Log in

Relevant bibliographies by topics / Hypouricemia / Journal articles

To see the other types of publications on this topic, follow the link: Hypouricemia.

Journal articles on the topic 'Hypouricemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Hypouricemia.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Kawasoe, Shin, Kazuki Ide, Tomoko Usui, Takuro Kubozono, Shiro Yoshifuku, Hironori Miyahara, Shigeho Maenohara, Mitsuru Ohishi, and Koji Kawakami. "Distribution and Characteristics of Hypouricemia within the Japanese General Population: A Cross-Sectional Study." Medicina 55, no. 3 (March 4, 2019): 61. http://dx.doi.org/10.3390/medicina55030061.

Full text

Abstract:

Background and objectives: There is insufficient epidemiological knowledge of hypouricemia. In this study, we aimed to describe the distribution and characteristics of Japanese subjects with hypouricemia. Materials and Methods: Data from subjects who underwent routine health checkups from January 2001 to December 2015 were analyzed in this cross-sectional study. A total of 246,923 individuals, which included 111,117 men and 135,806 women, met the study criteria. The participants were divided into quartiles according to their serum uric acid (SUA) levels. We subdivided the subjects with hypouricemia, which was defined as SUA level ≤ 2.0 mg/dL, into two groups and compared their characteristics, including their cardiovascular risks. Results: The hypouricemia rates were 0.46% overall, 0.21% for the men and 0.66% for the women (P < 0.001). The number of the subjects with hypouricemia showed two distributions at SUA levels of 0.4–1.1 mg/dL (lower hypouricemia group), which included a peak at 0.7–0.8 mg/dL, and at SUA levels of 1.4–2.0 mg/dL (higher hypouricemia group). The men in the higher hypouricemia group had lower body mass indexes (BMI) and triglyceride (TG) levels and had higher fasting blood glucose levels than those in the lower hypouricemia group. The women in the higher hypouricemia group were younger; had lower BMI, total protein, TG, total cholesterol and low-density lipoprotein cholesterol levels; and had higher estimated glomerular filtration rates levels compared to those in the lower hypouricemia group. Conclusions: The characteristics of the individuals in the lower and higher hypouricemia groups differed significantly, indicating different pathophysiologies within each group.

APA, Harvard, Vancouver, ISO, and other styles

2

Wakasugi, Minako, Junichiro James Kazama, Ichiei Narita, Tsuneo Konta, Shouichi Fujimoto, Kunitoshi Iseki, Toshiki Moriyama, et al. "Association between Hypouricemia and Reduced Kidney Function: A Cross-Sectional Population-Based Study in Japan." American Journal of Nephrology 41, no. 2 (2015): 138–46. http://dx.doi.org/10.1159/000381106.

Full text

Abstract:

Background: Hypouricemia, conventionally defined as a serum uric acid level of ≤2 mg/dl, is considered a biochemical disorder with no clinical significance. However, individuals with renal hypouricemia have a high risk of urolithiasis and exercise-induced acute kidney injury, both of which are risk factors for reduced kidney function. Methods: To test the hypothesis that individuals with hypouricemia would be at a higher risk of reduced kidney function, we conducted a population-based cross-sectional study using data from the Specific Health Checkups and Guidance System in Japan. Logistic analysis was used to examine the relationship between hypouricemia and reduced kidney function, defined as estimated glomerular filtration rate <60 ml/min/1.73 m2. Results: Among 90,710 men (mean age, 63.8 years) and 136,935 women (63.7 years), 193 (0.2%) and 540 (0.4%) were identified as having hypouricemia, respectively. The prevalence of hypouricemia decreased with age in women (p for trend <0.001), but not in men (p for trend = 0.24). Hypouricemia was associated with reduced kidney function in men (odds ratio, 1.83; 95% confidence interval, 1.23-2.74), but not in women (0.61; 0.43-0.86), relative to the reference category (i.e., serum uric acid levels of 4.1-5.0 mg/dl) after adjusting for age, drinking, smoking, diabetes, hypertension, hypercholesterolemia, obesity, and history of renal failure. Sensitivity analyses stratified by diabetic status yielded similar results. Conclusions: This study is the first to provide evidence that hypouricemia is associated with reduced kidney function in men. Further research will be needed to determine the long-term prognosis of individuals with hypouricemia.

