scholarly journals Gout - asymptomatic hyperuricemia with/without asymptomatic monosodium urate crystal deposition: To be treated or not?

2019 ◽  
Vol 147 (11-12) ◽  
pp. 777-781
Author(s):  
Marija Radak-Perovic ◽  
Mirjana Zlatkovic-Svenda
Keyword(s):  
Uric Acid ◽  
Imaging Techniques ◽  
Serum Uric Acid Level ◽  
Tumor Lysis Syndrome ◽  
Chronic Inflammatory Disease ◽  
Low Grade ◽  
Crystal Deposition ◽  
Uric Acid Crystal ◽  
Acid Crystal ◽  
Xanthine Oxidase Inhibitors

Elevation of serum uric acid level without clinically visible arthritis (known as asymptomatic hyperuricemia) is not traditionally considered to be gout disease, but only a possible cause of it, even though it may be accompanied by tissue uric acid crystal deposition. On the other hand, gout is traditionally recognized as recurrent, overt arthritis, visible only after a long period of time due to uric acid accumulation in joints. Advanced imaging techniques have substantially changed the perception of this problem, identifying gout as a low-grade chronic inflammatory disease from the very beginning, visible only by phases of acute arthritis attacks. According to ultrasonography, uric acid crystal hyperechoic aggregates (tophi) are seen not only in the symptomatic gout disease phase, but also in the preceding ? asymptomatic (latent) ? gout phase. New perception of the problem was approved by the recently described NETs (neutrophil extracellular traps) phenomenon. Also, hyperuricemia has recently been identified as a systemic disorder, responsible not only for the apparent gout arthritis, but also for the renal and cardiovascular disease occurrence and progression. Positive effect of urate-lowering therapy (xanthine oxidase inhibitors and uricosurics) on hypertension and chronic kidney disease indicates a possibility of its utility in asymptomatic hyperuricemia and asymptomatic gout therapy, apart from the use in clinically manifested gout treatment and for certain conditions, such as tumor lysis syndrome.

scholarly journals Detection of uric acid crystal deposition by ultrasonography and dual-energy computed tomography

Medicine ◽  
2018 ◽  
Vol 97 (42) ◽  
pp. e12834 ◽  
Author(s):  
Yu Wang ◽  
Xuerong Deng ◽  
Yufeng Xu ◽  
Lanlan Ji ◽  
Zhuoli Zhang
Keyword(s):  
Computed Tomography ◽  
Uric Acid ◽  
Dual Energy ◽  
Crystal Deposition ◽  
Uric Acid Crystal ◽  
Dual Energy Computed Tomography ◽  
Acid Crystal

scholarly journals A Review of Uric Acid, Crystal Deposition Disease, and Gout

2014 ◽  
Vol 32 (1) ◽  
pp. 31-41 ◽  
Author(s):  
Fernando Perez-Ruiz ◽  
Nicola Dalbeth ◽  
Tomas Bardin
Keyword(s):  
Uric Acid ◽  
Crystal Deposition ◽  
Uric Acid Crystal ◽  
Acid Crystal ◽  
Crystal Deposition Disease ◽  
Deposition Disease

scholarly journals Erythrodermic Psoriasis Causing Uric Acid Crystal Nephropathy

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
John Ellis ◽  
Jeffrey Lew ◽  
Sumir Brahmbhatt ◽  
Sarah Gordon ◽  
Troy Denunzio
Keyword(s):  
Uric Acid ◽  
Rare Complication ◽  
Tumor Lysis Syndrome ◽  
Keratinocyte Differentiation ◽  
Uric Acid Crystal ◽  
Acid Crystal ◽  
Crystal Nephropathy ◽  
Erythrodermic Psoriasis ◽  
Life Threatening ◽  
Psoriatic Lesions

