Role of neutrophil/lymphocyte ratio in prediction of disease progression in patients with stage–4 chronic kidney disease

2012 ◽  
Vol 26 (2) ◽  
pp. 358-365 ◽  
Author(s):  
Ismail Kocyigit ◽  
Eray Eroglu ◽  
Aydin Unal ◽  
Murat Hayri Sipahioglu ◽  
Bulent Tokgoz ◽  
...  
2018 ◽  
Vol 12 (3) ◽  
pp. 420-426 ◽  
Author(s):  
Diego Barbieri ◽  
Marian Goicoechea ◽  
Maria Dolores Sánchez-Niño ◽  
Alberto Ortiz ◽  
Eduardo Verde ◽  
...  

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1674
Author(s):  
Tao Han Lee ◽  
Jia-Jin Chen ◽  
Chao-Yi Wu ◽  
Chih-Wei Yang ◽  
Huang-Yu Yang

The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.


Renal Failure ◽  
2019 ◽  
Vol 41 (1) ◽  
pp. 238-243 ◽  
Author(s):  
Ryota Yoshitomi ◽  
Masaru Nakayama ◽  
Teppei Sakoh ◽  
Akiko Fukui ◽  
Eisuke Katafuchi ◽  
...  

2012 ◽  
Vol 108 (10) ◽  
pp. 605-615 ◽  
Author(s):  
Hélène Plé ◽  
Manon Maltais ◽  
Aurélie Corduan ◽  
Guy Rousseau ◽  
François Madore ◽  
...  

SummaryBleeding and thrombotic disorders are major complications affecting patients with chronic kidney disease (CKD). Exposure of circulating platelets to uraemic toxins and contact with artificial surfaces during dialysis induce platelet abnormalities and alter the platelet proteome. We hypothesised that these changes may be subsequent to changes in the composition and/or regulation of the platelet transcriptome. In this study, we investigated the circulating platelets of 10 CKD patients (i.e. five chronic haemodialysis patients and five stage 4 CKD uraemic patients) and five age- and sex-matched healthy subjects. We observed an alteration of the platelet messenger RNA (mRNA) and microRNA transcriptome in CKD patients. Impaired in uraemic platelets, the levels of some mRNAs and of most microRNAs appeared to be corrected by dialysis, which is consistent with a beneficial effect of dialysis and a mRNA regulatory role of platelet microRNAs. Reduced in platelets of uraemic patients, phosphatidylcholine transfer protein (PCTP) and WD repeat-containing protein 1 (WDR1) were found to be regulated by microRNAs, the latter of which involving hsa-miR-19b, a microRNA increased in platelets of uraemic patients and involved in platelet reactivity. These results suggest that an alteration of microRNA-based mRNA regulatory mechanisms may underlie the platelet response to uremia and entail the development of platelet-related complications in CKD.


2010 ◽  
Vol 25 (6) ◽  
pp. 1896-1903 ◽  
Author(s):  
S. Prajczer ◽  
U. Heidenreich ◽  
W. Pfaller ◽  
P. Kotanko ◽  
K. Lhotta ◽  
...  

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 811
Author(s):  
Diego Ingrosso ◽  
Alessandra F. Perna

Renal disease is the common denominator of a number of underlying disease conditions, whose prevalence has been dramatically increasing over the last two decades. Two aspects are particularly relevant to the subject of this review: (I) most cases are gathered under the umbrella of chronic kidney disease since they require—predictably for several lustrums—continuous clinical monitoring and treatment to slow down disease progression and prevent complications; (II) cardiovascular disease is a terrible burden in this population of patients, in that it claims many lives yearly, while only a scant minority reach the renal disease end stage. Why indeed a review on DNA methylation and renal disease? As we hope to convince you, the present evidence supports the role of the existence of various derangements of the epigenetic control of gene expression in renal disease, which hold the potential to improve our ability, in the future, to more effectively act toward disease progression, predict outcomes and offer novel therapeutic approaches.


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