APA, Harvard, Vancouver, ISO, and other styles

3

Shimizu, Yoshio, Keiichi Wakabayashi, Ayako Totsuka, Yoko Hayashi, Shusaku Nitta, Kazuaki Hara, Maiko Akira, Yasuhiko Tomino, and Yusuke Suzuki. "Exercise-Induced Acute Kidney Injury in a Police Officer with Hereditary Renal Hypouricemia." Case Reports in Nephrology and Dialysis 9, no. 2 (July 29, 2019): 92–101. http://dx.doi.org/10.1159/000501877.

Full text

Abstract:

Hereditary renal hypouricemia is characterized by hypouricemia with hyper-uric acid clearance due to a defect in renal tubular transport. Patients with hereditary renal hypouricemia have a higher risk of exercise-induced acute kidney injury (EAKI) and reduced kidney function. Although the best preventive measure is avoiding exercise, there are many kinds of jobs that require occupational exercise. A 27-year-old male police officer suffered from stage 3 AKI after performing a 20-m multistage shuttle run test. His mother had previously been diagnosed as having renal hypouricemia at another facility. The patient had reported having hypouricemia during a health check at a previous police station, but his serum uric acid concentration was within the normal range at our hospital. After treatment, he recovered from EAKI and exhibited low serum uric acid and hyper-uric acid clearance. Since the patient desired to continue his career requiring strenuous exercise, it was difficult to establish a preventive plan against the recurrence of EAKI. Patients with hereditary renal hypouricemia who must undergo strenuous occupational anaerobic exercise are at higher risk of developing EAKI than other workers. The risks of EAKI among patients with hypouricemia should be considered when undergoing physical occupational training.

APA, Harvard, Vancouver, ISO, and other styles

4

Kawamura, Yusuke, Akiyoshi Nakayama, Seiko Shimizu, Yu Toyoda, Yuichiro Nishida, Asahi Hishida, Sakurako Katsuura-Kamano, et al. "A Proposal for Practical Diagnosis of Renal Hypouricemia: Evidenced from Genetic Studies of Nonfunctional Variants of URAT1/SLC22A12 among 30,685 Japanese Individuals." Biomedicines 9, no. 8 (August 13, 2021): 1012. http://dx.doi.org/10.3390/biomedicines9081012.

Full text

Abstract:

Background: Renal hypouricemia (RHUC) is characterized by a low serum uric acid (SUA) level and high fractional excretion of uric acid (FEUA). Further studies on FEUA in hypouricemic individuals are needed for a more accurate diagnosis of RHUC. Methods: In 30,685 Japanese health-examination participants, we genotyped the two most common nonfunctional variants of URAT1 (NFV-URAT1), W258X (rs121907892) and R90H (rs121907896), in 1040 hypouricemic individuals (SUA ≤ 3.0 mg/dL) and 2240 individuals with FEUA data. The effects of NFV-URAT1 on FEUA and SUA were also investigated using linear and multiple regression analyses. Results: Frequency of hypouricemic individuals (SUA ≤ 3.0 mg/dL) was 0.97% (male) and 6.94% (female) among 30,685 participants. High frequencies of those having at least one allele of NFV-URAT1 were observed in 1040 hypouricemic individuals. Furthermore, NFV-URAT1 significantly increased FEUA and decreased SUA, enabling FEUA and SUA levels to be estimated. Conversely, FEUA and SUA data of hypouricemic individuals are revealed to be useful to predict the number of NFV-URAT1. Conclusions: Our findings reveal that specific patterns of FEUA and SUA data assist with predicting the number of nonfunctional variants of causative genes for RHUC, and can also be useful for practical diagnosis of RHUC even before genetic tests.

