Research progress of risk factors and early diagnostic biomarkers of gout-induced renal injury

Abstract

Gout renal injury has an insidious onset, no obvious symptoms, and laboratory abnormalities in the early stages of the disease. The injury is not easily detected, and in many cases, the patients have entered the renal failure stage at the time of diagnosis. Therefore, the detection of gout renal injury–related risk factors and early diagnostic biomarkers of gout renal injury is essential for the prevention and early diagnosis of the disease. This article reviews the research progress in risk factors and early diagnostic biomarkers of gout renal injury.

The Heterogeneity of Symptom Burden and Fear of Progression Among Kidney Transplant Recipients: A Latent Class Analysis

“…This study is the first to identify an association between hyperuricemia and symptom burden. High uric acid can promote the development of kidney disease by inducing inflammatory response and oxidative stress, 56 lead to glomerular hypertrophy and renal tubular interstitial fibrosis, hinder endothelial nitric oxide production, lead to endothelial cell dysfunction, affect graft function, and even lead to graft loss, 57 which will undoubtedly increase the psychological pressure of patients. Hyperuricemia can also lead to hypertension, 56,58 cardiovascular disease, 58 and diabetes, 59 thus aggravating the symptom burden of KTRs.…”

Metabolomic profiles in serum and urine uncover novel biomarkers in children with nephrotic syndrome

“…The kidney is the main organ for extensive metabolization and clearance of small molecules. Therefore, metabolomics is a precious approach in the research of kidney diseases, for example diabetic kidney disease, CKD and gout renal injury 18,34,35 . Changes in the serum or urine metabolites concentration may result from impaired kidney functions and can be used as predictors of kidney diseases.…”

“…Some biomarkers reported in kidney injury, for example, betaine, the best discriminator of gout kidney injury, are involved in the enriched disease pathways—Glycine, serine and threonine metabolism of SSNS 35 . 1‐aminopyrene was reported as a mediator of progressive CKD by aryl hydrocarbon receptor activation, 36 consistency with the tubulointerstitial fibrosis (TIF) pathogenesis 37 .…”

Characterizations of microRNAs involved in the molecular mechanisms underlying the therapeutic effects of noni (Morinda citrifolia L.) fruit juice on hyperuricemia in mice

“…The whole blood sample was collected from each mouse 1 h after the 7th administration of required treatments, coagulated at room temperature for about 1 h, and then centrifuged for 5 min at 3000 rpm/min to obtain the serum. The contents of serum UA ( 1 ), XOD ( 9 ), Cr ( 28 ), and BUN ( 29 ) in the serum of each mouse were measured by the specific detection kits purchased from Nanjing Jiancheng Biotechnology Co., Ltd. (Nanjing, China) according to the manufacturer’s instructions.…”

“…Hyperuricemia in either males or females is generally defined based on the solubility of uric acid (UA), i.e., the serum UA concentration over 7.0 mg/dL or 416 mmol/L ( 1 ), which is caused by either excessive UA production ( 2 ) and/or decreased excretion in kidney and intestine, ultimately leading to excessive increase of serum UA concentration ( 3 , 4 ). Furthermore, hyperuricemia is well known as an important risk factor for the development of various medical disorders, e.g., hypertension, diabetes, cardiovascular complication, metabolic syndrome, atherosclerosis, stroke, gout, and kidney diseases ( 5–7 ), even though it is recommended that the asymptomatic hyperuricemia may not be treated ( 8 ).…”