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UROLOGY, NEPHROLOGY AND ANDROLOGY (155 journals)                     

Showing 1 - 155 of 155 Journals sorted alphabetically
Acta Urológica Portuguesa     Open Access   (Followers: 1)
Actas Urológicas Españolas     Full-text available via subscription   (Followers: 3)
Actas Urológicas Españolas (English Edition)     Full-text available via subscription   (Followers: 1)
Advances in Chronic Kidney Disease     Full-text available via subscription   (Followers: 11)
Advances in Urology     Open Access   (Followers: 13)
African Journal of Nephrology     Open Access  
African Journal of Urology     Open Access   (Followers: 7)
AJP Renal Physiology     Hybrid Journal   (Followers: 8)
Aktuelle Urologie     Hybrid Journal   (Followers: 11)
American Journal of Kidney Diseases     Hybrid Journal   (Followers: 42)
American Journal of Men's Health     Open Access   (Followers: 9)
American Journal of Nephrology     Full-text available via subscription   (Followers: 36)
Andrologia     Hybrid Journal   (Followers: 2)
Andrology     Hybrid Journal   (Followers: 4)
Andrology & Gynecology : Current Research     Hybrid Journal   (Followers: 4)
Andrology and Genital Surgery     Open Access   (Followers: 7)
Andrology-Open Access     Open Access  
Annales d'Urologie     Full-text available via subscription  
Arab Journal of Nephrology and Transplantation     Open Access   (Followers: 1)
Arab Journal of Urology     Open Access   (Followers: 7)
Archives of Clinical Nephrology     Open Access   (Followers: 2)
Archivio Italiano di Urologia e Andrologia     Open Access   (Followers: 1)
Archivos Españoles de Urología     Open Access  
Asian Journal of Andrology     Open Access   (Followers: 1)
Asian Journal of Urology     Open Access   (Followers: 3)
Bangladesh Journal of Urology     Open Access   (Followers: 5)
BANTAO Journal     Open Access  
Basic and Clinical Andrology     Open Access  
BJU International     Hybrid Journal   (Followers: 35)
BMC Nephrology     Open Access   (Followers: 9)
BMC Urology     Open Access   (Followers: 15)
Canadian Journal of Kidney Health and Disease     Open Access   (Followers: 6)
Canadian Urological Association Journal     Open Access   (Followers: 2)
Cancer Urology     Open Access   (Followers: 2)
Cardiorenal Medicine     Full-text available via subscription   (Followers: 1)
Case Reports in Nephrology     Open Access   (Followers: 5)
Case Reports in Nephrology and Dialysis     Open Access   (Followers: 9)
Case Reports in Urology     Open Access   (Followers: 12)
Clinical and Experimental Nephrology     Hybrid Journal   (Followers: 4)
Clinical Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 19)
Clinical Medicine Insights : Urology     Open Access   (Followers: 3)
Clinical Nephrology     Full-text available via subscription   (Followers: 8)
Clinical Nephrology and Urology Science     Open Access   (Followers: 6)
Clinical Queries: Nephrology     Hybrid Journal   (Followers: 1)
Cuadernos de Cirugía     Open Access   (Followers: 3)
Current Opinion in Nephrology & Hypertension     Hybrid Journal   (Followers: 10)
Current Opinion in Urology     Hybrid Journal   (Followers: 12)
Current Urology     Open Access   (Followers: 10)
Current Urology Reports     Hybrid Journal   (Followers: 5)
Der Nephrologe     Hybrid Journal  
Der Urologe     Hybrid Journal   (Followers: 7)
EMC - Urología     Full-text available via subscription  
Enfermería Nefrológica     Open Access   (Followers: 1)
European Urology     Full-text available via subscription   (Followers: 38)
European Urology Focus     Hybrid Journal   (Followers: 6)
European Urology Supplements     Full-text available via subscription   (Followers: 15)
Forum Nefrologiczne     Full-text available via subscription  
Geriatric Nephrology and Urology     Hybrid Journal   (Followers: 7)
Giornale di Clinica Nefrologica e Dialisi     Open Access  
Herald Urology     Open Access   (Followers: 2)
Hong Kong Journal of Nephrology     Open Access   (Followers: 3)
Human Andrology     Partially Free   (Followers: 2)
IJU Case Reports     Open Access  
Indian Journal of Nephrology     Open Access   (Followers: 2)
Indian Journal of Urology     Open Access   (Followers: 5)
International Brazilian Journal of Urology     Open Access   (Followers: 5)
International Journal of Nephrology     Open Access   (Followers: 2)
International Journal of Nephrology and Renovascular Disease     Open Access   (Followers: 2)
International Journal of Urology     Hybrid Journal   (Followers: 12)
International Urology and Nephrology     Hybrid Journal   (Followers: 7)
Jornal Brasileiro de Nefrologia     Open Access  
Journal für Urologie und Urogynäkologie/Österreich     Hybrid Journal  
Journal of Clinical Nephrology     Open Access   (Followers: 1)
Journal of Clinical Urology     Hybrid Journal   (Followers: 14)
Journal of Endoluminal Endourology     Open Access  