APA, Harvard, Vancouver, ISO, and other styles

5

Morales, Manuel, and Victor Garcia-Nieto. "Hypouricemia and Cancer." Oncology 53, no. 4 (1996): 345–48. http://dx.doi.org/10.1159/000227585.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

SPERLING, O. "Hereditary renal hypouricemia." Molecular Genetics and Metabolism 89, no. 1-2 (September 2006): 14–18. http://dx.doi.org/10.1016/j.ymgme.2006.03.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Shichiri, Masayoshi. "Diabetic Renal Hypouricemia." Archives of Internal Medicine 147, no. 2 (February 1, 1987): 225. http://dx.doi.org/10.1001/archinte.1987.00370020045033.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Shichiri, M. "Diabetic renal hypouricemia." Archives of Internal Medicine 147, no. 2 (February 1, 1987): 225–28. http://dx.doi.org/10.1001/archinte.147.2.225.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Stiburkova, Blanka, Jana Bohata, Iveta Minarikova, Andrea Mancikova, Jiri Vavra, Vladimír Krylov, and Zdenek Doležel. "Clinical and Functional Characterization of a Novel URAT1 Dysfunctional Variant in a Pediatric Patient with Renal Hypouricemia." Applied Sciences 9, no. 17 (August 23, 2019): 3479. http://dx.doi.org/10.3390/app9173479.

Full text

Abstract:

Renal hypouricemia (RHUC) is caused by an inherited defect in the main (reabsorptive) renal urate transporters, URAT1 and GLUT9. RHUC is characterized by decreased concentrations of serum uric acid and an increase in its excretion fraction. Patients suffer from hypouricemia, hyperuricosuria, urolithiasis, and even acute kidney injury. We report the clinical, biochemical, and genetic findings of a pediatric patient with hypouricemia. Sequencing analysis of the coding region of SLC22A12 and SLC2A9 and a functional study of a novel RHUC1 variant in the Xenopus expression system were performed. The proband showed persistent hypouricemia (67–70 µmol/L; ref. range 120–360 µmol/L) and hyperuricosuria (24–34%; ref. range 7.3 ± 1.3%). The sequencing analysis identified common non-synonymous allelic variants c.73G > A, c.844G > A, c.1049C > T in the SLC2A9 gene and rare variants c.973C > T, c.1300C > T in the SLC22A12 gene. Functional characterization of the novel RHUC associated c.973C > T (p. R325W) variant showed significantly decreased urate uptake, an irregular URAT1 signal on the plasma membrane, and reduced cytoplasmic staining. RHUC is an underdiagnosed disorder and unexplained hypouricemia warrants detailed metabolic and genetic investigations. A greater awareness of URAT1 and GLUT9 deficiency by primary care physicians, nephrologists, and urologists is crucial for identifying the disorder.

APA, Harvard, Vancouver, ISO, and other styles

10

Yoon, Jaeho, Raul Cachau, Victor A. David, Mary Thompson, Wooram Jung, Sun-Ha Jee, Ira O. Daar, Cheryl A. Winkler, and Sung-Kweon Cho. "Characterization of a Compound Heterozygous SLC2A9 Mutation That Causes Hypouricemia." Biomedicines 9, no. 9 (September 6, 2021): 1172. http://dx.doi.org/10.3390/biomedicines9091172.

