A novel role for uric acid in acute kidney injury associated with tumour lysis syndrome

Shimada, Michiko; Johnson, Richard J.; May, W. Stratford; Lingegowda, Vijaykumar; Sood, Puneet; Nakagawa, Takahiko; Van, Quoc C.; Dass, Bhagwan; Ejaz, A. Ahsan

doi:10.1093/ndt/gfp330

Cited by 121 publications

(78 citation statements)

References 60 publications

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“…About one-third of patients with a high risk of tumour lysis syndrome develop AKI [206,207]. In this clinical condition, hyperuricaemia is one of the factors which contribute to AKI by different mechanisms [208]. In two randomized controlled studies and 2 recent metaanalyses, rasburicase administration was associated with a more rapid and profound decrease in uricaemia as compared with allopurinol [209][210][211].…”

Section: (Grade 1−) Strong Agreementmentioning

confidence: 99%

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Ichai

Vinsonneau

Souweine

et al. 2016

Anaesthesia Critical Care & Pain Medicine

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Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years. The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen and serum creatinine, have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. However, using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, also called "functional renal insufficiency" or "pre-renal insufficiency". This situation is characterized by an oliguria and an increase in creatininemia as a consequence of a reduction in renal blood flow related to systemic haemodynamic abnormalities. In this situation, "renal insufficiency" seems rather inappropriate as kidney function is not impaired. On the contrary, the kidney delivers an appropriate response aiming to recover optimal systemic physiological haemodynamic conditions. Considering the kidney as insufficient is erroneous because this suggests that it does not work correctly, whereas the opposite is occurring, because the kidney is healthy even in a threatening situation. With current definitions of AKI, normalization of volaemia is needed before defining AKI in order to avoid this pitfall.

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Section: (Grade 1−) Strong Agreementmentioning

confidence: 99%

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Ichai

Vinsonneau

Souweine

et al. 2016

Anaesthesia Critical Care & Pain Medicine

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“…Furthermore, elevated UA increases the risk of chronic kidney disease (2,25,35). To date, studies of UA in the kidney have mainly concentrated on intrarenal deposition of UA crystals that could stimulate renal interstitial fibrosis (29,33). However, the direct effect of circulating UA on mesangial cells (MCs) remains unclear.…”

mentioning

confidence: 99%

Activation of ERK1/2 by NADPH oxidase-originated reactive oxygen species mediates uric acid-induced mesangial cell proliferation

Zhuang

Feng

Ding

et al. 2014

American Journal of Physiology-Renal Physiology

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A, Huang S. Activation of ERK1/2 by NADPH oxidase-originated reactive oxygen species mediates uric acid-induced mesangial cell proliferation. Am J Physiol Renal Physiol 307: F396-F406, 2014. First published February 26, 2014 doi:10.1152/ajprenal.00565.2013.-Hyperuricemia is associated with kidney complications including glomerulosclerosis and mesangial cell (MC) proliferation by poorly understood mechanisms. The present study investigated the underlying mechanisms that mediate uric acid (UA)-induced MC proliferation. A rat MC line, HBZY-1, was treated with various concentrations of UA in the presence or absence of a specific extracellular-regulated protein kinase 1/2 (ERK1/2) inhibitor (U0126), apocynin. UA dose dependently stimulated MC proliferation as shown by increased DNA synthesis and number of cells in the S and G 2 phases in parallel with the upregulation of cyclin A2 and cyclin D1. In addition, UA time dependently promoted MC proliferation and significantly increased phosphorylation of ERK1/2 but not c-Jun NH 2-terminal kinase and p38 MAPK in MCs as assessed by immunoblotting. Inhibition of ERK1/2 signaling via U0126 markedly blocked UA-induced MC proliferation. More importantly, UA induced intracellular reactive oxygen species (ROS) production of MCs dose dependently, which was completely blocked by apocynin, a specific NADPH oxidase inhibitor. Toll-like receptor (TLR)2 and TLR4 signaling had no effect on NADPH-derived ROS and UA-induced MC proliferation. Interestingly, pretreatment with apocynin inhibited ERK1/2 activation, the upregulation of cyclin A2 and cyclin D1, and MC proliferation. In conclusion, UA-induced MC proliferation was mediated by NADPH/ROS/ERK1/2 signaling pathway. This novel finding not only reveals the mechanism of UAinduced MC cell proliferation but also provides some potential targets for future treatment of UA-related glomerular injury.

