Hypertension control is the most important and effective treatment for chronic kidney diseases.Compared with hypertension patients without kidney diseases,it requires a stricter blood pressure control in those with kidney diseases.The treatment principles are:(i)To lower the blood pressure is the top priority;and(ii)the impacts of various antihypertensive drugs on individual patients.The antihypertensive drugs should be chosen taking into consideration of the following factors:the extent of hypertension,whether the hypertension occurs abruptly or permanently,the heart and renal functions and any significant metabolic disorders.Among the existing drugs,diuretic is usually hampered by renal dysfunction;ACEI/ARB seems to be more effective on patients with proteinuria,but it should be used with caution in patients with severe renal insufficiency;CCB is effective and can quickly lower blood pressure,therefore it is an essential drug for hypertension treatment;?-blocker is not considered as a main drug for hypertension with kidney diseases.Combination use of anti-hypertensive drug is common to many CKD with hypertension,among them ACEI/ARB+diuretic,ACEI/ARG+CCB are the most common combinations.ACEI+ARB exhibit a better proteinuria reduction effect;however it is not indicated in patients with severe cardiovascular lesion.Hypertension treatment should take into consideration of individual differences and should be adjusted according to individual responses.Salt intake control also plays an important role in the successful treatment of hypertension with kidney diseases.

AIM To explore the effect of ACE inhibitor on early kidney hypertrophy and its mechanism in diabetic rats. METHODS Rats were randomly divided into three groups: uninephrectomized rats, streptozotocin induced diabetic rats and diabetic rats treated with benazepril (an ACE inhibitor, 10 mg?kg -1 ?d -1 , ig). Activity of ACE was determined by the fluorimetric assay. Expression of TGF? 1 mRNA and TGF? 1 and p21 CIP1 protein was measured by Northern blot analysis and Western blot analysis, respectively. RESULTS After 1 week, the diabetic rats developed a body weight loss, kidney weight/body weight increased and renal cortex ACE activity elevated despite a decrease in plasma ACE activity. Northern blot analysis showed that renal cortex TGF? 1 mRNA expression in the diabetic rats was enhanced by 1.3 times, compared with uninephrectomized rats. Western blot analysis showed that TGF? 1 and p21 CIP1 protein expression were also increased. Administration of benazepril for one week significantly suppressed kidney hypertrophy. ACE activity in the plasma, renal cortex and medulla was reduced by 89%,70% and 70 5%, respectively. Expression of TGF? 1 mRNA as well as expression of TGF? 1 and p21 CIP1 protein was reduced by 47 7%, 49 5% and 60 0%, respectively. CONCLUSION Our results suggest that the suppression of ACE inhibitor on diabetic kidney hypertrophy might partially be associated with a decrease in the expression of TGF? 1 and p21 CIP1 in diabetic rats renal cortex. However, its exact mechanism remains to be further explored.

AIM: To study effect of benazepril (an ACE inhibitor) on expression of insulin receptor (IR) and its substrate-1(IRS-1) protein in renal tissue cell membrane in diabetic rats. METHODS: The rats were randomly divided into following groups: control (n=6), streptozotocin induced diabetic (n=7) and diabetic treated with benazepril (n=7). Body weight, kidney weight and kidney weight/body weight were observed after 4 weeks of treatment. ACE activities in plasma, renal tissue were measured by the fluorimetric assay. The expressions of IR and IRS-1 protein were determined by Western blot analysis in renal tissue cell membrane. RESULTS: After 4 weeks of treatment, benazepril significantly ameliorated kidney hypertrophy in diabetic rats. ACE activities in plasma, renal tissue were redunced by approximately 92.00% and 88.77%, respectively. Western blot analysis showed that the expressions of IR and IRS-1 protein were increased by 2.1 and 1.5 folds in renal tissue cell membrane in diabetic rats. However, benazepril reduced expression of IR and IRS-1 protein by 45.74% and 47.66%, respectively. CONCLUSIONS: Increased expression of IR and IRS-1 protein might be related to abnormally active glucose metabolism in diabetic rat kidney. Down-regulation of expression of IR and IRS-1 protein might be one of important machnisms of Benazepril nephroprotection on diabetic rats.

Objective To probe the changes of RAGEmRNA expression in renal tissue of.streptozotocin (STZ)-induced diabetic rats. Methods Quantitative reverse transcription polymerase chain reaction (RT-PCR) was used in control rats and diabetic rats for 12 weeks. Results After 4 weeks of diabetes inducement, RACEmRNA level showed a continuous increase both in diabetic renal cortex and medulla. However, this enhancement could not be observed in 2 weeks of diabetes. In addition, after 8 weeks diabetic rats had significantly higher glycated Hb(GHb). Conclusion Gene expression of RAGE in renal tissue of diabetic rats is altered and the excessive gene expression of RAGE may enhance the AGEs-RAGE interactions which would contribute to the development of diabetic nephropathy. Furthermore, this change occurs as a result of hyperglycemia-induced AGEs formation.