Full text

Abstract:

Renal hypouricemia is a rare genetic disorder. Hypouricemia can present as renal stones or exercise-induced acute renal failure, but most cases are asymptomatic. Our previous study showed that two recessive variants of SLC22A12 (p.Trp258*, pArg90His) were identified in 90% of the hypouricemia patients from two independent cohorts: the Korean genome and epidemiology study (KoGES) and the Korean Cancer Prevention Study (KCPS-II). In this work, we investigate the genetic causes of hypouricemia in the rest of the 10% of unsolved cases. We found a novel non-synonymous mutation of SLC2A9 (voltage-sensitive uric acid transporter) in the whole-exome sequencing (WES) results. Molecular dynamics prediction suggests that the novel mutation p.Met126Val in SLCA9b (p.Met155Val in SLC2A9a) hinders uric acid transport through a defect of the outward open geometry. Molecular analysis using Xenopus oocytes confirmed that the p.Met126Val mutation significantly reduced uric acid transport but does not affect the SLC2A9 protein expression level. Our results will shed light on a better understanding of SLC2A9-mediated uric acid transport and the development of a uric acid-lowering agent.

APA, Harvard, Vancouver, ISO, and other styles

11

Ishihara, M., T. Shinoda, T. Aizawa, T. Shirota, Y. Nagasawa, and T. Yamada. "Hypouricemia in NIDDM Patients." Diabetes Care 11, no. 10 (November 1, 1988): 796–97. http://dx.doi.org/10.2337/diacare.11.10.796.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Wakida, Naoki, Do Gia Tuyen, Masataka Adachi, Taku Miyoshi, Hiroshi Nonoguchi, Toshiaki Oka, Osamu Ueda, et al. "Mutations in Human Urate Transporter 1 Gene in Presecretory Reabsorption Defect Type of Familial Renal Hypouricemia." Journal of Clinical Endocrinology & Metabolism 90, no. 4 (April 1, 2005): 2169–74. http://dx.doi.org/10.1210/jc.2004-1111.

Full text

Abstract:

Abstract To date, 11 loss of function mutations in the human urate transporter 1 (hURAT1) gene have been identified in subjects with idiopathic renal hypouricemia. In the present studies we investigated the clinical features and the mutations in the hURAT1 gene in seven families with presecretory reabsorption defect-type renal hypouricemia and in one family with the postsecretory reabsorption defect type. Twelve affected subjects and 26 family members were investigated. Mutations were analyzed by PCR and the direct sequencing method. Urate-transporting activities of wild-type and mutant hURAT1 were determined by [14C]urate uptake in Xenopus oocytes. Mutational analysis revealed three previously reported mutations (G774A, A1145T, and 1639–1643 del-GTCCT) and a novel mutation (T1253G) in families with the presecretory reabsorption defect type. Neither mutations in the coding region of hURAT1 gene nor significant segregation patterns of the hURAT1 locus were detected in the postsecretory reabsorption defect type. All hURAT1 mutants had significantly reduced urate-transporting activities compared with wild type (P < 0.05; n = 12), suggesting that T1253G is a loss of function mutation, and hURAT1 is responsible for the presecretory reabsorption defect-type familial renal hypouricemia. Future studies are needed to identify a responsible gene for the postsecretory reabsorption defect-type familial renal hypouricemia.

APA, Harvard, Vancouver, ISO, and other styles

13

Maesaka, John K., Anthony J. Cusano, Harold L. Thies, Frederick P. Siegal, and Albert W. Dreisbach. "Hypouricemia in Acquired Immunodeficiency Syndrome." American Journal of Kidney Diseases 15, no. 3 (March 1990): 252–57. http://dx.doi.org/10.1016/s0272-6386(12)80770-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Bugdayci, Guler, Yasemin Balaban, and Ozlem Sahin. "Causes of Hypouricemia Among Outpatients." Laboratory Medicine 39, no. 9 (September 2008): 550–52. http://dx.doi.org/10.1309/h3ttuvdbe75d6n6p.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Takeda, Eiji, Yasuhiro Kuroda, Motomi Ito, Kenji Toshima, Toshiyuki Watanabe, Michinori Ito, Etsuo Naito, Ichiro Yokota, Tai Ju Hwang, and Masuhide Miyao. "Hereditary renal hypouricemia in children." Journal of Pediatrics 107, no. 1 (July 1985): 71–74. http://dx.doi.org/10.1016/s0022-3476(85)80617-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

YAMAMOTO, KAZUHIKO, and HIROKO MOROOKA. "An investigation of incidental hypouricemia." Juntendo Medical Journal 36, no. 4 (1991): 540–50. http://dx.doi.org/10.14789/pjmj.36.540.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Windpessl, Martin, Marco Ritelli, Manfred Wallner, and Marina Colombi. "A Novel Homozygous SLC2A9 Mutation Associated with Renal-Induced Hypouricemia." American Journal of Nephrology 43, no. 4 (2016): 245–50. http://dx.doi.org/10.1159/000445845.

