additional, Callard, P., additional, Jouanneau, C., additional, Verpont, M.-C., additional, Hertig, A., additional, Rondeau, E., additional, Grosjean, F., additional, Torreggiani, M., additional, Esposito, V., additional, Mangione, F., additional, Serpieri, N., additional, Villa, L., additional, Sileno, G., additional, Marchi, G., additional, Fasoli, G., additional, Esposito, C., additional, Dal Canton, A., additional, Sancho-Martinez, S., additional, Striker, G., additional, Vlassara, H., additional, Zheng, F., additional, Park, D. J., additional, Kim, J. H., additional, Jung, M. H., additional, Seo, J. W., additional, Kim, H.-j., additional, Chang, S.-H., additional, Han, B.-G., additional, Yang, J.-W., additional, Yu, J.-M., additional, Choi, S.-O., additional, Christo, J. S., additional, Rusai, K., additional, Prokai, A., additional, Szebeni, B., additional, Meszaros, K., additional, Fekete, A., additional, Treszl, A., additional, Vannay, A., additional, Muller, V., additional, Reusz, G., additional, Heemann, U., additional, Tulassay, T., additional, Lutz, J., additional, Szabo, A. J., additional, Ranghino, A., additional, Bruno, S., additional, Grange, C., additional, Dolla, C., additional, Cantaluppi, V., additional, Biancone, L., additional, Tetta, C., additional, Segoloni, G. P., additional, Camussi, G., additional, Pinto, V., additional, Teixeira, V., additional, Almeida, W., additional, Fujikura, T., additional, Sun, Y., additional, Iwakura, T., additional, Yasuda, H., additional, Fujigaki, Y., additional, Simone, S., additional, Rascio, F., additional, Loverre, A., additional, Cosola, C., additional, Cariello, M., additional, Castellano, G., additional, Ditonno, P., additional, Schena, F. P., additional, Gesualdo, L., additional, Grandaliano, G., additional, Pertosa, G., additional, Choi, J.-Y., additional, Kim, J., additional, Jin, D.-C., additional, Cha, J.-H., additional, Kaynar, K., additional, Aliyazicioglu, R., additional, Ersoz, S., additional, Ulusoy, S., additional, Al, S., additional, Ozkan, G., additional, Cansiz, M., additional, Fuchs, T. C., additional, Emde, B., additional, Czasch, S., additional, von Landenberg, F., additional, Hewitt, P., additional, Abu-Salah, N., additional, Bishara, B., additional, Awad, H., additional, Ghrayeb, N., additional, Assady, S., additional, Armaly, Z., additional, Better, O., additional, and Abassi, Z., additional

Published
2011
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24. The Effect of Indomethacin on Hepatitis B Virus Replication in Chronic Healthy Carriers.

Author

Kapicioğlu, S., Sari, M., Kaynar, K., Baki, A., and Özoran, Y.

Subjects
INDOMETHACIN, HEPATITIS B virus, CARRIER state (Communicable diseases), VIRAL replication, THERAPEUTICS
Abstract

Background: A chronic HBsAg carrier state, a major cause of viral spread in a community, is one of the consequences of hepatitis B virus (HBV) infection. Although successful immunization programs have been initiated to eliminate the virus, there is still a large number of people with HBV infection worldwide. This study was designed to investigate the effect of indomethacin treatment on HBV markers in humans, in comparison with a control group. Methods: In total, 65 chronic `healthy' HBV carriers were involved in the study. Patients were divided randomly into two groups. Group I (n = 42) received oral indomethacin 75 mg daily for 6 months. Group II (n = 23) acted as control. Patients in both groups were followed up for 6 months, during which laboratory tests, including viral parameters, were performed periodically. Liver biopsy was done in 17 patients (11/42 of the indomethacin group and 6/23 of the control group). Results: All liver biopsies showed grade 0-2 and stage 0-1 HBV in both groups (P > 0.05). HBsAg positivity did not change in any patient in either group. Five patients who had positive HBeAg in group I became negative 4 months later, while patients in group II continued to be positive at 6 months (P < 0.001). Similarly, all patients receiving indomethacin exhibited a total anti-HBeAg immunoglobulin response at 6 months, while the control group remained the same during this period (P < 0.05). HBV DNA, as detected by polymerase chain reaction in 20/22 (91%), was negative in group I at the end of 6 months. No change was observed in group II (P = 0.007). Conclusions: Although no biochemical analyses were performed on prostaglandins in the present study, the results suggest that the prostaglandin pathway may be involved in the pathogenesis of the immune response against HBV, and that the suppression of viral replication is achieved as indicated by the disappearance of HBeAg and HBV DNA in healthy chronic HBV carriers. [ABSTRACT FROM AUTHOR]

Published
2000
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25. Bilateral asymptomatic giant renal artery aneurysm

Author

Özkan, G., Ulusoy, S., Dinç, H., Kaynar, K., BİRCAN SONMEZ, and Akagündüz, K.

