scholarly journals Elevated serum fibrinogen level is an independent risk factor for IgA nephropathy

Oncotarget ◽  
2017 ◽  
Vol 8 (58) ◽  
pp. 99125-99135 ◽  
Author(s):  
Ji Zhang ◽  
Chaosheng Chen ◽  
Qiongxiu Zhou ◽  
Shubei Zheng ◽  
Yinqiu Lv ◽  
...  
2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yaling Zhai ◽  
Xingchen Yao ◽  
Yuanyuan Qi ◽  
Jingge Gao ◽  
Yazhuo Chen ◽  
...  

Introduction. The identification of reliable prognostic factors is a crucial requirement for patients with IgA nephropathy (IgAN). Here, we explored the relationship between serum chloride levels and prognosis in patients with IgAN. Methods. We recruited all patients with primary IgAN, as diagnosed by renal biopsy, between 1st January 2015 and 1st April 2019. Patients were divided two groups (high chloride group and low chloride group) based on the best cut-off values from survival receiver operating characteristic (ROC) curves. The baseline clinicopathological characteristics of two groups were then compared. Cox proportional hazard models were used to determine the prognostic value of serum chloride levels in patients with IgAN. Finally, we screened reliable prognostic indicators and built a clinical prediction model and validated the performance of the model. Results. Compared with patients in the high chloride group, patients in the low chloride group had significantly lower levels of 24-hour urinary total protein (24 h-UTP), serum creatinine (sCr), and higher levels of hemoglobin (Hb), albumin (all p < 0.05 ), and less proportion of Oxford classification grade E1 (endothelial cell proliferation) and T2 (renal tubule atrophy or renal interstitial fibrosis). Cox analysis revealed that serum   chloride   level ≥ 105.4   mmol / L was a significant and independent risk factor for prognosis in patients with IgAN ( p < 0.05 ). Serum chloride, sCr, T, hypertension, and Hb were used to generate a predictive model for prognosis. The c -indices of our predictive model were 0.80, 0.86, and 0.78, for 1, 2, and 3 years, respectively; Brier scores were 0.06, 0.09, and 0.16, respectively. Conclusions. A serum   chloride   level ≥ 105.4   mmol / l was identified as a significant and independent risk factor for the prognosis of patients with IgAN. A predictive prognosis model was generated using serum chloride, sCr, T, hypertension, and Hb; this model exhibited a good predictive effect.


2020 ◽  
Vol 27 (30) ◽  
pp. 5056-5066 ◽  
Author(s):  
Pan Jing ◽  
Min Shi ◽  
Liang Ma ◽  
Ping Fu

Hyperuricemia, defined as the presence of elevated serum uric acid (sUA), could lead to urate deposit in joints, tendons, kidney and other tissues. Hyperuricemia as an independent risk factor was common in patients during the causation and progression of kidney disease. Uric acid is a soluble final product of endogenous and dietary purine metabolism, which is freely filtered in kidney glomeruli where approximately 90% of filtered uric acid is reabsorbed. Considerable studies have demonstrated that soluble uric acid was involved in the pathophysiology of renal arteriolopathy, tubule injury, tubulointerstitial fibrosis, as well as glomerular hypertrophy and glomerulosclerosis. In the review, we summarized the mechanistic insights of soluble uric acid related renal diseases.


2020 ◽  
Author(s):  
Yaling Zhai ◽  
Xingchen Yao ◽  
Yuanyuan Qi ◽  
Jingge Gao ◽  
Yazhuo Chen ◽  
...  