Journal of Endourology     Hybrid Journal   (Followers: 2)
Journal of Endourology Case Reports     Hybrid Journal  
Journal of Genital System & Disorders     Hybrid Journal   (Followers: 3)
Journal of Integrative Nephrology and Andrology     Open Access   (Followers: 2)
Journal of Kidney Cancer and VHL     Open Access  
Journal of Lower Genital Tract Disease     Hybrid Journal  
Journal of Nephrology     Hybrid Journal   (Followers: 4)
Journal of Nephrology Research     Open Access   (Followers: 3)
Journal of Pediatric Nephrology     Open Access   (Followers: 3)
Journal of Renal Care     Hybrid Journal   (Followers: 8)
Journal of Renal Nursing     Full-text available via subscription   (Followers: 12)
Journal of Renal Nutrition     Hybrid Journal   (Followers: 29)
Journal of Renal Nutrition and Metabolism     Open Access   (Followers: 1)
Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 27)
Journal of The Egyptian Society of Nephrology and Transplantation     Open Access  
Journal of Translational Neurosciences     Open Access  
Journal of Urology     Full-text available via subscription   (Followers: 53)
Journal of Urology & Nephrology     Open Access   (Followers: 2)
Kidney Disease and Transplantation     Open Access   (Followers: 4)
Kidney Diseases     Open Access   (Followers: 3)
Kidney International     Hybrid Journal   (Followers: 44)
Kidney International Reports     Open Access   (Followers: 3)
Kidney Medicine     Open Access  
Kidney Research Journal     Open Access   (Followers: 6)
Kidneys (Počki)     Open Access   (Followers: 1)
Nature Reviews Nephrology     Full-text available via subscription   (Followers: 19)
Nature Reviews Urology     Full-text available via subscription   (Followers: 13)
Nefrología (English Edition)     Open Access  
Nefrología (Madrid)     Open Access  
Nephro-Urology Monthly     Open Access   (Followers: 1)
Nephrology     Hybrid Journal   (Followers: 12)
Nephrology Dialysis Transplantation     Hybrid Journal   (Followers: 25)
Nephron     Hybrid Journal   (Followers: 4)
Nephron Clinical Practice     Full-text available via subscription   (Followers: 4)
Nephron Experimental Nephrology     Full-text available via subscription   (Followers: 4)
Nephron Extra     Open Access   (Followers: 1)
Nephron Physiology     Full-text available via subscription   (Followers: 4)
Neurourology and Urodynamics     Hybrid Journal   (Followers: 1)
OA Nephrology     Open Access   (Followers: 2)
Open Access Journal of Urology     Open Access   (Followers: 6)
Open Journal of Nephrology     Open Access   (Followers: 5)
Open Journal of Urology     Open Access   (Followers: 7)
Open Urology & Nephrology Journal     Open Access  
Pediatric Urology Case Reports     Open Access   (Followers: 7)
Portuguese Journal of Nephrology & Hypertension     Open Access   (Followers: 1)
Progrès en Urologie     Full-text available via subscription  
Progrès en Urologie - FMC     Full-text available via subscription  
Prostate Cancer and Prostatic Diseases     Hybrid Journal   (Followers: 6)
Renal Failure     Open Access   (Followers: 12)
Renal Replacement Therapy     Open Access   (Followers: 4)
Research and Reports in Urology     Open Access   (Followers: 4)
Revista de Nefrología, Diálisis y Trasplante     Open Access   (Followers: 1)
Revista Mexicana de Urología     Open Access   (Followers: 1)
Revista Urologia Colombiana     Open Access  
Saudi Journal of Kidney Diseases and Transplantation     Open Access   (Followers: 2)
Scandinavian Journal of Urology     Hybrid Journal   (Followers: 8)
Seminars in Nephrology     Hybrid Journal   (Followers: 11)
The Prostate     Hybrid Journal   (Followers: 8)
Therapeutic Advances in Urology     Open Access   (Followers: 4)
Trends in Urology & Men's Health     Partially Free   (Followers: 1)
Ukrainian Journal of Nephrology and Dialysis     Open Access   (Followers: 1)
Uro-News     Hybrid Journal   (Followers: 2)
Urolithiasis     Hybrid Journal   (Followers: 2)
Urologia Internationalis     Full-text available via subscription   (Followers: 2)
Urologia Journal     Hybrid Journal  
Urologic Clinics of North America     Full-text available via subscription   (Followers: 4)
Urologic Nursing     Full-text available via subscription   (Followers: 4)
Urologic Radiology     Hybrid Journal  
Urological Science     Open Access  
Urologicheskie Vedomosti     Open Access  
Urologie in der Praxis     Hybrid Journal  
Urologie Scan     Hybrid Journal  
Urology     Hybrid Journal   (Followers: 34)
Urology Annals     Open Access   (Followers: 4)
Urology Case Reports     Open Access   (Followers: 3)
Urology Practice     Full-text available via subscription   (Followers: 2)
Urology Times     Free   (Followers: 3)
Urology Video Journal     Open Access   (Followers: 1)
World Journal of Nephrology and Urology     Open Access   (Followers: 15)
World Journal of Urology     Hybrid Journal   (Followers: 12)

