Humans ; Infectious Disease Transmission, Vertical ; prevention & control ; Kidney Diseases ; prevention & control ; virology ; Viruses ; pathogenicity

To investigate the effects of mycophenolate mofetil (MMF) on the process of renal interstitial fibrosis, unilateral ureteral obstruction (UUO) model was established in rats. Twenty Sprague-Dawley rats underwent UUO and received vehicle (n = 10) or MMF (20 mg.kg-1.d-1, by daily gastric gavage, n = 10) during a period of 5 days following surgery, and the additional 10 rats were served as sham-operated group. The rats were killed 5 days after surgery. Immunohistochemistry was performed on renal tissue for proliferating cell nuclear antigen (PCNA), alpha-smooth muscle actin (alpha-SMA) and type I and III collagen (col I, col III). Histological studies were also done by MASSON staining. Five days after surgery, proliferating cells in tubules, interstitium as well as interstitial myofibroblast (MyoF) infiltration and interstitial col I, col III deposition were all significantly reduced by MMF treatment. MMF also alleviated the histological changes of UUO rats. These results suggested that the reduction of interstitial MyoF infiltration may be an important event by which MMF prevents renal injury caused by UUO and MMF could be used to limit the progression of renal fibrosis.
Fibrosis ; Kidney/*pathology ; Kidney Diseases/etiology ; Kidney Diseases/pathology ; Kidney Diseases/*prevention & control ; Mycophenolic Acid/*analogs & derivatives ; Mycophenolic Acid/*pharmacology ; Random Allocation ; Rats, Sprague-Dawley ; Ureteral Obstruction/*complications

Child ; China ; Chronic Disease ; Congresses as Topic ; Humans ; Kidney Diseases ; prevention & control ; Kidney Failure, Chronic ; prevention & control ; Renal Insufficiency, Chronic ; prevention & control

Maintenance of healthy endothelium is essential to vascular homeostasis, and preservation of endothelial cell function is critical for transplant allograft function. Damage of microvascular endothelial cells is now regarded as a characteristic feature of acute vascular rejection and chronic allograft nephropathy, which is an important predictor of graft loss and is often associated with transplant vasculopathy. In this review, we will discuss the role of microvascular endothelium, in renal allograft dysfunction, particularly as it relates to markers of endothelial dysfunction and endothelial repair mechanisms. We also discuss the potential for therapies targeting endothelial dysfunction and transplant graft vasculopathy.
Humans ; Kidney/*blood supply ; *Kidney Transplantation ; Research Support, Non-U.S. Gov't ; Transplantation, Homologous ; Vascular Diseases/*prevention & control/*therapy

OBJECTIVETo lessen the occurrence of contrast-induced nephropathy (CIN), the preventive measures of CIN were reviewed.

DATA SOURCESThe data used in this review were from PubMed with relevant English articles and from Chinese Knowledge Information (CNKI) published from 1989 to 2009. The search terms were "contrast medium", "contrast-induced nephropathy" and "prevention". Articles involved in prevention of CIN were selected.

STUDY SELECTIONCIN is the third most common cause of acute kidney injury and is associated with an unfavorable prognosis. The best treatment is prophylaxis because CIN can not be reversed or ameliorated.

RESULTSThirty articles were included. Among various preventive measures, pericatheterization hydration is almost universally accepted as an appropriate and safe measure to prevent CIN, although there is no agreement as to composition, amount, and timing of hydration. Based on the use of concomitant nephrotoxic agents or high doses of contrast medium (CM) is one of risk factors for CIN, discontinuation of potentially nephrotoxic drugs 2 - 3 days before and after the procedure until renal function recover, and using the lowest possible dose of CM can decrease the risk of CIN. It is promising that removing the majority of CM from the coronary sinus, before it enters the systemic circulation, during coronary angiography can reduce the risk for CIN in animal studies and in limited clinical trials. Inconsistent data exist with respect to application of some vasodilators (endothelin antagonists and adenosine antagonists) and antioxidants (N-acetylcysteine and statins) in preventing CIN in high-risk patients, and new vasodilators and antioxidants continue to be tested.

CONCLUSIONSPericatheterization hydration, discontinuation of nephrotoxic drugs, and using the lowest possible dose of CM are effective measures to lessen the risk for CIN. Other prophylactic strategies and some drugs are promising, but further confirmation is required.

