Hyperuricemia is associated with progression of IgA nephropathy

Bakan, Ali; Oral, Alihan; Elçioğlu, Ömer Celal; Takır, Mümtaz; Köstek, Osman; Özkök, Abdullah; Başçı, Semih; Şumnu, Abdullah; Öztürk, Savaş; Sipahioğlu, Murat Hayri; Türkmen, Aydın; Voroneanu, Luminița; Covic, Adrian; Kanbay, Mehmet

doi:10.1007/s11255-015-0939-7

Cited by 30 publications

(26 citation statements)

References 19 publications

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“…Several epidemiological studies in the general population and in patients with CKD show that uric acid is a major independent risk factor for the development and progression of renal disease [29], [30], [31], [32], [33]. This association was seen in studies with patients with diabetes mellitus as well [29], [34], [35], [36].…”

Section: Epidemiological Data Associating Hyperuricemia With Ckdmentioning

confidence: 89%

Asymptomatic hyperuricemia and chronic kidney disease: Narrative review of a treatment controversial

Eleftheriadis¹,

Golphinopoulos²,

Pissas³

et al. 2017

Journal of Advanced Research

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Section: Epidemiological Data Associating Hyperuricemia With Ckdmentioning

confidence: 89%

Asymptomatic hyperuricemia and chronic kidney disease: Narrative review of a treatment controversial

Eleftheriadis¹,

Golphinopoulos²,

Pissas³

et al. 2017

Journal of Advanced Research

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“…There was an increasing attention on the relationship between hyperuricemia [12] and chronic kidney disease [13]. High concentration of serum UA may lead to nephropathy and renal function impairment by directly mechanical damage or indirectly inflammation and cell phenotype inversion, resulting in the reduction of UA excretion and forming a vicious cycle.…”

Section: Discussionmentioning

confidence: 99%

Risk factors of progressive IgA nephropathy which progress to end stage renal disease within ten years: a case–control study

Shu

Zhang

et al. 2017

BMC Nephrol

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BackgroundThere were few related studies aiming to severe IgA nephropathy (IgAN) which could progress rapidly to end stage renal disease (ESRD) within ten years. To find valuable clinical or pathological factors and promising precautions is essential.MethodsA single center case–control study was performed. Fifty ESRD patients with the primary cause of IgAN and a short renal survival time of less than ten years after diagnose were enrolled in the case group. One hundred IgAN patients with a renal survival time of more than ten years were enrolled in the control group. IgA Oxford classification scores, clinical data at baseline and during the follow-up were collected. Multivariate logistic regression was used to investigate factors associated with the development of ESRD.ResultsThere were significant differences in baseline clinical data between these two groups, as well as the constituent ratio of Oxford MEST-score. Distinct differences were observed in time-average uric acid(TA-UA), time-average hemoglobin(TA-Hb), time-average albumin(TA-Alb), time-average total cholesterol(TA-TC) and time-average urinary protein(TA-P) during the follow-up. In multivariate logistic models, IgA Oxford score M1(OR = 5.10, P = 0.018) and eGFR(OR = 0.97, P = 0.039) at biopsy, TA-UA (OR = 2.06, P = 0.026) and TA-Hb (OR = 0.53, P = 0.022) during the follow-up were identified independent factors for developing ESRD.ConclusionIgAN patients with pathological assessment of M1, low baseline eGFR, TA-Hb and high TA-UA were more likely to progress to ESRD, and should be paid more attention. Appropriate regulations of UA, Hb and urine protein after diagnose may be a promising treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-016-0429-x) contains supplementary material, which is available to authorized users.

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“…Hyperuricemia appears to be a common manifestation in IgAN patients, even when their GFR are normal and has been considered as a risk factor for IgAN progression [10,11,22,23]. However, a clear evaluation of the role of uric acid with histopathological Oxford classification on IgAN progression is still lacking and the causative role of uric acid in IgAN progression Table 3.…”

Section: Discussionmentioning

confidence: 99%

The Clinical Significance of Uric Acid and Complement Activation in the Progression of IgA Nephropathy

Çalışkan¹,

Celik²,

Öztop

et al. 2016

Kidney Blood Press Res

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Background/Aims: The aim of this study is to investigate the utility of clinical [age, gender, mean arterial pressure (MAP)] and laboratory parameters [eGFR, hemoglobin (Hgb), serum levels of creatinine, uric acid, albumin, proteinuria, hematuria] and also histopathological lesions (Oxford classification parameters, crescents, intensity and pattern of staining for C3, C1Q, IgA, IgG, IgM) as progression markers in patients with IgA Nephropathy (IgAN). Methods: A total of 111 IgAN patients with a follow-up period >1 year or who reached kidney failure [GFR category G5 chronic kidney disease (CKD)] <1 year were investigated. Primary endpoint was the development of kidney failure or eGFR decline ≥50% from the baseline. Kaplan-Meier and Cox proportional hazards analyses were performed. Results: Mean follow-up period was 33±29 months. Thirty-seven (33.3%) patients progressed to kidney failure and 4 (3.6%) patients developed eGFR decline ≥50% from the baseline after a median of 23 and 65 months, respectively. In multivariate Cox regression analysis, baseline levels of Hgb (HR:0.782, 95% CI 0.559-0.973, p=0.037), serum uric acid (HR:1.293, 95% CI 1.023-1.621, p=0.046), eGFR (HR:0.966, 95% CI 0.947-0.984, p=0.004) and intensity of C3 staining (HR:1.550, 95% CI 1.198-1.976, p=0.049) predicted primary endpoint. Serum uric acid level was associated independently with T score (β=0.303, p=0.005) in patients with eGFR>30 ml/min/m². Conclusions: Hyperuricemia and the deposition of C3 are independent risk factors for IgAN progression.

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Hyperuricemia is associated with progression of IgA nephropathy

Abstract: Baseline serum uric acid concentration is directly proportional to the rate of decline in renal functions in patients with IgAN. Uric acid-lowering treatments may be beneficial for the prevention of progression of IgAN. However, randomized controlled studies are needed for this purpose.

Cited by 30 publications

References 19 publications

Asymptomatic hyperuricemia and chronic kidney disease: Narrative review of a treatment controversial

Asymptomatic hyperuricemia and chronic kidney disease: Narrative review of a treatment controversial

Risk factors of progressive IgA nephropathy which progress to end stage renal disease within ten years: a case–control study

The Clinical Significance of Uric Acid and Complement Activation in the Progression of IgA Nephropathy

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