Aims:We prospectively examined the relationship between metabolic syndrome (MetS) and incident chronic kidney disease (CKD) among middle-aged and elderly Chinese, and conducted a systematic review and meta-analysis of all cohort studies on this topic. Materials and Methods:Our research data were derived from the China Health and Retirement Longitudinal Study. Participants (n=5752, age ≥45 years) without CKD (defined as estimated glomerular filtration rate <60 ml/min/1.73m 2 ) at baseline were followed up for 4 years. We applied logistic regressions to examine the association of MetS with incident CKD. In addition, we pooled our effect estimates and those from previous cohort studies in the meta-analysis. Results:In a 4-years follow-up, 61 (4.27%) developed CKD in participants with MetS versus 102 (2.36%) in participants without MetS. After adjustment for potential confounders, odds ratio for incident CKD was 1.82 [95% confidence interval (95% CI): 1.19-2.78] comparing participants with MetS with those without MetS.There was a linear positive association between the number of MetS components and incident CKD (p for trend <0.001). In the updated meta-analysis of 25 studies among 350,655 participants with 29,368 incident cases of CKD, the pooled relative risk of developing CKD in participants with MetS was 1.34 (95% CI: 1.28-1.39), compared with those without MetS.Conclusions: Individuals with MetS had higher risk of incident CKD in middle-aged and elderly Chinese adults, which was supported by a comprehensive review of cohort studies from multiple populations. It may be advisable to routinely monitor renal functions among individuals with MetS.

Objective To prospectively examine the association of high sensitivity C‐reactive protein (hs‐CRP) with incident type 2 diabetes mellitus (T2DM) among middle‐aged and elderly Chinese, and validate the association in an updated meta‐analysis of prospective studies. Methods We used data from the China Health and Retirement Longitudinal Study, started in 2011–2012 with follow ups in 2013–2014 and 2015–2016. Multivariable Cox proportional hazard regressions were applied to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between hs‐CRP level and incident T2DM. An updated meta‐analysis was conducted to combine our estimates with those in previous prospective studies. Results Included in the analyses were 7985 participants (mean age: 59.38 years; men: 46.73%). Higher hs‐CRP was associated with increased risk of T2DM (multivariable‐adjusted HR, 1.30; 95% CI: 1.03, 1.64 for comparing extreme quartiles). The association was stronger in participants with body mass index (BMI) of 24.0 kg/m2 or higher than those with a BMI lower than 24.0 kg/m2 (p for interaction = 0.038). In a meta‐analysis of 28 cohorts, 2 case‐cohort, and 6 nested case‐control studies among 125,356 participants with 10,759 cases, the pooled relative risk for T2DM was 1.77 (95% CI: 1.60, 1.96) for the highest versus lowest level of hs‐CRP. Conclusions Hs‐CRP was associated with higher risk of T2DM in middle‐aged and elderly Chinese, and this association was confirmed by an updated meta‐analysis of prospective studies. Our findings highlight the role of elevated hs‐CRP in the development of T2DM.

Background We prospectively examined the association between serum uric acid (SUA) levels and chronic kidney disease (CKD) in China and updated the evidence through a comprehensive meta-analysis of prospective studies worldwide. Methods Our original analyses were based on data from the China Health and Retirement Longitudinal Study. The primary exposure of interest was SUA at baseline, and the main outcome was incident CKD. Logistic regression models were used to examine the association between SUA levels and incident CKD. A meta-analysis was performed to pool our effect estimate and those from other cohort studies. Results During a 4-year follow-up, 180 participants developed incident CKD. Participants in the highest SUA quartile were 2.73 times as likely to develop incident CKD compared to those in the lowest quartile (multivariable-adjusted OR, 2.73; 95% CI, 1.65–4.50). Each 1 mg/dL increment in the SUA levels was associated with a 49% increased risk of incident CKD (multivariable-adjusted OR, 1.49; 95% CI, 1.28–1.74). In the meta-analysis of 30 cohort studies (including the current study), pooled relative risks (95% CIs) of incident CKD were 1.15 (1.10–1.21) for SUA each 1 mg/dL increment, 1.22 (1.14–1.30) for the highest versus lowest SUA group, and 1.17 (1.12–1.23) for hyperuricemia versus no hyperuricemia. Conclusions Baseline SUA levels were associated with higher risk of incident CKD in middle-aged and elderly Chinese adults, and this positive association was confirmed in the meta-analysis of multiple cohort studies. Our findings may imply that SUA levels need to be routinely monitored for future CKD risk.

BackgroundAdrenocorticotropic hormone (ACTH)-independent Cushing’s syndrome (CS) with bilateral cortisol-secreting adenomas has been rarely reported in the literatures. Precise recognition and management of this disorder constitute a challenge to clinicians due to the difficulty of exact location of the functional lesions.Case presentationWe herein report a new case of a Chinese female patient with a complaint of exertional dyspnea for over 10 years. ACTH-independent CS was diagnosed based on undetectable ACTH and unsuppressed cortisol levels by dexamethasone. Computed tomography (CT) scan indicated bilateral adrenal masses, and adrenal venous sampling (AVS) adjusted by plasma aldosterone revealed hypersecretion of cortisol from both adrenal glands. Bilateral cortisol-secreting adrenal adenomas were suspected and confirmed by the postoperative pathology in subsequent two-step bilateral laparoscopic adrenalectomy. The symptoms and signs of CS relieved after surgery with continuous glucocorticoid replacement.ConclusionsAVS adjusted by plasma aldosterone could be a useful technique in diagnosing ACTH-independent CS with bilateral adrenal adenomas prior to surgery. And the aldosterone ratio could be used to confirm the success of adrenal vein cannulation in this situation.

Background Co-existing Cushing’s syndrome and primary aldosteronism caused by bilateral adrenocortical adenomas, secreting cortisol and aldosterone, respectively, have rarely been reported. Precise diagnosis and management of this disorder constitute a challenge to clinicians due to its atypical clinical manifestations and laboratory findings. Case presentation We here report a Chinese male patient with co-existing Cushing’s syndrome and primary aldosteronism caused by bilateral adrenocortical adenomas, who complained of intermittent muscle weakness for over 3 years. Computed tomography scans revealed bilateral adrenal masses. Undetectable ACTH and unsuppressed cortisol levels by dexamethasone suggested ACTH-independent Cushing’s syndrome. Elevated aldosterone to renin ratio and unsuppressed plasma aldosterone concentration after saline infusion test suggested primary aldosteronism. Adrenal venous sampling adjusted by plasma epinephrine revealed hypersecretion of cortisol from the left adrenal mass and of aldosterone from the right one. A sequential bilateral laparoscopic adrenalectomy was performed. The cortisol level was normalized after partial left adrenalectomy and the aldosterone level was normalized after subsequent partial right adrenalectomy. Histopathological evaluation of the resected surgical specimens, including immunohistochemical staining for steroidogenic enzymes, revealed a left cortisol-producing adenoma and a right aldosterone-producing adenoma. The patient’s symptoms and laboratory findings resolved after sequential adrenalectomy without any pharmacological treatment. Conclusions Adrenal venous sampling is essential in diagnosing bilateral functional adrenocortical adenomas prior to surgery. Proper interpretation of the laboratory findings is particularly important in these patients. Immunohistochemistry may be a valuable tool to identify aldosterone/cortisol-producing lesions and to validate the clinical diagnosis. Electronic supplementary material The online version of this article (10.1186/s12902-019-0395-y) contains supplementary material, which is available to authorized users.