           

Similar Journals
Journal Cover
Nephron Experimental Nephrology
Number of Followers: 4  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 1660-2129 - ISSN (Online) 1660-2129
Published by Karger Homepage  [120 journals]
  • Macrophage Depletion Ameliorates Glycerol-Induced Acute Kidney Injury in
           Mice
    • Abstract: Background: This study was conducted to elucidate the role of renal macrophages in the development of acute kidney injury (AKI) in a glycerol (Gly)-induced rhabdomyolysis mouse model. Methods: The experimental model of rhabdomyolysis requires injecting 50% Gly (10 ml/kg) intramuscularly into mice. Control mice were injected into the tail vein with the liposomal vehicle. Liposome-encapsulated clodronate (LEC)-only mice were injected with LEC. Gly-only mice were injected with Gly into a hind limb. LEC+Gly-treated mice were injected intravenously with 100 µl of LEC 24 h prior to Gly injection. Mice were sacrificed 24 h after Gly injection. Results: Gly injection increased the serum creatinine level, and induced tubular damage. Renal CD45+CD11b+Ly6c+ or CD45+CD11b+Ly6c+F4/80+ macrophages were decreased by pretreatment with LEC in both normal and injured kidneys. Macrophage depletion prevented Gly-induced apoptotic death of tubular epithelial cells by decreasing caspase-9, ERK and p53, while increasing Bcl-2 expression. Expression of the inflammatory mediators NF-#954;B, MCP-1, ICAM-1, iNOS and COX-2 were also decreased with LEC pretreatment of mice injected with Gly. Conclusion: These results support the hypothesis that depletion of macrophages prevents renal dysfunction by abrogating apoptosis and attenuating inflammation during AKI.
      Nephron Exp Nephrol 2014;128:21-29
      PubDate: Wed, 05 Nov 2014 00:00:00 +010
       
  • Contents Vol. 128, 2014
    • Abstract:
      Nephron Exp Nephrol 2014;128:I-VI
       