Background. Erythrodermic psoriasis is a rare and severe variant of psoriasis. It is characterized by widespread skin erythema, scaling, pustules, or exfoliation of more than 75% of the body’s surface area. This condition has life-threatening complications to include hemodynamic, metabolic, immunologic, and thermoregulatory disturbances. One metabolic complication, hyperuricemia, occurs from rapid keratinocyte differentiation and infiltration of inflammatory cells into psoriatic lesions. Although renal injury caused by shunting of blood to the skin has been reported, there are no reports of erythrodermic psoriasis causing crystal-induced nephropathy. We present a case of erythrodermic psoriasis and hyperuricemia complicated by uric acid crystal nephropathy. Case Presentation. A 57-year-old male with long-standing psoriatic arthritis presented with diffuse scaling of his skin. He was being treated with adalimumab, leflunomide, and topical clobetasol, but had recently stopped taking his medications. Physical exam revealed yellow scaling covering his entire body with underlying erythema and tenderness without mucosal involvement. Labs were notable for a creatinine of 3.3 mg/dL, with no prior history of renal disease, and uric acid of 12.7 mg/dL. He was admitted to the intensive care unit given >80% of body surface area involvement and acute renal failure. Despite aggressive fluid resuscitation, renal function did not improve, and creatinine peaked at 4.61 mg/dL. Urine microscopy showed diffuse polymorphic uric acid crystals, consistent with uric acid crystal-induced nephropathy. He was started on rasburicase, urinary alkalinization, and fluids. His renal function improved dramatically; urine output, uric acid, and electrolytes normalized. He was discharged on topical clobetasol and leflunomide and started on secukinumab with little to no skin involvement. Conclusion. This case presents the rare complication of crystal-induced nephropathy in a patient with erythrodermic psoriasis. Uric acid crystal nephropathy is well described in diseases with rapid cell turnover such as tumor lysis syndrome. It is thought that rapid keratinocyte differentiation and inflammatory infiltration of psoriatic lesions produced life-threatening electrolyte abnormalities similar to tumor lysis syndrome. Early recognition of this rare complication is critical, and aggressive fluid resuscitation, urine alkalinization, and uric acid lowering agents should be administered immediately.

scholarly journals Acute Uric Acid Nephropathy following Epileptic Seizures: Case Report and Review

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Chinmay Patel ◽  
Caitlin P. Wilson ◽  
Naveed Ahmed ◽  
Yousef Hattab
Keyword(s):  
Uric Acid ◽  
Uric Acid Level ◽  
Acid Level ◽  
Serum Uric Acid Level ◽  
Tumor Lysis Syndrome ◽  
Kidney Injury ◽  
Young Male ◽  
Epileptic Seizures ◽  
Uric Acid Nephropathy ◽  
Acute Uric Acid Nephropathy

Acute hyperuricemia most commonly occurs in patients who experience tumor lysis syndrome. Hyperuricemia along with other electrolyte abnormalities like hyperkalemia, hypocalcemia, and hyperphosphatemia leads to acute kidney injury (AKI) due to acute uric acid nephropathy which is associated with significant morbidity. High risk patients are thus closely monitored for signs of these laboratory abnormalities. Extreme exercise, rhabdomyolysis, and seizures are rare causes of acute hyperuricemia. Serum uric acid level is not routinely monitored as a part of postictal labs. We report an unusual case of AKI in a young male with recurrent seizures and no associated rhabdomyolysis who was found to have acute uric acid nephropathy. Timely administration of Rasburicase prevented the need for dialysis in this patient and led to complete renal recovery. This case illustrates the importance of doing a urine microscopy and checking uric acid level in patients with recurrent seizures who develop unexplainable AKI, as timely management helps improve outcome. We also briefly review the pathophysiology of seizure related hyperuricemia and acute uric acid nephropathy.

scholarly journals Contribution of Mast Cell-Derived Interleukin-1β to Uric Acid Crystal-Induced Acute Arthritis in Mice

2014 ◽  
Vol 66 (10) ◽  
pp. 2881-2891 ◽  
Author(s):  
Laurent L. Reber ◽  
Thomas Marichal ◽  
Jeremy Sokolove ◽  
Philipp Starkl ◽  
Nicolas Gaudenzio ◽  
...  
Keyword(s):  
Mast Cell ◽  
Uric Acid ◽  
Interleukin 1Β ◽  
Uric Acid Crystal ◽  
Acute Arthritis ◽  
Acid Crystal

Urate nephropathy

2015 ◽  
Author(s):  
Duk-Hee Kang ◽  
Mehmet Kanbay
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Crystal Deposition ◽  
Asymptomatic Patients ◽  
Xanthine Oxidase Inhibitors ◽  
Comorbidity Burden ◽  
Urate Nephropathy ◽  
Systemic Disorder ◽  
Urate Crystal ◽  
Uric Acid Nephropathy

Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.

scholarly journals P2772A novel approach for uric acid crystal detection in human coronary arteries with polarization-sensitive micro-OCT

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
K Nishimiya ◽  
G Sharma ◽  
K Singh ◽  
H Osman ◽  
J A Gardecki ◽  
...  
Keyword(s):  
Uric Acid ◽  
Coronary Arteries ◽  
Uric Acid Crystal ◽  
Acid Crystal ◽  
Novel Approach
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