Prazosin Protects the Liver Against Renal Ischemia/Reperfusion Injury in Rats.

Acute kidney injury (AKI) is a common subsequent problem after many medical conditions. AKI is associated with distant organ dysfunction where systemic inflammation and oxidative stress play major roles. In this study, the effect of Prazosin, an α1-Adrenergic receptor antagonist, was investigated on the liver injury induced by kidney ischemia-reperfusion (I/R) in rats. Male adult Wistar rats (n=21) were divided into three groups: sham, kidney I/R, and kidney I/R pre-treated with Prazosin (1 mg/kg). Kidney I/R was induced by vascular clamping of the left kidney for 45 min to reduce the blood flow. Oxidative and antioxidant factors along with apoptotic (Bax, Bcl-2, caspase3), and inflammatory (NF-κß, IL-1ß, and IL-6) factors were measured in the liver at protein levels. Prazosin could reserve liver function (p<0.01) and increase glutathione level (p<0.05) after kidney I/R significantly. Malonil dialdehyde (MDA), a lipid peroxidation marker, was diminished more significantly in Prazosin-treated rats compared to the kidney I/R group (p<0.001). Inflammatory and apoptotic factors were diminished by Prazosin pre-treatment in the liver tissue (p<0.05). Pre-administration of Prazosin could preserve liver function and decrease its inflammatory and apoptotic factors under kidney I/R conditions.

The impact of gut microbiota on kidney function and pathogenesis.

Chronic kidney diseases (CKDs) are a global health problem. Besides diverse leading reasons in initiation and progression of CKDs, it is evident that they might largely originate from changes in the gut microbial community (microbiota). Mounting evidence indicates that a bidirectional relationship exists between host and microbiome in humans and animals with CKDs. Changes in the microbiota composition and structure (dysbiosis) produce excessive amounts of uremic toxins (e.g. indoxyl sulfate, p-cresyl sulfate and trimethylamine-N-oxide) but less reno-protective metabolites that are implicated in oxidative stress, uremia, inflammation, deterioration of kidney function, kidney diseases progression, a higher prevalence of cardiovascular risk, and mortality in patients with CKD. The present review focuses on the pathogenic association between gut microbiota and kidney diseases like CKD, IgA nephropathy, and kidney stone disease. Certainly, novel insights into the impact of the gut microbiota in kidney diseases can be helpful to develop therapeutic strategies in order to avoid and/or treat aforementioned conditions.

Circulating miR-150, miR-192, miR-200b, and miR-423-3p as Non-invasive Biomarkers of Chronic Allograft Dysfunction.

BACKGROUND AND AIMS: Chronic allograft dysfunction (CAD) is the major cause of renal allograft loss and can only be diagnosed by invasive histological examinations. The current study aimed to determine whether or not the circulating miR-125a, miR-150, miR-192, miR-200b, miR-423-3p and miR-433 could serve as predictors of graft outcome in the renal transplant recipients with CAD. METHODS: To evaluate the expression levels of miRNAs, we used quantitative real-time PCR (qPCR) and analyzed the plasma samples of 53 renal transplant recipients, including: 27 recipients with stable graft function (SGF), 26 recipients with biopsy-proven interstitial fibrosis and tubular atrophy (IFTA) and 15 healthy controls. Possible correlation between the clinicopathological parameters and the studied circulating miRNAs was also evaluated. RESULTS: miR-150 (p <0.001), miR-192 (p = 0.003), miR-200b (p = 0.048) and miR-423-3p (p <0.001) were differentially expressed between IFTA and SGF plasma samples. Creatinine correlated with miR-192 (r = 0.414, p = 0.036) and miR-423-3p (r = -0.431, p = 0.028). Moreover, the estimated glomerular filtration rate (eGFR) significantly correlated with the circulating miR-192 (r = -0.390, p = 0.049) and miR-423 (r = 0.432, p = 0.028). Receiver operating characteristic (ROC) analysis indicated that four miRNAs possessed the best diagnostic value for discriminating IFTA from SGF recipients with the areas under the curve (AUC) of 0.87 and high sensitivity and specificity values of 78% and 91%, respectively. CONCLUSIONS: The results suggest that aberrant plasma levels of these miRNAs are associated with the renal allograft dysfunction. Therefore, they are proposed to be considered as potential diagnostic biomarkers for monitoring of renal graft function.

BK virus nephropathy is not always alone.

INTRODUCTION: BK virus associated allograft nephropathy (BKVAN) is an important cause of allograft lost that often occurs in the first year of transplantation. The state of over immunosuppression also predispose these patients to various opportunistic viral infection Objectives: This research aimed to study the renal transplanted patients for BK viremia and BKVAN. PATIENTS AND METHODS: This observational study was conducted between January 2013 to December 2014 to study the renal transplanted patients for BK viremia and BKVAN. In our center patients received combination of de-sensitization therapy including antithymocyte globulin (ATG), rituximab (RITU), basiliximab, therapeutic plasma exchange, and methylprednisolone (MTP), in high risks or only MTP therapy in immunologically low risk patients. RESULTS: Of total number of 26 patients (20-52 years, M/F 17/9), seven patients received ATG and seven patient received intensive desensitizing protocols, BKVAN and BK viremia happened in three and two patients in above groups subsequently, only one patient developed BKVAN in low risk group. We also observed; cytomegalovirus (CMV) and parvovirus B19 infection and hemophagocytic syndrome (HPS), thrombotic microangiopathy (TMA) and endocarditis in our patients with BKVAN and BK viremia. CONCLUSION: Awareness about the possibility of BK virus nephropathy and appropriate immunosuppression minimization are crucial components of management. Consideration of other opportunistic infections and specific syndromes are also very important.