Full text

Abstract:

Background: Hereditary renal hypouricemia (RHUC) is a genetically heterogenous disorder characterized by defective uric acid (UA) reabsorption resulting in hypouricemia and increased fractional excretion of UA; acute kidney injury (AKI) and nephrolithiasis are recognized complications. Type 1 (RHUC1) is caused by mutations in the SLC22A12 gene, whereas RHUC2 is caused by mutations in the SLC2A9 gene. Patient ethnicity is diverse but only few Caucasian families with an SLC2A9 mutation have been reported. Methods: The current report describes the clinical history, biochemical and molecular genetics findings of a native Austrian family with RHUC2. The propositus presented with 2 episodes of exercise-induced AKI and exhibited profound hypouricemia. Mutational screening of the SLC22A12 and SLC2A9 genes was performed. Results: The molecular analyses revealed the homozygous c.512G>A transition that leads to the p.Arg171His missense substitution in SLC2A9, confirming the diagnosis of RHUC2. Segregation study of the causal mutation revealed that the mother and elder sister were heterozygous carriers, whereas the younger sister was found to be homozygous. Conclusion: We report the identification of a novel mutation in SLC2A9 as the cause of RHUC2 in a native Austrian family. We show that glucose transporter 9 mutations cause severe hypouricemia in homozygous individuals and confirm the high risk of AKI in male individuals harbouring these mutations. In our literature review, we provide an overview of the putative underlying pathophysiology, potential renal complications, findings on kidney biopsy as well as potential long-time renal sequelae.

APA, Harvard, Vancouver, ISO, and other styles

18

Maalouli, Christian, Karin Dahan, Arnaud Devresse, and Valentine Gillion. "Mutation in the SLC2A9 Gene: A New Family with Familial Renal Hypouricemia Type 2." Case Reports in Nephrology 2021 (September 23, 2021): 1–3. http://dx.doi.org/10.1155/2021/4751099.

Full text

Abstract:

Familial renal hypouricemia is a rare genetic disorder characterized by a defect in renal tubular urate reabsorption. Some patients present with exercise-induced acute kidney injury and nephrolithiasis. Type II is caused by mutations in the SLC2A9 gene. Here, we report the case of a young patient who developed acute kidney injury after exercise secondary to familial renal hypouricemia type II. The same mutation was found in other asymptomatic members of his family. We review the medical literature on this condition. This case highlights the importance of considering uric acid disorders in the work-up of acute kidney injury after exercise.

APA, Harvard, Vancouver, ISO, and other styles

19

Zhou, Yunan, Xueguang Zhang, Rui Ding, Zuoxiang Li, Quan Hong, Yan Wang, Wei Zheng, et al. "Using Next-Generation Sequencing to Identify a Mutation in Human MCSU that is Responsible for Type II Xanthinuria." Cellular Physiology and Biochemistry 35, no. 6 (2015): 2412–21. http://dx.doi.org/10.1159/000374042.