Abstract IntroductionFinding reliable prognostic factors is crucial for IgA nephropathy (IgAN). Here, we determined the relationship between prognosis of IgAN with serum chloride.MethodsPrimary IgAN diagnosed by renal biopsy from January 1, 2015 to April 1, 2019 were recruited. Patients were divided into lower group and higher group based on the best cut-off value of survival receiver operating characteristics (ROC) curves. The baseline clinicopathological characteristics were retrospectively compared. Cox proportional hazard models were used to demonstrate the prognostic value of serum chloride in IgAN. Prognosis prediction model was built by multivariate Cox regression. ResultsCompared to higher group , age、24-hour urinary protein and serum creatinine(Cr) in the lower group were significantly lower, hemoglobin(Hb)、albumin were significantly higher(all P<0.05),the degree of endothelial cell proliferation (E) and renal tubule atrophy or renal interstitial fibrosis (T) were significantly lighter (all P<0.05). Univariate and multivariate Cox analysis revealed that serum chloride ≥105.4 mmol/l was an independent risk factor for the prognosis of IgAN(P<0.05). Serum chloride, Cr, T, hypertension, and Hb were screened out as features in predictive prognosis model. The c-index of the model was 0.85、0.82 and 0.77 for 1、2 and 3 years respectively, and brier scores were 0.06 、0.09 and 0.16 respectively. ConclusionsSerum chloride ≥105.4 mmol/l was an independent risk factor for the prognosis of IgAN. A predictive prognosis model including serum chloride, Cr, T, hypertension and Hb exhibited a relatively good prediction effect.


Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3364-3368 ◽  
Author(s):  
Mario von Depka ◽  
Ulrike Nowak-Göttl ◽  
Roswith Eisert ◽  
Christian Dieterich ◽  
Monika Barthels ◽  
...  

Elevation of serum lipoprotein (a) (Lp[a]) is a known risk factor predisposing to cardiovascular and cerebrovascular disease. However, little is known about the role of increased Lp(a) in venous thromboembolism (VTE). This study evaluated the role of Lp(a) among a panel of established hereditary thrombogenic defects in patients with VTE. A total of 685 consecutive patients with at least one episode of VTE and 266 sex- and age-matched healthy controls were screened with regard to activated protein C resistance, protein C, protein S, and antithrombin deficiency, elevated serum levels of Lp(a), and the factor V G1691A, MTHFR C677T, and prothrombin G20210A mutations. Elevated Lp(a) levels above 30 mg/dL were found in 20% of all patients, as compared to 7% among healthy controls (P < .001, odds ratio [OR] 3.2, 95% confidence interval [CI], 1.9-5.3). The coexistence of FV G1691A and elevated Lp(a) was significantly more prevalent among patients with VTE than in the control group (7% versus 0.8%; P < .001, OR 9.8, 95% CI, 2.4-40.7). No other established prothrombotic risk factor was found to be significantly combined with increased Lp(a). These data suggest that Lp(a) concentrations greater than 30 mg/dL are a frequent and independent risk factor for VTE. Furthermore, elevated Lp(a) levels might contribute to the penetrance of thromboembolic disease in subjects being affected by other prothrombotic defects, such as FV G1691A mutation.


Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3364-3368 ◽  
Author(s):  
Mario von Depka ◽  
Ulrike Nowak-Göttl ◽  
Roswith Eisert ◽  
Christian Dieterich ◽  
Monika Barthels ◽  
...  

Abstract Elevation of serum lipoprotein (a) (Lp[a]) is a known risk factor predisposing to cardiovascular and cerebrovascular disease. However, little is known about the role of increased Lp(a) in venous thromboembolism (VTE). This study evaluated the role of Lp(a) among a panel of established hereditary thrombogenic defects in patients with VTE. A total of 685 consecutive patients with at least one episode of VTE and 266 sex- and age-matched healthy controls were screened with regard to activated protein C resistance, protein C, protein S, and antithrombin deficiency, elevated serum levels of Lp(a), and the factor V G1691A, MTHFR C677T, and prothrombin G20210A mutations. Elevated Lp(a) levels above 30 mg/dL were found in 20% of all patients, as compared to 7% among healthy controls (P &lt; .001, odds ratio [OR] 3.2, 95% confidence interval [CI], 1.9-5.3). The coexistence of FV G1691A and elevated Lp(a) was significantly more prevalent among patients with VTE than in the control group (7% versus 0.8%; P &lt; .001, OR 9.8, 95% CI, 2.4-40.7). No other established prothrombotic risk factor was found to be significantly combined with increased Lp(a). These data suggest that Lp(a) concentrations greater than 30 mg/dL are a frequent and independent risk factor for VTE. Furthermore, elevated Lp(a) levels might contribute to the penetrance of thromboembolic disease in subjects being affected by other prothrombotic defects, such as FV G1691A mutation.


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