Dexamethasone protects the glycocalyx on the kidney microvascular endothelium during severe acute pancreatitis.

OBJECTIVE: This study demonstrated that dexamethasone (DEX) protects the endothelial glycocalyx from damage induced by the inflammatory stimulus tumor necrosis factor-α (TNF-α) during severe acute pancreatitis (SAP), and improves the renal microcirculation. METHODS: Ninety mice were evenly divided into 3 groups (Sham, SAP, and SAP+DEX). The SAP mice model was established by ligature of pancreatic duct and intraperitoneal injection of cerulein. Renal perfusion and function, and morphological changes of the glycocalyx were evaluated by laser Doppler velocimetry, electron microscopy, and histopathology (hematoxylin and eosin (H&E) staining), respectively. Serum levels of syndecan-1 and TNF-α were assessed by enzyme-linked immunosorbent assay (ELISA). The protective effects of dexamethasone on the glycocalyx and renal microcirculation were evaluated. RESULTS: Significantly high levels of serum TNF-α were detected 3 h after the onset of SAP. These levels might induce degradation of the glycocalyx and kidney hypoperfusion, resulting in kidney microcirculation dysfunction. The application of dexamethasone reduced the degradation of the glycocalyx and improved perfusion of kidney. CONCLUSIONS: Dexamethasone protects the endothelial glycocalyx from inflammatory degradation possibly initiated by TNF-α during SAP. This is might be a significant discovery that helps to prevent tissue edema and hypoperfusion in the future.

Xuezhikang () reduced renal cell apoptosis in streptozocin-induced diabetic rats through regulation of Bcl-2 family.

OBJECTIVE: To investigate the effect of Xuezhikang (, XZK) on renal cell apoptosis in diabetic rats and the possible mechanism. METHODS: Sixty-six rats were randomly divided into 3 groups: the normal, model and XZK groups. In each group, the rats were further randomly divided into 3-month and 6-month subgroups, respectively. Diabetes of rats was induced by a single intraperitoneal injection of 1% streptozocin at 60 mg/kg body weight. Rats in the XZK group received gastric perfusion of XZK (1200 mg/kg body weight) everyday for 3 or 6 months, while rats in the normal and model groups received equal volume of saline. Twenty-four hours' urine was collected for urinary albumin excretion (UAE) measurement. Periodic acid-Schiff (PAS) and Masson's trichrome staining were used for saccharides and collagen detection. Cell apoptosis of renal cortex was investigated by TdT-mediated dUTP nick end labeling (TUNEL) staining. Bax and Bcl-2 expressions were detected by immunohistochemistry and Western blot, respectively. Cytochrome C (Cyt C) and caspase-9 concentration were detected by Western blot. RESULTS: Compared with the model group, XZK treatment could significantly decrease the kidney hypertrophy index, 24 h UAE, renal cell apoptosis, cytoplasmic Cyt C level and active caspase-9 level, as well as suppress the increment of Bax and up-regulate the expression of Bcl-2, leading to the suppression of Bax/Bcl-2 ratio at 3 and 6 months (P<0.05 or P<0.01). Moreover, XZK treatment could alleviate the deposition of PAS-stained saccharides and Masson's trichromestained collagen to different extent. CONCLUSIONS: Renal cell apoptosis was observed in diabetic kidney, in which mitochondrial apoptotic pathway might be involved. XZK treatment could attenuate pathological changes in diabetic kidney and reduce renal cell apoptosis, probably via the suppression of Bax/Bcl-2 ratio, which lead to inhibition of Cyt C release and following caspase-9 activation.

[Clinical features and risk factors of renal damage in elderly and non-elderly patients with type 2 diabetes mellitus].