Contrast Media ; adverse effects ; Humans ; Iodine ; adverse effects ; Kidney Diseases ; chemically induced ; prevention & control

OBJECTIVEMatrine has an anti-fibrosis effect, such as hepatic cirrhosis and derma fibrosis, while its effect on glomerulosclerosis is unknown. The purpose of this study was to analyze the renoprotective effects of matrine on experimental glomerulosclerosis in rats and inquire into its mechanisms.

METHODSThe rats were randomly assigned to following groups: normal control group, model control group, benazepril treatment group, matrine 100 mg/kg treatment group and matrine 50 mg/kg treatment group. The rats of normal control group were subjected to sham operation and were injected with normal saline via the tail vein one week later. The rats of the other groups were uninephrectomized and injected with adriamycin (5 mg/kg) via the tail vein one week later. The dose of benazepril was 6 mg/kg. Both matrine and benazepril were given by gastric perfusion from the first day after the operation. The level of urinary protein was measured at the 2nd, 4th and 6th week after the operation. The serum total protein and albumin, serum creatinine, blood urea nitrogen (BUN) were tested only at the 6th week after operation. Renal pathology changes were evaluated at the 6th week as well. Immunohistochemistry was used to detect the expression of fibronectin (FN), laminin (LN), connective tissue growth factor (CTGF) and transforming growth factor-beta1 (TGF-beta1) in glomeruli.

RESULTSMatrine and benazepril not only reduced the excretion of urinary protein and the level of serum creatinine and BUN, but also significantly ameliorated glomerular mesangial proliferation and glomerular sclerosis (P < 0.05, respectively). Immunohistochemical staining indicated that there was an increasing FN, LN, CTGF and TGF-beta1 expression in model control group as compared to the three treatment groups (P < 0.05). Matrine 100 mg/kg treatment group and benazepril treatment group showed much more advantages than matrine 50 mg/kg treatment group (P < 0.05), but there was no significant difference between the former two groups (P > 0.05).

CONCLUSIONMatrine has a renoprotective effect on experimental glomerulosclerosis in rats, the possible mechanism might relate to the reduction of the TGF-beta1 negative function via CTGF, which will inhibit the activation and proliferation of glomerular intrinsic cells, decrease the secretion of ECM accordingly.

Alkaloids ; pharmacology ; Animals ; Benzazepines ; pharmacology ; Kidney ; drug effects ; Kidney Diseases ; prevention & control ; Kidney Glomerulus ; drug effects ; Protective Agents ; pharmacology ; Quinolizines ; pharmacology ; Rats ; Renal Agents ; pharmacology

Child ; Disease Progression ; Humans ; Kidney ; abnormalities ; physiopathology ; Kidney Diseases ; congenital ; physiopathology ; therapy ; Kidney Failure, Chronic ; etiology ; physiopathology ; prevention & control ; Ureteral Obstruction ; etiology ; physiopathology ; therapy

The nuclear hormone receptor PPARgamma is activated by several agonists, including members of the thiazolidinedione group of insulin sensitizers. Pleiotropic beneficial effects of these agonists, independent of their blood glucose-lowering effects, have recently been demonstrated in the vasculature. PPARgamma agonists have been shown to lower blood pressure in animals and humans, perhaps by suppressing the renin-angiotensin (Ang)-aldosterone system (RAAS), including the inhibition of Ang II type 1 receptor expression, Ang-II-mediated signaling pathways, and Ang-II-induced adrenal aldosterone synthesis/secretion. PPARgamma agonists also inhibit the progression of atherosclerosis in animals and humans, possibly through a pathway involving the suppression of RAAS and the thromboxane A2 system, as well as the protection of endothelial function. Moreover, PPARgamma-agonist-mediated renal protection, especially the reduction of albuminuria, has been observed in diabetic nephropathy, including animal models of the disease, and in non-diabetic renal dysfunction. The renal protective activities may reflect, at least in part, the ability of PPARgamma agonists to lower blood pressure, protect endothelial function, and cause vasodilation of the glomerular efferent arterioles. Additionally, anti-neoplastic effects of PPARgamma agonists have recently been described. Based on the multiple therapeutic actions of PPARgamma agonists, they will no doubt lead to novel approaches in the treatment of lifestyle-related and other diseases.
Animals ; Atherosclerosis/prevention & control ; Humans ; Hypertension/drug therapy ; Hypoglycemic Agents/*pharmacology ; Kidney Diseases/etiology ; PPAR gamma/*agonists ; PPAR-beta/agonists

AIMTo investigate the protective effect of low molecular weight heparin (LMWH) on nephropathy in rats with pregnancy induced hypertension and to study its possible mechanism.