Subjects
cardiovascular system, Case Report, cardiovascular diseases
Abstract

The incidence of renal artery aneurysm is very low. Approximately in 20% of these patients hypertension is observed. The diameter of aneurysm increases with accompanying complication rates. The most feared complication is rupture. The risk of rupture also increases with the diameter of aneurysm. We report an aneurysm with the biggest diameter reported in the literature. The patient had a 12 cm-diameter of aneurysm in one kidney and did not show any symptoms including hypertension until she was seventy years old.

31. A comparison of the effects of losartan and ramipril on blood pressure, renal volume and progression in polycystic kidney disease: A 5-Year follow-up.

Author

Ulusoy, S., Ozkan, G., Kosucu, P., Kaynar, K., and Eyuboglu, I.

Subjects
*LOSARTAN, *RAMIPRIL, *DISEASE progression, *POLYCYSTIC kidney disease, *DRUG efficacy, *BLOOD pressure, *FOLLOW-up studies (Medicine)
Abstract

Background: The major cause of hereditary renal failure is autosomal dominant polycystic kidney disease (ADPKD). Many factors affect renal progression in these patients. Among these, hypertension and an increase in renal volume are interrelated in terms of their effects on renal progression. We aimed to investigate the effects of losartan and ramipril on renal volume and progression in patients with ADPKD. Materials and Methods: Data from 18 hypertensive patients with ADPKD were evaluated. Eleven of the 18 hypertensive patients were on losartan and 7 on ramipril treatment. Demographic parameters, use of antihypertensives and other medications, the course of blood pressure (BP), biochemical parameters, creatinine clearance (CrCL), findings at computed tomography and renal volume were recorded at baseline and at 1 and 5 years. Results: Target BP values were maintained over 5 years. The annual decrease in CrCL was 1.33 mL/min in the losartan group compared with 6.59 mL/min in the ramipril group. There was no significant difrerence between the groups in terms of annual decrease in CrCL. Annual increase in renal volume was 252.04 cm3 in the losartan group and 167.36 cm3 in the ramipril group. There was no significant difference between the groups in terms of the increase in renal volumes at 1 and 5 years. Conclusion: Our study demonstrated that losartan and ramipril provided effective BP control. In addition, the results of our study demonstrated that despite the increase in renal volume, losartan and ramipril may have regressed renal progression via other factors. [ABSTRACT FROM AUTHOR]

Published
2012

32. Bilateral asymptomatic giant renal artery aneurysm.

Author

Özkan, G., Ulusoy, S., Dinç, H., Kaynar, K., Sönmez, B., and Akagündüz, K.

Subjects
*RENAL artery aneurysms, *RUPTURED aneurysms, *ULTRASONIC imaging, *POSITRON emission tomography, *QUALITATIVE research
Abstract

The incidence of renal artery aneurysm is very low. Approximately in 20% of these patients hypertension is observed. The diameter of aneurysm increases with accompanying complication rates. The most feared complication is rupture. The risk of rupture also increases with the diameter of aneurysm. We report an aneurysm with the biggest diameter reported in the literature. The patient had a 12 cm-diameter of aneurysm in one kidney and did not show any symptoms including hypertension until she was seventy years old. [ABSTRACT FROM AUTHOR]

Published
2011

37. A novel mutation in a patient with familial renal hypouricemia type 2.

Author

Kaynar K, Güvercin B, Şahin M, Turan N, and Açíkyürek F

Subjects
Allantoin, Glucose Transport Proteins, Facilitative genetics, Humans, Mutation, Organic Cation Transport Proteins genetics, Renal Tubular Transport, Inborn Errors, Uric Acid, Urinary Calculi, Acute Kidney Injury genetics, Organic Anion Transporters genetics
Abstract

Introduction: Hypouricemia may be caused by disorders leading to decreased UA production, oxidation of UA to allantoin by drugs or increased renal tubular loss of filtered UA, renal hypouricemia (RHUC). RHUC may be resulted from familial or acquired disorders. Familial RHUC cases are classified according to the gene affected as type 1 (SLC22A12 gene) and type 2 (SLC2A9). Clinical importance of RHUC entity is mainly determined by emerging of acute kidney injury (AKI) after strenuous exercise and urolithiasis., Case Presentation: Here, we report a case of RHUC with increased fractional excretion of uric acid value of more than 100%, serum uric acid level of nearly zero, and exercise-induced AKI episodes clinically and a new unpublished homozygous (biallelic) mutation of c.1419+2T>G (IVS11+2T>G) in the SLC2A9 gene genetically for the first time to our knowledge., Conclusion: Clinicians should be aware of this rare entity defined as hereditary RHUC in order to provide long term renoprotection by advisements like simple precautions such as avoiding severe exercises., (Copyright © 2021 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Published
2022
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38. A case report of antineutrophil cytoplasmic antibody-associated vasculitis and glomerular immune depositions.

