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The safety of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) used in hemodialysis (HD) patients was evaluated. Medline, Embase, the Cochrane Library, some databases of clinical trial registries, grey literatures, other reference lists of eligible articles and review articles for the randomized clinical trials (RCTs) on comparison of ACEIs/ARBs or placebo in HD patients were retrieved. RCTs reporting the risk of hyperkalemia by using ACEIs/ARBs in HD patients were selected. Eight articles met the eligibility criteria and were subjected to meta-analysis by using the Cochrane Collaboration's RevMan 4.2 software package. The results showed that there was no significant difference in hyperkalemia in HD patients between ACEIs or ARBs group and control group (ACEIs vs. control: RD=0.03, 95% CI=-0.13-0.18, Z=0.34, P=0.73; ARBs vs. control: RD=-0.02, 95% CI=-0.07-0.03, Z=0.75, P=0.45). However, there was no significant difference in the serum potassium between ACEIs or ARBs group and control group in HD patients (ACEIs vs. control: WMD=0.10, 95% CI=0.06-0.15, Z=4.64, P<0.00001; ARBs vs. control: WMD=-0.24, 95% CI=-0.37-0.11, Z=3.58, P=0.0003). The use of ACEIs or ARBs could not cause an increased risk of hyperkalemia in HD patients, however the serum potassium could be increased with use of ACEIs in HD patients. Therefore the serum potassium concentration should still be closely monitored when ACEIs are taken during the maintenance HD.
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In order to analyze the cai]ses of delayed diagnosis and raise the level of early diagnosis of atypical multiple myeloma (MM), the differences of presenting features between the patients presented to nephrologists and those presented to hematologists were compared. MM patients in our hospital were studied retrospectively. Those who referred renal impairment were divided into two groups: group I presented to nephrologists prior to MM diagnosis (n=29) and group II presented to hematologists directly (n=62). The age, sex, initial symptoms, haematological and biochemical parameters, the phenotype of paraprotein, bone marrow biopsy and cytology were undertaken and analyzed. The results showed that the median time between the initial symptoms and diagnosis in the patients of group I was longer than that in group II (P<0.001); patients in group I had significantly lower incidence of bone pain (P<0.01) and worse renal function (P<0.05) on presentation. There were lower level of myeloma cells (P<0.05), lower incidence of hypergammaglobulinemia (P<0.05), lower positive rate of monoclonal immunoglobulin (M protein) (P<0.05) and M protein level (P<0.05) in the patients of group I than those in group II. The ratio of monoclonal to lambda monoclonal proteins in a population was 1:3.67 in patients of group I, whereas 1:0.90 in patients of group II (P<0.01). Moreover, patients with λ type had a higher degree of renal insufficiency than those with κ type (P<0.05). It was suggested that the median time between the initial symptoms and diagnosis in the patients presented to nephrologists was longer than that in those presented to hematologists; the patients presented to nephrologists had the lower incidence of bone pain, lower level of myeloma cells and M protein, which made early diagnosis more difficult; more patients presented to nephrologists had the majority of λ light chain type, moreover, patients with λ light chain type had a higher incidence of renal insufficiency.
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Teaching urinary system diseases by problem-based learning method for eight-year program medical students was applied in nephrology department in affiliated Tongji hospital of Huazhong university of science and technology since 2008.They had accumulated experiences in compiling teaching plan,fostering teachers,practicing teaching and evaluating teaching.These steps may future intensify education reform on long schooling system and improve teaching quality of eight-year program.
RESUMO
The safety of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) used in hemodialysis (HD) patients was evaluated. Medline, Embase, the Cochrane Library, some databases of clinical trial registries, grey literatures, other reference lists of eligible articles and review articles for the randomized clinical trials (RCTs) on comparison of ACEIs/ARBs or placebo in HD patients were retrieved. RCTs reporting the risk of hyperkalemia by using ACEIs/ARBs in HD patients were selected. Eight articles met the eligibility criteria and were subjected to meta-analysis by using the Cochrane Collaboration's RevMan 4.2 software package. The results showed that there was no significant difference in hyperkalemia in HD patients between ACEIs or ARBs group and control group (ACEIs vs. control: RD=0.03, 95% CI=-0.13-0.18, Z=0.34, P=0.73; ARBs vs. control: RD=-0.02, 95% CI=-0.07-0.03, Z=0.75, P=0.45). However, there was no significant difference in the serum potassium between ACEIs or ARBs group and control group in HD patients (ACEIs vs. control: WMD=0.10, 95% CI=0.06-0.15, Z=4.64, P<0.00001; ARBs vs. control: WMD=-0.24, 95% CI=-0.37-0.11, Z=3.58, P=0.0003). The use of ACEIs or ARBs could not cause an increased risk of hyperkalemia in HD patients, however the serum potassium could be increased with use of ACEIs in HD patients. Therefore the serum potassium concentration should still be closely monitored when ACEIs are taken during the maintenance HD.
