scholarly journals Molecular Biological and Clinical Understanding of the Pathophysiology and Treatments of Hyperuricemia and Its Association with Metabolic Syndrome, Cardiovascular Diseases and Chronic Kidney Disease

2021 ◽  
Vol 22 (17) ◽  
pp. 9221
Author(s):  
Hidekatsu Yanai ◽  
Hiroki Adachi ◽  
Mariko Hakoshima ◽  
Hisayuki Katsuyama

Uric acid (UA) is synthesized mainly in the liver, intestines, and vascular endothelium as the end product of an exogenous purine from food and endogenously from damaged, dying, and dead cells. The kidney plays a dominant role in UA excretion, and the kidney excretes approximately 70% of daily produced UA; the remaining 30% of UA is excreted from the intestine. When UA production exceeds UA excretion, hyperuricemia occurs. Hyperuricemia is significantly associated with the development and severity of the metabolic syndrome. The increased urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) expression, and glycolytic disturbances due to insulin resistance may be associated with the development of hyperuricemia in metabolic syndrome. Hyperuricemia was previously thought to be simply the cause of gout and gouty arthritis. Further, the hyperuricemia observed in patients with renal diseases was considered to be caused by UA underexcretion due to renal failure, and was not considered as an aggressive treatment target. The evidences obtained by basic science suggests a pathogenic role of hyperuricemia in the development of chronic kidney disease (CKD) and cardiovascular diseases (CVD), by inducing inflammation, endothelial dysfunction, proliferation of vascular smooth muscle cells, and activation of the renin-angiotensin system. Further, clinical evidences suggest that hyperuricemia is associated with the development of CVD and CKD. Further, accumulated data suggested that the UA-lowering treatments slower the progression of such diseases.

2006 ◽  
Vol 15 (4) ◽  
pp. 361-365 ◽  
Author(s):  
Carmen A Peralta ◽  
Manjula Kurella ◽  
Joan C Lo ◽  
Glenn M Chertow

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Heather A. LaGuardia ◽  
L. Lee Hamm ◽  
Jing Chen

Metabolic syndrome is characterized by a clustering of cardiovascular risk factors, including abdominal obesity, elevated blood pressure and glucose concentrations, and dyslipidemia. The presence of this clinical entity is becoming more pervasive throughout the globe as the prevalence of obesity increases worldwide. Moreover, there is increased recognition of the complications and mortality related to this syndrome. This paper looks to examine the link between metabolic syndrome and the development of chronic kidney disease.


2007 ◽  
Vol 71 (7) ◽  
pp. 693-700 ◽  
Author(s):  
C. Kitiyakara ◽  
S. Yamwong ◽  
S. Cheepudomwit ◽  
S. Domrongkitchaiporn ◽  
N. Unkurapinun ◽  
...  

2006 ◽  
Vol 21 (12) ◽  
pp. 3608-3609 ◽  
Author(s):  
M. Kanauchi ◽  
K. Kanauchi ◽  
K. Kimura ◽  
T. Inoue ◽  
Y. Saito

2020 ◽  
Vol 66 (8) ◽  
pp. 1100-1107
Author(s):  
Sibel Gökçay Bek ◽  
Berna Üstüner ◽  
Necmi Eren ◽  
Zeynep Sentürk ◽  
Betül Kalender Gönüllü

SUMMARY BACKGROUND Hepcidin is an important regulator of iron homeostasis. OBJECTIVES This cross-sectional study was conducted to evaluate the association between hepcidin and components of metabolic syndrome in patients with chronic kidney disease (CKD). DESIGN AND SETTING 103 CKD patients and 59 healthy volunteers were included in the study from the University Hospital. METHODS Serum hepcidin levels were measured by enyzme-linked immunosorbent assay (ELISA) test. As for the study parameters, age, sex, body mass index, renal diseases, serum biochemistry, complete blood count, iron and total iron-binding capacity, ferritin, high-sensitive C-reactive protein (hsCRP), C- reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were evaluated. RESULTS The mean age of the patients was 58.63 ± 11.8 years. Hepcidin level was significantly associated with hypertension and higher uric acid levels (P < 0.05). There was a positive correlation between hepcidin and urea, uric acid, creatinine, ferritin, CRP, ESR, phosphorus, triglyceride, low-density lipoprotein (LDL), proteinuria and albuminuria in 24-hour urine collection. A negative correlation was found between hepcidin and estimated glomerular filtration rate (eGFR), hemoglobin, hematocrit, calcium, 25 OH vitamin D, pH, and bicarbonate levels. CONCLUSION Hepcidin, a well-known hormone regulator of iron metabolism, may play an important role in the pathogenesis of metabolic syndrome in patients with CKD, and further studies might delineate in-depth its potential as a promising early marker in these patients.


2020 ◽  
Vol 22 (1) ◽  
pp. 52-67
Author(s):  
Letícia Bitencourt Cota ◽  
Ana Luisa Pedrosa ◽  
Stephanie Bruna Camilo Soares de Brito ◽  
Ana Cláudia Fontoura Fróes ◽  
Sarah Tayná de Carvalho ◽  
...  

Background: It becomes increasingly evident that the SARS-CoV-2 infection is not limited to the respiratory system. In addition to being a target of the virus, the kidney also seems to have substantial influence on the outcomes of the disease. Methods: Data was obtained by a comprehensive and non-systematic search in the PubMed, Cochrane, Scopus and SciELO databases, using mainly the terms “SARS-CoV-2”, “COVID-19”, “chronic kidney disease”, “renal transplantation”, acute kidney injury” and “renal dysfunction”. Discussion: The membrane-bound angiotensin converting enzyme 2 is the receptor for SARS-CoV-2, and this interaction may lead to an imbalance of the Renin Angiotensin System (RAS), associated with worse clinical presentations of COVID-19, including acute pulmonary injury, hyperinflammatory state and hematological alterations. In the framework of renal diseases, development of acute kidney injury is associated mostly with immune alterations and direct cytopathic lesions by the virus, leading to higher mortality. As for chronic kidney disease, the patients at a non-terminal stage have worse prog-nosis, while the hemodialysis patients appear to have mild courses of COVID-19, probably due to lower chances of being affected by the cytokine storm. Furthermore, the current scenario is unfavorable to kidney donation and transplantation. The relationship between COVID-19 and immunosuppression in kidney transplantation recipients has been greatly discussed to determine whether it increases mortality and how it interacts with immunosuppressive medications. Conclusion: The kidney and the RAS exert fundamental roles in the SARS-CoV-2 infection and more research is required to have a complete understanding on the repercussions caused by COVID-19 in renal diseases.


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