  • Inhalation of Hydrogen Gas Is Beneficial for Preventing Contrast-Induced
           Acute Kidney Injury in Rats
    • Abstract: Background: The present study aimed at investigating the effect of a novel antioxidant, hydrogen (H2) gas, on the severity of contrast-induced acute kidney injury (CIAKI) in a rat model. Methods: CIAKI was induced in rats by intravenous injection of a contrast medium, Ioversol, in addition to reagents inhibiting prostaglandin and nitric oxide synthesis. During the injection of these reagents, the rats inhaled H2 gas or control gas. Results: One day after the injection, serum levels of urea nitrogen were significantly lower in H2 gas-inhaling CIAKI rats (17.6 ± 2.3 mg/dl) than those in control gas-treated CIAKI rats (36.0 ± 7.3 mg/dl), although they both were elevated as compared to untreated rats (14.9 ± 0.9 mg/dl). Consistently, creatinine clearance in H2 gas-treated CIAKI rats was higher than that in control gas-treated counterparts. Renal histological analysis revealed that the formation of proteinaceous casts and tubular necrosis was improved by H2 gas inhalation. Mechanistic analyses showed that inhalation of H2 gas significantly reduced renal cell apoptosis, expression of cleaved caspase 3, and expression of an oxidative stress marker, 8-hydroxydeoxyguanosine, in injured kidneys. Conclusion: Results suggest that H2 gas inhalation is effective in ameliorating the severity of CIAKI in rats by reducing renal cell apoptosis and oxidative stress.
      Nephron Exp Nephrol 2014;128:116-122
       
  • Stimulation of Cyclooxygenase 2 Expression in Rat Peritoneal Mesothelial
           Cells
    • Abstract: Objective: Since peritoneal dialysis causes peritoneal fibrosis, we examined how glucose (osmotic factor), mannitol (osmotic control), and angiotensin II (AngII) regulate proinflammatory cyclooxygenase 2 (COX-2) in primary rat peritoneal mesothelial cells. Materials and Methods: For this study, we used the following material (n = 4-8 cell lines): cells, passages 1-2; 125I-AngII receptor surface binding (AT1R antagonist losartan, AT2R antagonist PD123319; both 10 µM); intracellular calcium probe calcium-5; COX-2 immunoblotting (ß-actin normalized); real-time PCR of COX-2 gene PTGS2, and NF-#954;B inhibitor Ro-1069920 (5 µM). Results: AngII surface receptors were predominantly AT1R (minimally AT2R). AngII and glucose increased COX-2 protein expression concentration dependently; mannitol also increased COX-2 expression. Maximal COX-2 protein expression was observed after 6 h (AngII) and 24 h (glucose, mannitol). The time course of increases in PTGS2 mRNA levels reflected that of COX-2 protein expression. At optimal exposure conditions (time/concentration), glucose was 5-fold more efficacious in stimulating COX-2 protein expression than AngII or mannitol. Losartan fully inhibited COX-2 protein responses to AngII and mannitol, but minimally inhibited responses to glucose. Ro-1069920 fully inhibited COX-2 protein responses to each effector. Conclusion: AngII, glucose, and osmotic stress (mannitol) activate COX-2; NF-#954;B may be an ideal site for COX-2 blockade, and COX-2 activation by osmotic stress requires AT1R, but activation by glucose is more robust and mechanistically complex.
      Nephron Exp Nephrol 2014;128:89-97
       
  • Polyuria in Hantavirus Infection Reflects Disease Severity and Is
           Associated with Prolonged Hospital Stay: A Systematic Analysis of 335
           Patients from Southern Germany
    • Abstract: Background/Aims: Puumala virus (PUUV) infection leads to nephropathia epidemica (NE), especially in endemic areas in Central Europe. The clinical course of NE is characterized by acute kidney injury (AKI) with thrombocytopenia followed by polyuria to a different degree. The prevalence of polyuria and its associated risk factors have not been reported in a large cohort of NE patients. Methods: Clinical and laboratory data during the acute phase of the disease were obtained from the medical reports and files of 335 patients who received in-hospital treatment during acute hantavirus infection. Comprehensive statistical models were developed to estimate the probability of polyuria. Results: The median age at diagnosis was 47 years (interquartile range, IQR 40-59) and 48% of the patients developed polyuria with a urinary output of 5,100 ml/day (IQR 4,200-7,300). The hospital stay was significantly longer in the polyuric group compared to the nonpolyuric group [8 days (IQR 6-10) vs. 6 days (IQR 5-8); p = 0.04]. Using logistic regression analysis, male gender (odds ratio, OR = 1.6; 95% confidence interval, CI 1.05-2.58; p = 0.03), oliguria/anuria during NE (OR = 2.56; 95% CI 1.65-4.01; p < 0.001), severe AKI (OR = 1.87; 95% CI 1.22-2.9; p < 0.001), and hematuria (OR = 1.78; 95% CI 1.02-3.15; p = 0.04) were significantly associated with the development of polyuria. In a multivariate model, the probability of polyuria was 0.19 (SEM ± 0.05) in female patients presenting with mild/moderate AKI without anuria/oliguria. Conclusions: Almost 50% of hospitalized NE patients developed polyuria, which was associated with a prolonged hospital stay. The probability of the development of polyuria was lowest in female patients with mild/moderate, non-oliguric/anuric AKI.
      Nephron Exp Nephrol 2014;128:111-115
       