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“…Ürik asit, fizyolojik pH'ta tamama yakın iyonize olmasına rağmen, renal tübüller-deki asidik ortamda çözünemez hale gelir. Ürik asidin çökmesi, intratübüler tıkanma ve sonrasında artmış böbrek vasküler direnci ve azalmış glomerüler filtrasyon hızı ile sonuçlanır (22). Tümör lizis sendromunda hiperfosfatemi ve hipokalsemi de gelişir.…”

Section: Tümör Li̇zi̇s Sendromuunclassified

Lung Cancer And Nephrologıc Dıseases

Nalcaci¹,

Tuglular²

2016

Toraks Cer Bult

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The incidence reported about the malignancy rates in patients with chronic renal insufficiency vary among different series. In a wide series about renal insufficiency in lung cancer, of the 445 lung cancer patients, 14.4% had a serum creatinine (SCR) level 1.25 mg/dL. However, when Cockcroft-Gault and Modification of Diet in Renal Disease formulas were applied, 62.1% and 55.9% respectively had abnormal renal function, according to the KDOQI-KDIGO Kidney Disease Outcomes Quality Initiative (KDOQI) and Kidney Disease: Improving Global Outcomes (KDIGO) definition. Because ~50% of all anticancer drugs are predominantly excreted in urine as an unchanged drug or active metabolite(s), any reduction in renal clearance can result in the accumulation of potentially toxic species and overdosage. Thus, the dosage of chemotherapeutic agents used in these patients with renal insufficiency frequently requires dosage reduction to avoid severe toxicities. The clinical course and survival in patients with lung cancer and chronic kidney disease (CKD) appear to be comparable with those in patients with lung cancer, but without kidney dysfunction. As with all hospitalized patients, those with cancer are at a risk of developing acute kidney injury (AKI) from hypotension, sepsis, or administration of radiocontrast, antifungal, and antibacterial agents. Nephrotoxicity is the most common dose-limiting side effect of cisplatin administration. The primary site for the clearance of cisplatin is the kidney. The most common clinical scenario is the gradual onset of nonoliguric AKI; however, electrolyte wastage is observed, particularly with high dosages of cisplatin. Glomerulonephritis, generally presenting as nephrotic syndrome, is associated with the presence of various types of cancer. The strongest association is with membranous nephropathy and solid tumors (lung, colon, breast, and prostate).Keywords: Lung cancer, acute renal failure, chronic renal failure, glomerulophritis ÖzetKronik böbrek yetmezliği olan hastalardaki malignite insidansı için çeşitli araştırmalarda farklı oranlar bildirilmektedir. 2014'teki geniş bir seride düşük glomerüler filtrasyon hızı (eGFR) (mL/dk/1,73 m2) artmış böbrek kanseri riski ile iliş-kili bulunmuş ancak prostat, meme, akciğer, kolorektal veya herhangi bir kanserle ilişkili bulunmamıştır. Akciğer kanseri olan hastalardaki renal yetmezlik oranı ile ilgili yapılan bir çalışmada 445 akciğer kanserli hastanın verileri incelenmiş-tir. Hastaların %13,4 ünün serum kreatinin seviyeleri 1,25 mg/dL' nin altında saptanmasına rağmen KDOQI-KDIGO tanımına göre böbrek fonksiyonlarını ölçen Cockroft-Gault ve a modification of diet in renal disease (MDRD) formülleri uygulandığında hastaların sırasıyla %62,1 ve %55,9' unda böbrek fonksiyonlarında bozukluk saptanmıştır. Antikanser ilaçlarının yaklaşık %50'si temel olarak değişmeden veya aktif metabolit halinde idrar ile atıldıklarından böbrek klirensindeki herhangi bir azalma toksik maddelerin birikimi ve doz aşımı ile sonuçlanabilmektedir. Ciddi toksisiteleri önle...

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A novel role for uric acid in acute kidney injury associated with tumour lysis syndrome

Cited by 121 publications

References 60 publications

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Activation of ERK1/2 by NADPH oxidase-originated reactive oxygen species mediates uric acid-induced mesangial cell proliferation

Lung Cancer And Nephrologıc Dıseases

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