METHODSThe levels of the expression of renal ERK1/2 protein and mRNA were detected in PIH rats which were made by injection of L-NAME, normal pregnant rats and rats treated with LMWH by immunohistochemistry, Western blotting and reverse transcription-polymerase chain reaction(RT-PCR). The renal tissue was observed by using light microscopy.

RESULTSThe expression level of renal ERK1/2 protein and mRNA in LMWH-treated rats were significantly lower than that in PIH rats, while the expression level of renal ERK1/2 protein and mRNA in PIH rats was significantly higher than that in normal pregnant rats (P < 0.01), the intensity of ERK1/2 expression had no obvious differences among 3 groups. The average arterial pressure and urine protein in LMWH group were decreased, but no decrease was observed in normal rats. Mesangial expansion and basal membrane thickening were obviously retarded in LMWH- treated group.

CONCLUSIONLMWH has renal protective effect on PIH rats, whose mechanism may be associated partly with a down-regulation of ERK expression.

Animals ; Female ; Heparin, Low-Molecular-Weight ; therapeutic use ; Hypertension, Pregnancy-Induced ; drug therapy ; pathology ; Kidney ; pathology ; Kidney Diseases ; etiology ; prevention & control ; Pregnancy ; Rats ; Rats, Wistar

OBJECTIVETo explore the effect of curcumin (CMN) on contrast-induced nephropathy (CIN) in rats and explore the potential mechanisms focusing on heme oxygenase-1 (HO-1) expression.

METHODSMale SD rats (n = 24) were randomly divided into four groups (n = 6 each): control group (group A), diatrizoate group (DTZ, group B), DTZ + CMN group (group C), DTZ + CMN + zinc protoporphyrin IX group (group D). All rats were fed with normal chow for 1 week, right kidney was excised under anesthesia and rats were fed with normal chow for another 4 weeks. Afterwards, rats in group A was fed with normal chow, and rats in group B to D were fed with low-salt diet. All rats were injected furosemide 2 mg×kg(-1)×d(-1) for 7 days intramuscularly. At the beginning of the 7(th) day, rats in group C were injected intramuscularly with CMN 20 mg/kg, rats in group D were injected with CMN (20 mg/kg) + zinc protoporphyrin IX (7.5 mg/kg) while rats in group A and B were injected with equal volume of physiological saline. At the end of the 7(th) day, indometacin (10 mg/kg) was injected into tail vein of all rats. One hour later, 60% DTZ (8 ml/kg) was injected to rats in the group B, C and D while equal volume saline was injected to rats in group A through common carotid artery. After 48 hours, blood was drawn from the hearts of deeply anesthetized rats and kidney tissue was obtained for histology, HO-1, Bax, Bcl-2 expression and the apoptotic index measurements.

RESULTSThe serum creatinine of group B, C and D [(83.67 ± 4.50) µmol/L, (63.67 ± 4.76) µmol/L, (104.17 ± 4.58) µmol/L] was significantly higher than that of group A [(41.50 ± 5.58) µmol/L, all P < 0.05], the serum creatinine was significantly higher in group B than in group C and lower than in group D (all P < 0.05). HO-1 expression of group B, C and D was significantly higher than that of group A (all P < 0.05), significantly higher in group C than in group B and D (all P < 0.05). HO-1 activity of group A, B and C was significantly higher than that of group D(all P < 0.05), HO-1 activity was significantly higher in group B than in group A and significantly lower in group B than in group C (all P < 0.05). Bax, Bcl-2 expression and apoptosis index of group B, C and D were significantly higher than that of group A (all P < 0.05), while Bcl-2/Bax of group B, C and D were significantly lower than that of group A (all P < 0.05). Bcl-2 and Bcl-2/Bax were significantly higher while apoptosis index was significantly lower in group C than in group B (all P < 0.05). Bax and apoptosis index were significantly higher and Bcl-2, Bcl-2/Bax were significantly lower in group D than in group B (all P < 0.05).

CONCLUSIONCMN could protect against contrast-induced nephropathy through reducing renal cell apoptosis via upregulating HO-1 expression and activating HO-1 activity in rats.

Animals ; Contrast Media ; administration & dosage ; Curcumin ; pharmacology ; Disease Models, Animal ; Heme Oxygenase (Decyclizing) ; metabolism ; Kidney ; metabolism ; Kidney Diseases ; chemically induced ; prevention & control ; Male ; Rats ; Rats, Sprague-Dawley