Assuntos
Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Antagonistas de Receptores de Angiotensina , Usos Terapêuticos , Inibidores da Enzima Conversora de Angiotensina , Usos Terapêuticos , Hiperpotassemia , Diálise RenalRESUMO
Objective To assess the renal protective effects of mycophenolate mofetil(MMF) in diabetic model rats and to explore its mechanism. Methods SD rats were divided randomly into there groups: control group,diabetic model group and diabetic group treated with MMF. In 12 weeks, blood glucose(BG), blood urea nitrogen(BUN), serum creatinine(Scr), index number of kidney hypertrophy(kidey weight to body weight, KW/BW),creatinine clearance(Ccr) and 24- hour urinary protein (24Upro) were detected. Kidney tissure were examined by microscopy. The protein exprssion of intercellular adhesion molecule-1 (ICAM-1) and proliferating cell nuclear antigen(PCNA) in renal tissure were determined by immunohistochemical technique. The mRNA expression of ICAM-1 in kidney tissure were semi-quantitatively determined with reverse transcription-polymerase chain reaction(RT-PCR). Results Compared with control group, BG、KW/BW、24Upro、BUN、Scr and Ccr were significantly increased in diabetic model rats(P
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The effects of benazepril on P42/44MAPK, angiotensin Ⅱ expression in renal tissue and renal pathological change of the experimental diabetic rats were assessed and the possible mechanism of benazepril's renoprotective effect was explored. Adult male Wistar rats, 11-12 weeks age,weighing initially 160 to 200 g were randomly allocated into 2 groups: control group (A, n=6) and experimental group (n= 12). Diabetic rats in experimental group were rendered diabetic by intraperitoneal injection of Streptozotocin (60 mg/kg body weight), and randomly subdivided into B group (diabetic control) and C group (diabetic rats treated with benazepril, 6 mg/kg every day).Studies were performed 8 weeks after induction of diabetes. Twenty-four h urine of every rat was collected to detect urine creatinine. Serum glucose concentration and serum creatinine were determined by collecting blood samples from the inferior vena cava. Body and kidney weight were recorded. Creatinine clearance (Ccr) and ratio of kidney weight to body weight were calculated. Plasma and renal tissue angiotensin Ⅱ concentration was assayed by radioimmunoassay (RIA). The phospo-p44/42MAPK protein expression was detected by Western-blot. The results showed that benazepril had no significant effect on the blood glucose level in diabetic rats in two experimental groups.Ccr and ratio of kidney weight to body weight were increased in group B (P＜0. 01) as coapared with normal rats at the end of the 8th week. At the end of the 8th week, Ccr in group C was lower than that in group B (P＜0.01). The ratio of kidney weight to body weight in group C was lower than that in group B at the 8th week. There were glomeruli hypertrophy and slight or moderate mesangium proliferation in diabetic rats, while there was fragmentally proliferative mesangium in group C at the end of the 8th week. Renal tissue angiotensin Ⅱ concentration was significantly increased in group B, while benazepril could significantly decrease the concentration of angiotensin Ⅱ in renal tissue. The expression of the phospo-p44/42MAPK protein in group B was increased as compared with group A, while it was decreased in group C as compared with group B. P42/44MAPK pathway participated in the pathogenesis of diabetic nephropathy. Benazepril can eliminate high filtration of glomeruli, decrease proteinuria, and eliminate renal hypertrophy as well as renal destruction. Renoprotective effect of benazepril in diabetic rats may be partly related to the inhibition of angiotensin Ⅱ -P42/44MAPK pathway.
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The apoptosis and the expression of tumor suppressor gene p53 in hypercholesterolemia (HC)-induced renal injury were investigated in rats. A high cholesterol diet (HCD)-induced HC rat model was made and serum lipid, urinary protein excretion (UPE) and N-aceto-β-D-glucosidase (NAG) were measured. The levels of malondialdehyde (MDA), as an index of lipid peroxidation, in renal cortex and serum were compared between the two diet groups. Apoptosis and p53 expression were determined by TUNEL and immunohistochemistry, respectively. In the HCD-induced HC group, serum total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C) as well astriglyceride (TG) were significantly increased, while the level of high density lipoprotein-cholesterol (HDL-C) decreased. Meanwhile, increased excretions of UPE and NAG in urine were observed, which were accompanied with a decrease in urinary creatinine clearance (Ccr) and indicated both glomerular and tubular damages. In addition, apoptotic cell death coexisted in the kidney, as revealed by increased TUNEL positive cells. Finally, an increase in p53 expression was observed in tubuli, but not in glomeruli. Both TUNEL positive cells and p53 expression were found to be correlated to the level of renal cortical MDA (r=0.817, P<0.01 and r=0.547, P<0.01, respectively). The major manifestation of HCD-induced renal injury is apoptosis. The lipid peroxidation is a critical event to induce DNA damage and p53 is involved in the pathogenesis of lipid-induced renal injury.