Full text

Abstract:

Background: Hypouricemia is caused by various diseases and disorders, such as hepatic failure, Fanconi renotubular syndrome, nutritional deficiencies and genetic defects. Genetic defects of the molybdoflavoprotein enzymes induce hypouricemia and xanthinuria. Here, we identified a patient whose plasma and urine uric acid levels were both extremely low and aimed to identify the pathogenic gene and verify its mechanism. Methods: Using next-generation sequencing (NGS), we detected a mutation in the human molybdenum cofactor sulfurase (MCSU) gene that may cause hypouricemia. We cultured L02 cells, knocked down MCSU with RNAi, and then detected the uric acid and MCSU concentrations, xanthine oxidase (XOD) and xanthine dehydrogenase (XDH) activity levels, and xanthine/hypoxanthine concentrations in cell lysates and culture supernatants. Results: The NGS results showed that the patient had a mutation in the human MCSU gene. The in vitro study showed that RNAi of MCSU caused the uric acid, human MCSU concentrations, the XOD and XDH activity levels among cellular proteins and culture supernatants to be extremely low relative to those of the control. However, the xanthine/hypoxanthine concentrations were much higher than those of the control. Conclusions: We strongly confirmed the pathogenicity of the human MCSU gene.

APA, Harvard, Vancouver, ISO, and other styles

20

HISATOME, Ichiro, Yasushi TANAKA, Kazuhide OGINO, Masaki SHIMOYAMA, Koh HIROE, Mariko TSUBOI, Yasutaka YAMAMOTO, et al. "Hematuria in Patients with Renal Hypouricemia." Internal Medicine 37, no. 1 (1998): 40–46. http://dx.doi.org/10.2169/internalmedicine.37.40.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

MATSUDA, OSAMU. "A case of idiopathic renal hypouricemia." Nihon Naika Gakkai Zasshi 83, no. 12 (1994): 2156–58. http://dx.doi.org/10.2169/naika.83.2156.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Albert, Daniel, Paige N. Scudder, Pamela Bagley, and Kenneth G. Saag. "Vascular Consequences of Hyperuricemia and Hypouricemia." Rheumatic Disease Clinics of North America 45, no. 3 (August 2019): 453–64. http://dx.doi.org/10.1016/j.rdc.2019.04.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Arranz-Caso, J. A., F. J. Fernández de Paz, V. Barrio, L. M. Cuadrado-Gomez, F. Albarran-Hernandez, and M. Alvarez de Mon. "Severe Renal Hypouricemia Secondary to Hyperbilirubinemia." Nephron 71, no. 3 (1995): 354–56. http://dx.doi.org/10.1159/000188743.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Magoula, Ifigenia, George Tsapas, Konstantinos Paletas, and Konstantinos Mavromatidis. "Insulin-Dependent Diabetes and Renal Hypouricemia." Nephron 59, no. 1 (1991): 21–26. http://dx.doi.org/10.1159/000186512.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Smetana, Shmuel S. "Hypouricemia due to Renal Tubular Defect." Archives of Internal Medicine 145, no. 7 (July 1, 1985): 1200. http://dx.doi.org/10.1001/archinte.1985.00360070070011.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Gaspar, Gabriel S. "Hypouricemia due to Renal Tubular Defect." Archives of Internal Medicine 146, no. 6 (June 1, 1986): 1241. http://dx.doi.org/10.1001/archinte.1986.00360180261060.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Gaspar, G. S. "Hypouricemia due to renal tubular defect." Archives of Internal Medicine 146, no. 6 (June 1, 1986): 1241a—1241. http://dx.doi.org/10.1001/archinte.146.6.1241a.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Han, Moon Hee, Sang Uk Park, Deok-Soo Kim, Jae Won Shim, Jung Yeon Shim, Hye Lym Jung, and Moon Soo Park. "A case of idiopathic renal hypouricemia." Korean Journal of Pediatrics 50, no. 5 (2007): 489. http://dx.doi.org/10.3345/kjp.2007.50.5.489.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Tykarski, A. "Mechanism of Hypouricemia in Hodgkin’s Disease." Nephron 50, no. 3 (1988): 217–19. http://dx.doi.org/10.1159/000185161.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Hisatome, Ichiro, Kazuhide Ogino, Hiroshi Kotake, Riichiro Ishiko, Makoto Saito, Junichi Hasegawa, Hiroto Mashiba, and Shoji Nakamoto. "Cause of Persistent Hypouricemia in Outpatients." Nephron 51, no. 1 (1989): 13–16. http://dx.doi.org/10.1159/000185233.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Sebesta, Ivan, Blanka Stiburkova, Josef Bartl, Kimiyoshi Ichida, Makoto Hosoyamada, Judy Taylor, and Anthony Marinaki. "Diagnostic Tests for Primary Renal Hypouricemia." Nucleosides, Nucleotides and Nucleic Acids 30, no. 12 (December 2011): 1112–16. http://dx.doi.org/10.1080/15257770.2011.611483.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Kaneko, Kazunari, Naho Taniguchi, Yuko Tanabe, Takahide Nakano, Masafumi Hasui, and Kandai Nozu. "Oxidative imbalance in idiopathic renal hypouricemia." Pediatric Nephrology 24, no. 4 (April 2009): 869–71. http://dx.doi.org/10.1007/s00467-008-1032-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Chiba, Toshinori, Hirotaka Matsuo, Shushi Nagamori, Akiyoshi Nakayama, Yusuke Kawamura, Seiko Shimizu, Masayuki Sakiyama, et al. "Identification of a Hypouricemia Patient with SLC2A9 R380W, A Pathogenic Mutation for Renal Hypouricemia Type 2." Nucleosides, Nucleotides and Nucleic Acids 33, no. 4-6 (April 4, 2014): 261–65. http://dx.doi.org/10.1080/15257770.2013.857781.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Dissanayake, Lashodya V., Denisha R. Spires, Oleg Palygin, and Alexander Staruschenko. "Effects of uric acid dysregulation on the kidney." American Journal of Physiology-Renal Physiology 318, no. 5 (May 1, 2020): F1252—F1257. http://dx.doi.org/10.1152/ajprenal.00066.2020.