OBJECTIVE: To investigate the clinical features and risk factors of renal damage in the elderly and non-elderly patients with type 2 diabetes mellitus. METHODS: The data were collected from a survey of 10-year retrospective study of chronic complications of hospitalized type 2 diabetics organized by Chinese Diabetes Society. A total of 1351 patients of type 2 diabetes were selected and divided into an elderly group (>or=60 year) and a non-elderly group (<60 year). The patients were also divided into three groups according to urinary albumin excretion rate (AER): normoalbuminuria group (AER<30 mg/24 h), microalbuminuria group (30or=300 mg/24 h). eGFR was estimated by the equation from the MDRD study. Clinical and laboratory parameters of all patients were analyzed. RESULTS: (1) The proportions of renal insufficiency in both normoalbuminuria and microalbuminuria groups of type 2 diabetes in the elderly patients were significantly higher than those in the non-elderly patients (26.7% vs 15.8%, P<0.01; 30.5% vs 21.3%, P<0.05 respectively); (2) in type 2 diabetic patients with renal insufficiency and normoalbuminuria, the diabetes duration (7.7 vs 3.8 years), systolic blood pressure [(146+/-24) mm Hg vs (134+/-23) mm Hg], diastolic blood pressure [(84+/-13) mm Hg vs (80+/-11) mm Hg], proportion of hypertension (37.8% vs 21.1%), diabetic retinopathy (34.1% vs 23.9%), cardiovascular diseases (31.6% vs 11.3%) and cerebrovascular disease (24.4% vs 9.9%) were significantly higher in the elderly group than in the non-elderly group (P<0.05 or 0.01); (3) multiple logistic regression analysis revealed that the duration of diabetes (OR=1.046, P=0.013) and systolic blood pressure (OR=1.014, P=0.002) were independently associated with renal insufficiency in the elderly type 2 diabetic patients with normoalbuminuria, whereas systolic blood pressure (OR=1.042, P=0.000) and 2-hour postprandial blood glucose (OR=1.048, P=0.002) were independent risk factors for renal insufficiency of non-elderly patients. CONCLUSION: The elderly type 2 diabetic patients are likely to suffer renal insufficiency initially from a lower glomerular filtration rate than the non-elderly patients. Systolic blood pressure is the main risk factor in both elderly and non-elderly type 2 diabetes with normoalbuminuria and a decreased renal function. Controlling blood pressure may delay the decline of renal function.

[Renal insufficiency and its associated factors in type 2 diabetic patients with normoalbuminuria.].

OBJECTIVE: To investigate the prevalence of renal insufficiency and its associated factors in type 2 diabetes mellitus with normoalbuminuria using estimated glomerular filtration rate (eGFR). METHODS: We retrospectively analyzed 10-year data of chronic complications in type 2 diabetics in-patient from the Chinese Diabetes Society. eGFR was estimated using the equation from Modification of Diet in Renal Disease (MDRD) study. The clinical characteristics as well as associated factors for low eGFR were analyzed among the normoalbuminuric type 2 diabetic patients. RESULTS: A total of 1351 type 2 diabetic patients were included, 755 patients with normoalbuminuria, 466 patients with microalbuminuria and 130 patients with macroalbuminuria respectively. Among the patients, 310 (22.9%) had low eGFR (GFR < 60 mlxmin(-1) x 1.73 m(-2)), 19.7% (149/755) in the patients with normoalbuminuria, 21.9% (102/466) in microalbuminuria and 45.4% (59/130) in macroalbuminuria. Patients with normoalbuminuria and low eGFR suffered more chronic complications than those with normoalbuminuria and normal eGFR, mainly retinopathy, cerebrovascular diseases and sensory neuropathy. Stepwise logistic regression analysis revealed that age (OR = 1.042, P < 0.001), diabetic duration (OR = 1.038, P = 0.045), systolic blood pressure (OR = 1.017, P < 0.001) were independently associated with renal impairment among the patients with normoalbuminuria. Body mass index (OR = 0.868, P < 0.001) and HbA1c (OR = 0.898, P = 0.021) were also related with renal insufficiency. CONCLUSION: A considerable proportion in type 2 diabetic patients without albuminuria may exist renal impairment, and eGFR estimation could benefit the evaluation of renal function in such patients.