The Crystallization of Monosodium Urate

Martillo, Miguel; Nazzal, Lama; Crittenden, Daria B.

doi:10.1007/s11926-013-0400-9

Cited by 252 publications

(205 citation statements)

References 56 publications

Supporting

Mentioning

188

Contrasting

Unclassified

Order By: Relevance

“…It has been claimed that UA has two faces of the coin; the good aspect is that UA acts as radical scavenger at risk of disability to intrinsically generate vitamin C in the higher primates [11,12,14,15]. The bad aspect is that increased level of SUA tends to get crystalized and causes a variety of unwanted diseases such as gout, urinary stones and inflammatory processes [16]. Cause and effect relationship between hyperuricemia and CKD remains unresolved and will be discussed in more detail later.…”

Section: Metabolism Of Uamentioning

confidence: 99%

Time to target uric acid to retard CKD progression

et al. 2016

View full text Add to dashboard Cite

Uric acid (UA) remains a possible risk factor of chronic kidney disease (CKD) but its potential role should be elucidated given a fact that multidisciplinary treatments assure a sole strategy to inhibit the progression to end-stage renal disease (ESRD). In clinical setting, most observational studies showed that elevation of serum uric acid (SUA) independently predicts the incidence and the development of CKD. The meta-analysis showed that SUA-lowering therapy with allopurinol may retard the progression of CKD but did not reach conclusive results due to small-sized studies. Larger scale, randomized placebo-controlled trials to assess SUA-lowering therapy are needed. Our recent analysis by propensity score methods has shown that the threshold of SUA should be less than 6.5 mg/dL to abrogate ESRD. In animal models an increase in SUA by the administration of oxonic acid, uricase inhibitor, or nephrectomy can induce glomerular hypertension, arteriolosclerosis including afferent arteriolopathy and tubulointerstitial fibrosis. The ever-growing discoveries of urate transporters prompt us to learn UA metabolism in the kidney and intestine. One example is that the intestinal ABCG2 may play a compensatory role at face of decreased renal clearance of UA in nephrectomized rats, the trigger of which is not a uremic toxin but SUA itself. This review will summarize the recent knowledge on the relationship between SUA and the kidney and try to draw a conclusion when and how to treat asymptomatic hyperuricemia accompanied by CKD. Finally we will address a future perspective on UA study including a Mendelian randomization approach.

show abstract

Section: Metabolism Of Uamentioning

confidence: 99%

Time to target uric acid to retard CKD progression

et al. 2016

View full text Add to dashboard Cite

show abstract

“…and viscosity of the synovial fluid (SF) [7,8]. These factors help to explain the preference of gout for the first metatarsophalangeal (MTP) joint, a low temperature peripheral joint [9].…”

mentioning

confidence: 99%

Molecular basis of oxidative stress in gouty arthropathy

et al. 2015

View full text Add to dashboard Cite

Gout is a disorder of urate metabolism in which persistent high urate levels in the extracellular fluids result in the deposition of monosodium urate (MSU) crystal in joints and periarticular tissues. In recent years, this disease represents an increasingly common health problem, so the pace of investigation in the field has accelerated tremendously. New research advances in the pathogenesis of hyperuricemia and in the understanding of how MSU crystals induce an acute gouty attack have been focused in this review on the processes of inflammation and involvement of the innate immune response; in addition, we discuss new knowledge about the role of the reactive oxygen species in establishing oxidative stress in MSU crystal-induced arthritis.

show abstract

“…In MSU, the temperature appears to play a role in crystal formation through effects on urate solubility. In vitro studies suggest that a reduction of even 2°C is sufficient to lower the solubility point [19]. Although, our preservation method, in a refrigerator at 4°C, is supported by a handful of small studies which assessed the impact of storage handling on crystals recognition [6,[12][13][14][15][16][17].…”

Section: Discussionmentioning

confidence: 93%

The added value of synovial fluid centrifugation for monosodium urate and calcium pyrophosphate crystal detection

et al. 2017

View full text Add to dashboard Cite

The aim of the study was to assess the added value of synovial fluid (SF) centrifugation for microscopic monosodium urate (MSU) and calcium pyrophosphate (CPP) crystal detection in patients with arthritis. This is a prospective observational study using SF samples from joints of patients undergoing joint arthrocentesis. Two blinded observers assessed the SF smears by polarized light microscopy for the presence of crystals before as well as after centrifugation. SF samples were collected from 98 patients with arthritis. After exclusion, 87 samples were eligible for inclusion. Of each sample, 2 smears before and after centrifugation were prepared and microscopically examined, resulting in 348 smears per observer. Observer 1 identified MSU crystals in 18.4% and CPP in 9.2% of the smears before as well as after centrifugation. No extra MSU crystal-positive smears were identified after centrifugation. However, centrifugation yielded 4 additional CPP crystal-positive smears. Observer 2 identified MSU crystals in 15.5% and CPP crystals in 6.3% of the smears before as well as after centrifugation. Centrifugation yielded 2 additional MSU crystal-positive smears and 4 CPP crystal-positive smears. Monosodium urate crystals were well recognized without centrifugation. Centrifugation of SF had limited additional value for increasing the amount of MSU-positive smears. However, CPP crystals were identified in a higher number of smears after centrifugation than before. Therefore, centrifugation may be of additional value in selected patients with suspected calcium pyrophosphate deposition disease and to a lesser extent for gout.

show abstract

The Crystallization of Monosodium Urate

Cited by 252 publications

References 56 publications

Time to target uric acid to retard CKD progression

Time to target uric acid to retard CKD progression

Molecular basis of oxidative stress in gouty arthropathy

The added value of synovial fluid centrifugation for monosodium urate and calcium pyrophosphate crystal detection

Contact Info

Product

Resources

About