Objective To investigate the expression of transforming growth factor ?_1(TGF?_1)in renal cortex from uninephrectomized diabetic rats. Methods Wistar rats were divided into uninephrectomized rats(group A), streptozotocin diabetic rat(group B). Blood glucose, serum insulin level and body weight, kidney weight, kidney weight/body weight as well as renal tissue protein contents were observed after 1, 4 weeks of streptozotocin injection. The expression of TGF?_1, precollagen 1?(Ⅳ) and fibronectin mRNA were measured by Northern blot analysis, and TGF?_1 protein by Western blot analysis in kidney cortex. In addition, ACE activities were determined by fluorimetric assay in plasma, kidney cortex and medulla. Results Group B demonstrated significantly elevated blood glucose and decreased serum insulin level. Kidney weight、kidney weight/body weight and renal tissue protein contents progressively increased despite total body weight loss. There was significant(P

Purpose To evaluate apoptosis in renal tissue of diffuse proliferative lupus nephritis and therelationship between the existence of apoptosis cells in renal tissue and histopathological or clinical changes.Methods Apoptosis was detected by in situ nick-end labeling techniques (TUNEL) in renal biopsies from 25patients with type Ⅳ LN, 12 patients with IgAN, 4 patients with MsPGN, and 3 patients with APSGN. Normalrenal tissue obtained at nephrectorny for hypemephroma in 4 adults was used as control. In addition, proliferatingcells were identified by proliferating cell nuclear antigen(PCNA) in these patients. Results Compared to otherproliferative glomerulonephritis and control,the patients with lupus nephritis had less apoptosis cells, higher ratio ofPCNA+ cells/TdT+ cells/(P/T) in renal tissues;Ratio of P/T in glomeruli and tubulointerstitium correlated withthe chronicity index, r=0. 498 3(P = 0. 013 2), r = 0. 839 9(P＜ 0.001 ), r = 0. 661 4(P = 0. 003 3),respectively. Ratio of P/T in glomerulus and tubule had positive correlation with 24 hour urinary protein, r =0.855 4(P＜0.001),r=0.713 4(P=0. 001); negative correlation with Ccr, r = - 0. 488 0(P =0. 013 3)and r = - 0. 722 9(P = 0. 001), which in tubules positively correlated with Scr, r = 0. 410 7 (P = 0.041 4 ).Conclusions Apoptosis is insufficient in proliferative lupus nephritis. Intense proliferation without followingincrease in apoptosis may be related to chronic progressive renal histopatholcgical changes.

Objective To study the effect of oxidative modification of hydrochlorous acid (HOCl) on human serum albumin (HSA) and the relationship between the AOPPs and HOCl-treated HSA. Methods Purified HSA (60 mg/ml) was treated with HOCl (0, 1, 5, 10, 20, 30, 40, 50 and 60 mmol/L). Size-exclusion chromatography was applied to estimate molecular weights of oxidized products of HSA by HOCl and spectrum scan from 190 nm -400 nm was performed to observe the spectrum characteristics of all variants of HSA. Results Major products of HSA after exposure to HOC1 were dimer and hexmer of HSA. The first-order process could be employed to describe the oxidative dynamics of monomer and dimer of HSA oxidized by HOCl. To AOPPs formation mediated by oxidant was identified as pseudo first-order reaction. However, formation hexmer was much in accordance with second-order reaction. Hexmer was also a major contributor to AOPPs in all types of modified HSA. Spectral analysis showed that red shift of absorbance maximum of polymers of HSA occurred, suggesting that a possibility that polymers of HSA were cross linked by tyrosine residues in protein. Conclusions Protein aggregation is primary consequence of HSA after its exposure to HOCl. Hexmer of HSA is the major contributor to AOPPs.

Uninephrectomy was performed in a ll rats of this study, and diabetic model was induced in partial rats by streptozo tocin. Then these rats were divided into uninephrectomy group, diabetes group an d benazepril-treated diabetes group. After 4 weeks, renal tubulo-interstitial morphological change was observed and type Ⅳ collagen, fibronectin and transfor ming growth factor ? 1 (TGF-? 1) proteins as well as TGF-? 1 mRNA were d etermined. The results suggested that benazepril played a protective role in ren al tubulo-interstitial injury, which was associated partially with down-regula ted overexpression of TGF-? 1.

Objective To investigate the expression and translocation of protein kinase C (PKC) ?Ⅱ isoform in renal tissue of diabetic rats and the effects of blocking renin-angiotensin system (RAS) on them. Methods Diabetic rats induced with streptozotocin were randomized to 4 groups. (1) Diabetic control without treatment. (2) Treatment with irbesartan (40 mg?kg -1 ?d -1 ). (3)Treatment with fosinopril (40 mg?kg -1 ?d -1 ) and (4) Treatment with a combination of irbesartan and fosinopril (20 mg?kg -1 ?d -1 each). Six normoglycemic rats served as normal control. After 4 weeks, blood glucose and insulin were measured and expression and translocation of PKC?Ⅱ in renal cortex and medulla were assessed by immunohistochemistry and Western blot. Results The expressions of total and membrane fraction in renal cortex of diabetic control rats weredecreasedto66.0%and50.0% of the values of normal control rats respectively (both P

AIM:To study the effects of astragali radix extract(ARE)on renal resistance to atrial natriuretic peptide(ANP)in rats with experimental nephrotic syndrome.METHODS:Male Sprague-Dawley rats were randomly divided into normal control,adriamycin nephropathy(ADR),ADR treated with ARE(2.5 g? kg-1? d-1)and ADR treated with benazepril(10 mg? kg-1? d-1).After 6 weeks,rats received intravenous infusion of 2% body weight isotonic saline.Urinary cGMP excretion(UcGMPV),plasma ANP level,renal PDE5 activity and protein expression were also detected.RESULTS:ARE increased UNaV while ACEI was not natriuretic.Nephrotic rats had a blunted natriuretic response and reduced rate of UcGMPV after volume expansion despite higher plasma ANP concentration.ARE increased UcGMPV and restored partly natriuretic response to volume expansion.The activity and protein abundance of renal PDE5 were high in nephrotic rats.ARE significantly reduced the PDE5 activity and protein expression.CONCLUSION:ARE may ameliorate the renal resistance to ANP in rats with adriamycin nephropathy by inhibiting the PDE5.