Author

Kaynar K, Güvercin B, Demir S, Mungan S, and Çifçi ET

Abstract

Background: Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic disease leading to renal complications of pauci-immune focal and segmental necrotizing crescentic glomerulonephritis (PI-NCGN)., Case Description: We present a 57-year-old female patient with rapidly progressive glomerulonephritis, multiple systemic infections [candidiasis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)], severe weight loss, arthralgia, positive myeloperoxidase ANCA, acute deterioration of cardiac function and NCGN with heavy deposition of immunoglobulin (Ig) A and complement 3 (C3) in kidney biopsy. After two months of follow-up and appropriate treatments [methylprednisolone (60 mg/day), cyclophosphamide (15 mg/kg)], our patient recovered from multiple life-threatening infections, including candidiasis treated by fluconazole and SARS-CoV-2 treated by methylprednisolone and acute cardiac failure. In addition, she was saved from dialysis despite all poor prognostic factors., Conclusion: AAV might lead to immune complex deposition in kidneys due to different pathogenetic mechanisms like complement activation and immune complex formation, apart from losing tolerance to neutrophil proteins. HIPPOKRATIA 2022, 26 (2):86-88., Competing Interests: Authors declare no conflicts of interests., (Copyright 2022, Hippokratio General Hospital of Thessaloniki.)

Published
2022

42. A novel mutation in a patient with familial renal hypouricemia type 2.

Author

Kaynar K, Güvercin B, Şahin M, Turan N, and Açíkyürek F

Abstract

Introduction: Hypouricemia may be caused by disorders leading to decreased UA production, oxidation of UA to allantoin by drugs or increased renal tubular loss of filtered UA, renal hypouricemia (RHUC). RHUC may be resulted from familial or acquired disorders. Familial RHUC cases are classified according to the gene affected as type 1 (SLC22A12 gene) and type 2 (SLC2A9). Clinical importance of RHUC entity is mainly determined by emerging of acute kidney injury (AKI) after strenuous exercise and urolithiasis., Case Presentation: Here, we report a case of RHUC with increased fractional excretion of uric acid value of more than 100%, serum uric acid level of nearly zero, and exercise-induced AKI episodes clinically and a new unpublished homozygous (biallelic) mutation of c.1419+2T>G (IVS11+2T>G) in the SLC2A9 gene genetically for the first time to our knowledge., Conclusion: Clinicians should be aware of this rare entity defined as hereditary RHUC in order to provide long term renoprotection by advisements like simple precautions such as avoiding severe exercises., (Copyright © 2021 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Published
2021
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45. Don't forget syphilis in membranous nephropathy before immunosuppressants: Latent syphilis in a patient with proteinuria.

Author

Kaynar K, Güvercin B, Mungan S, and Ulusoy Ş

Subjects
Adult, Glomerulonephritis, Membranous diagnosis, Glomerulonephritis, Membranous pathology, Humans, Male, Proteinuria etiology, Syphilis Serodiagnosis, Syphilis, Latent diagnosis, Syphilis, Latent immunology, Glomerulonephritis, Membranous etiology, Syphilis, Latent complications
Published
2020
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47. In the presence of hypokalemia and hypomagnesemia; remember Gitelman syndrome.

Author

Güvercin B, Kaynar K, Güler Ö, and Kalyoncu M

Abstract

Background: Hypokalemia and hypomagnesemia caused due to renal losses with chloride-resistant metabolic alkalosis in normotensive patients should remind clinicians of the rare inherited tubulopathy, Gitelman syndrome. Its diagnosis is further strengthened by the presence of consanguinity and the absence of kaliuretic medications. A definitive diagnosis should be based on genetic testing., Case Report: We present the cases of three asymptomatic adult patients who were genetically (mutation in the SCL12A3 gene) diagnosed with Gitelman syndrome of different severity and response to therapy in terms of hypokalemia, hypomagnesemia, and metabolic alkalosis., Conclusion: This lifelong disease could cause life-threatening conditions due to the cardiac complications of hypokalemia in some of the affected patients. Therefore, it is necessary to be aware of the appropriate diagnosis and treatment for patients admitted to the clinic with hypokalemia, hypomagnesemia, hypocalciuria, and hyperreninemia. HIPPOKRATIA 2019, 23(4): 175-178., Competing Interests: Authors declare no conflict of interest., (Copyright 2019, Hippokratio General Hospital of Thessaloniki.)

Published
2019

48. The relationship between dermatological findings and serum interleukin 31 and serum uridine diphosphate glucose ceramide glucosyltransferase levels among patients with chronic kidney disease.