Full text

Abstract:

Recently, research has redirected its interests in uric acid (UA) from gout, an inflammatory disease in joints, to groups of closely interrelated pathologies associated with cardiovascular and kidney dysfunction. Many epidemiological, clinical, and experimental studies have shown that UA may play a role in the pathophysiology of the cardiorenal syndrome continuum; however, it is still unclear if it is a risk factor or a causal role. Hyperuricemia has been well studied in the past two decades, revealing mechanistic insights into UA homeostasis. Likewise, some epidemiological and experimental evidence suggests that hypouricemia can lead to cardiorenal pathologies. The goal of this review is to highlight why studying both hyperuricemia and hypouricemia is warranted as well as to summarize the relevance of UA to kidney function.

APA, Harvard, Vancouver, ISO, and other styles

35

Dinour, Dganit, Nicola K. Gray, Susan Campbell, Xinhua Shu, Lindsay Sawyer, William Richardson, Gideon Rechavi, et al. "Homozygous SLC2A9 Mutations Cause Severe Renal Hypouricemia." Journal of the American Society of Nephrology 21, no. 1 (November 19, 2009): 64–72. http://dx.doi.org/10.1681/asn.2009040406.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Sebesta, I., and B. Stiburkova. "469 DIAGNOSTIC APPROACH TO HEREDITARY RENAL HYPOURICEMIA." European Urology Supplements 9, no. 2 (April 2010): 166. http://dx.doi.org/10.1016/s1569-9056(10)60463-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Sebesta, Ivan. "Genetic Disorders Resulting in Hyper- or Hypouricemia." Advances in Chronic Kidney Disease 19, no. 6 (November 2012): 398–403. http://dx.doi.org/10.1053/j.ackd.2012.06.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Ducorps, M., C. Hélie, H. Mayaudon, and B. Bauduceau. "Severe hypouricemia: biochemical expression of asymptomatic xanthinuria." Clinical Chemistry 41, no. 12 (December 1, 1995): 1789–90. http://dx.doi.org/10.1093/clinchem/41.12.1789a.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