  • Beneficial Effects of AMP-Activated Protein Kinase Agonists in Kidney
           Ischemia-Reperfusion: Autophagy and Cellular Stress Markers
    • Abstract: Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK), where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However, whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1 g/kg) and metformin (0.3 g/kg), were administered 24 h prior to ischemia, with kidneys harvested at 24 h of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mammalian target of rapamycin (mTOR) C1 activity and p62/SQSTM1 expression. These results led us to propose that AMPK and autophagy are insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress-responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis, contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion.
      Nephron Exp Nephrol 2014;128:98-110
       
  • Wnt5a Is Necessary for Normal Kidney Development in Zebrafish and Mice
    • Abstract: Background: Wnt5a is important for the development of various organs and postnatal cellular function. Little is known, however, about the role of Wnt5a in kidney development, although WNT5A mutations were identified in patients with Robinow syndrome, a genetic disease which includes developmental defects in kidneys. Our goal in this study was to determine the role of Wnt5a in kidney development. Methods: Whole-mount in situ hybridization was used to establish the expression pattern of Wnt5a during kidney development. Zebrafish with wnt5a knockdown and Wnt5a global knockout mice were used to identify kidney phenotypes. Results: In zebrafish, wnt5a knockdown resulted in glomerular cyst formation and dilated renal tubules. In mice, Wnt5a global knockout resulted in pleiotropic, but severe, kidney phenotypes, including agenesis, fused kidney, hydronephrosis and duplex kidney/ureter. Conclusions: Our data demonstrated the important role of Wnt5a in kidney development. Disrupted Wnt5a resulted in kidney cysts in zebrafish and pleiotropic abnormal kidney development in mice.
      Nephron Exp Nephrol 2014;128:80-88
       
  • Protective Effects of Relaxin against Cisplatin-Induced Nephrotoxicity in
           Rats
    • Abstract: Background: Cisplatin (CDDP)-induced acute kidney injury (AKI) involves pro-inflammatory responses, apoptosis of renal tubular epithelial cells and vascular damage. AKI increases the risk of chronic kidney disease. Relaxin (RLX) has anti-apoptotic and anti-fibrosis properties. The aim of this study was to investigate the effects of RLX on CDDP-induced nephrotoxicity. Methods: We investigated the mitigating effects of RLX based on the etiopathology of AKI induced by CDDP, and also the anti-fibrotic effect of RLX on renal fibrosis after AKI. In the short-term experiments, rats were divided into the control group, CDDP group, and CDDP+RLX group. In the latter group, RLX was infused for 5 or 14 days using an implanted osmotic minipump. CDDP was injected intraperitoneally (6 mg/kg) after RLX or saline infusion. At 5 and 14 days post-CDDP, the kidneys were removed for analysis. The effect of RLX on renal fibrosis after AKI was evaluated at 6 weeks post-CDDP. Results: In short-term experiments, CDDP transiently increased plasma creatinine and blood urea nitrogen with peaks at day 5, and RLX prevented such rises. Semiquantitative analysis of the histological lesions indicated marked structural damage and apoptotic cells in the CDDP group, with the lesions being reduced by RLX treatment. Overexpression of Bax, interleukin-6 and tumor necrosis factor-α observed in the kidneys of the CDDP group was reduced in the CDDP+RLX group. In the long-term experiments, RLX significantly reduced renal fibrosis compared with the CDDP group. Conclusions: The results suggested that RLX provided protection against CDDP-induced AKI and subsequent fibrosis by reducing apoptosis and inflammation.
      Nephron Exp Nephrol 2014;128:9-20
       