Author

Güvercin B, Kaynar K, Arıca DA, Kural BV, Ulusoy Ş, Cansız M, Selçuk LB, Akyüz A, and Kolaylı CC

Abstract

Background: Cutaneous diseases are observed with increasing duration and severity of renal disease in patients with chronic kidney disease (CKD). This study aimed to elucidate dermatological manifestations at different stages of CKD and determine their relationship with interleukin 31 (IL-31), a T-cell cytokine that induces severe pruritus, and uridine diphosphate (UDP)-glucose ceramide glucosyltransferase (UGCG), an enzyme that metabolizes ceramide, which plays an important role in moisturizing epidermis., Methods: In this retrospective cohort study 145 patients with a mean age of 46 ± 17 years were categorized into hemodialysis (group 1), peritoneal dialysis (group 2),  kidney transplant (group 3), CKD (group 4), and healthy control (group 5) groups. Serum IL-31 and  UGCG levels were measured using enzyme-linked immunosorbent assay, and clinical dermatologists evaluated dermatological manifestations., Results: In the overall cohort, pruritus was significantly and inversely correlated with glomerular filtration rate and serum hemoglobin and albumin levels (p <0.005). Additionally, pruritus was significantly more frequent in group 2 than in group 5; and significantly less frequent in group 3 than in groups 1, 2, and 4 (p =0.01). In group 4, the patients with longitudinal nail ridges had significantly higher serum IL-31 levels than those without longitudinal nail ridges in their nails (p =0.02). Furthermore, in group 2, the patients with pruritus had significantly lower UGCG levels than those without pruritus (p =0.045)., Conclusion: IL-31 might play a role in the development of longitudinal nail ridges, whereas UGCG might provide protection from pruritus and xerosis in patients with CKD.  HIPPOKRATIA 2019, 23(2): 75-80., Competing Interests: All authors declare that there are no conflicts of interest related to the study., (Copyright 2019, Hippokratio General Hospital of Thessaloniki.)

Published
2019

50. The Frequency and Outcome of Acute Kidney Injury in a Tertiary Hospital: Which Factors Affect Mortality?

Author

Ulusoy S, Arı D, Ozkan G, Cansız M, and Kaynar K

Subjects
Acute Kidney Injury diagnosis, Acute Kidney Injury therapy, Aged, Female, Hospital Mortality, Humans, Kaplan-Meier Estimate, Kidney pathology, Male, Middle Aged, Retrospective Studies, Risk Factors, Treatment Outcome, Turkey epidemiology, Acute Kidney Injury epidemiology, Acute Kidney Injury mortality, Tertiary Care Centers
Abstract

Acute kidney injury (AKI) is a major cause of mortality and morbidity in hospitalized patients. Incidence and mortality rates vary from country to country, and according to different in-hospital monitoring units and definitions of AKI. The aim of this study was to determine factors affecting frequency of AKI and mortality in our hospital. We retrospectively evaluated data for 1550 patients diagnosed with AKI and 788 patients meeting the Kidney Disease: Improving Global Outcomes (KDIGO) guideline AKI criteria out of a total of 174 852 patients hospitalized in our institution between January 1, 2007 and December 31, 2012. Staging was performed based on KDIGO Clinical Practice for Acute Kidney Injury and RIFLE (Risk, Injury, Failure, Loss of kidney function and End-stage renal failure). Demographic and biochemical data were recorded and correlations with mortality were assessed. The frequency of AKI in our hospital was 0.9%, with an in-hospital mortality rate of 34.6%. At multivariate analysis, diastolic blood pressure (OR 0.89, 95% CI 0.87-0.92; P < 0.001), monitoring in the intensive care unit (OR 0.18, 95% CI 0.09-0.38; P < 0.001), urine output (OR 4.00, 95% CI 2.03-7.89; P < 0.001), duration of oliguria (OR 1.51, 95% CI 1.34-1.69; P < 0.001), length of hospitalization (OR 0.83, 95% CI 0.79-0.88; P < 0.001), dialysis requirement (OR 2.30, 95% CI 1.12-4.71; P < 0.05), APACHE II score (OR 1.16, 95% CI 1.09-1.24; P < 0.001), and albumin level (OR 0.32, 95% CI 0.21-0.50; P < 0.001) were identified as independent determinants affecting mortality. Frequency of AKI and associated mortality rates in our regional reference hospital were compatible with those in the literature. This study shows that KDIGO criteria are more sensitive in determining AKI. Mortality was not correlated with staging based on RIFLE or KDIGO. Nonetheless, our identification of urine output as one of the independent determinants of mortality suggests that this parameter should be used in assessing the correlation between staging and mortality., (Copyright © 2015 International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.)

Published
2015
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