HIRASAKI, Shoji, Norio KOIDE, Kiyoshi FUJITA, Hiromichi OGAWA, and Takao TSUJI. "Two Cases of Renal Hypouricemia with Nephrolithiasis." Internal Medicine 36, no. 3 (1997): 201–5. http://dx.doi.org/10.2169/internalmedicine.36.201.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Smetana, Shmuel S. "Hypouricemia due to Renal Tubular Defect-Reply." Archives of Internal Medicine 146, no. 6 (June 1, 1986): 1243. http://dx.doi.org/10.1001/archinte.1986.00360180263061.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Shichiri, Masayoshi, Hitoshi Iwamoto, and Tatsuo Shiigai. "Hypouricemia due to Increased Tubular Urate Secretion." Nephron 45, no. 1 (1987): 31–34. http://dx.doi.org/10.1159/000184067.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Yanase, Masahiro, Hajime Nakahama, Hiroshi Mikami, Yoshifumi Fukuhara, Yoshimasa Orita, and Hiromichi Yoshikawa. "Prevalence of Hypouricemia in Apparently Normal Population." Nephron 48, no. 1 (1988): 80. http://dx.doi.org/10.1159/000184876.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Colussi, Giacomo, Giuseppe Rombolà, Maria Elisabetta De Ferrari, and Luigi Minetti. "Hypouricemia Due to Increased Tubular Urate Secretion." Nephron 48, no. 3 (1988): 235–36. http://dx.doi.org/10.1159/000184920.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Hisatome, Ichiro, Tatsuo Kato, Hiroyuki Miyakoda, Toru Takami, Takaaki Abe, Yasushi Tanaka, Hiromoto Kosaka, et al. "Renal Hypouricemia with Both Drug-Insensitive Secretion and Defective Reabsorption of Urate: A Novel Type of Renal Hypouricemia." Nephron 64, no. 3 (1993): 447–51. http://dx.doi.org/10.1159/000187369.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Nakayama, Akiyoshi, Hirotaka Matsuo, Akira Ohtahara, Kazuhide Ogino, Masayuki Hakoda, Toshihiro Hamada, Makoto Hosoyamada, et al. "Clinical practice guideline for renal hypouricemia (1st edition)." Human Cell 32, no. 2 (February 19, 2019): 83–87. http://dx.doi.org/10.1007/s13577-019-00239-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Shichiri, Masayoshi, Hitoshi Iwamoto, and Fumiaki Marumo. "Diabetic Hypouricemia as an Indicator of Clinical Nephropathy." American Journal of Nephrology 10, no. 2 (1990): 115–22. http://dx.doi.org/10.1159/000168065.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Uribarri, Jaime, and Man S. Oh. "Renal Hypouricemia and Absorptive Hypercalciuria: A Real Syndrome." Nephron 63, no. 2 (1993): 172–75. http://dx.doi.org/10.1159/000187178.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

MORIWAKI, Yuji, Tetsuya YAMAMOTO, Sumio TAKAHASHI, Takahito NAKANO, Yoshiki AMURO, Toshikazu HADA, and Kazuya HIGASHINO. "A case of primary hepatocellular carcinoma with hypouricemia." Nihon Naika Gakkai Zasshi 75, no. 12 (1986): 1769–73. http://dx.doi.org/10.2169/naika.75.1769.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Park, Jung Hwan, Yong-Il Jo, and Jong-Ho Lee. "Renal effects of uric acid: hyperuricemia and hypouricemia." Korean Journal of Internal Medicine 35, no. 6 (November 1, 2020): 1291–304. http://dx.doi.org/10.3904/kjim.2020.410.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Juraschek, Stephen P., Tracie Kurano, Antony Rosen, and Allan C. Gelber. "Acute Gout After Renal Transplantation with Notable Hypouricemia." American Journal of Medicine 126, no. 10 (October 2013): e5-e6. http://dx.doi.org/10.1016/j.amjmed.2013.04.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!