  • Multiple Mechanisms in Renal Artery Stenosis-Induced Renal Interstitial
           Fibrosis
    • Abstract: Background/Aims: Renal artery stenosis (RAS), which may lead to renal fibrosis, is a common cause of end-stage renal disease in elderly patients. However, the potential mechanisms leading to the development of renal fibrosis and atrophy have not been clarified. Methods: A two-kidney, one-clip Goldblatt mouse model was established in the present study. Blood pressure, morphological and pathological alterations were examined on days 7, 14, and 28 after surgery. Peritubular capillary loss and pericyte changes after injury were evaluated. Inflammatory macrophage infiltration and Wnt/β-catenin signaling were also investigated. Results: A significant increase in blood pressure and obvious renal atrophy were observed on days 7, 14, and 28 after surgery. Following surgery, the clipped kidneys developed aggravated interstitial fibrosis and tubular epithelial injury over time. Moreover, RAS induced obvious peritubular capillary loss and inflammatory macrophage infiltration. Increased pericyte number was found in the clipped kidneys, but these cells detached from the endothelial cells and migrated to the interstitium. Wnt/β-catenin signaling was also significantly upregulated in the clipped kidneys after surgery. Conclusion: Our study provides a novel insight into the mechanisms linking peritubular capillary loss and pericyte changes in RAS-induced renal fibrosis. Our findings also suggest that inflammatory macrophages and Wnt/β-catenin signaling participate in these pathological processes. Therefore, multi-target therapeutic strategies may significantly contribute to the prevention of renal interstitial fibrosis and the preservation of renal function in patients with RAS.
      Nephron Exp Nephrol 2014;128:57-66
       
  • Increased Macrophage Activation Inhibited by Tacrolimus in the Kidney of
           Diabetic Rats
    • Abstract: Background/Aims: Accumulating evidence suggests that macrophage-induced inflammation may be the mechanism of development and progression of diabetic nephropathy. A previous study by our group has shown that tacrolimus, like cyclosporin A, has a renoprotective effect in diabetic rats. The present study aimed to elucidate the underlying molecular events. Methods: Diabetic rats were induced by using streptozotocin. Diabetic rats were subjected to oral tacrolimus treatment at a dose of 0.5 or 1.0 mg/kg daily for 4 weeks. Body weight, blood glucose, hemoglobin A1c (HbA1c) and renal pathology were assessed, followed by analyses of renal calcineurin (CaN) expression, changes in renal macrophage infiltration, proliferation and activation, and detection of renal TLR2+ and TLR4+ as well as NF-#954;B-p-p65+ in macrophages. Results: Diabetic rats had a reduced body weight and increased blood glucose and HbA1c levels, whereas tacrolimus treatment did not affect body weight or blood glucose and HbA1c. Increased relative kidney weight was only significantly reduced by tacrolimus treatment at a dose of 1.0 mg/kg, while the elevated albumin excretion rate was markedly attenuated after treatment with tacrolimus (0.5 and 1.0 mg/kg) in diabetic rats. Elevated glomerular volume was significantly attenuated by tacrolimus treatment with 0.5 and 1.0 mg/kg, and increased indices for tubulointerstitial injury were only ameliorated by tacrolimus treatment with 1.0 mg/kg. Western blot data showed that expression of CaN protein was induced 2.4-fold in the kidneys of positive control diabetic rats, whereas tacrolimus treatment at 0.5 and 1.0 mg/kg doses reduced the increased expression of CaN protein by 38.0 and 73.2%, respectively. Histologically there was a marked accumulation of ED-1+ cells (macrophages) in diabetic kidneys and tacrolimus treatment failed to inhibit it. In contrast, tacrolimus treatment at 0.5 and 1.0 mg/kg doses significantly inhibited the elevated ED-1+/PCNA+ cells and ED-1+/iNOS+ cells in the kidneys of diabetic rats, while tacrolimus treatment at a dose of 0.5 or 1.0 mg/kg significantly suppressed the increased ED-1+/TLR2+ cells, ED-1+/TLR4+ cells and ED-1+/NF-#954;B-p-p65+ cells in the kidneys of diabetic rats. Conclusion: The data from the current study demonstrated that tacrolimus could ameliorate early renal injury through a mechanism to suppress macrophage activation.
      Nephron Exp Nephrol 2014;128:46-56
       
 
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