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Background The most common and pernicious complication of Familial Mediterranean fever (FMF) is renal amyloidosis, usually affecting the kidneys, leading to end-stage renal failure. FMF-related renal amyloidosis needed to be diagnosed early. Optimal colchicine dose is effective in preventing and reversing renal amyloidosis. Galectin-3, profibrotic mediator, has regulatory functions in inflammation, fibrosis and tumorigenesis. Galectin-3 is a strong prognostic marker for heart failure. Galectin-3 plays role in diabetic nephropathy and chronic kidney disease. The aim of the study is to investigate whether galectin-3 is related to proteinuria and amyloidosis in FMF. Methods Seventy-five FMF patients who have no exclusion criteria and healthy controls ( n  = 36) were included. Serum galectin-3 was measured and morning spot urine was collected for determination of the protein/creatinine ratio (PCR). Results Serum Galectin-3 levels were significantly higher in FMF patients than the control group [969.66 (3825) pg/mL vs. 238 (921) pg/mL, respectively; P <0.001]. We classified into two groups: Group1 ( n  = 48) had FMF patients with proteniuria, Group2 ( n  = 27) had FMF patients without proteinuria. Group1 had higher levels of galectin-3 than Group2 [1106(3812) pg/mL vs. 867.3(1433) pg/mL, P  < 0.001]. Galectin-3 levels were correlated with PCR in whole group and FMF group ( r  = 0.785, P  < 0.001 and r  = 0.803, P  < 0.001). In ROC curve, best cutoff value = 581.50 pg/mL was used to detect proteinuria (sensitivity = 91.7 %, specificity = 71.4 %, AUC = 0.879) and optimal cutoff value = 1458.00 pg/mL was an indicator of nephrotic-range proteinuric (sensitivity = 100 %, specificity = 92.1 %, AUC = 0.983). Conclusion Galectin-3 is associated with proteinuria and renal amyloidosis in FMF. Galectin-3 may play role in pathogenesis of amyloidosis.

Objectives Renal ischemia followed by reperfusion leads to acute renal failure in both native kidneys and renal allograft. We investigated the effect of curcumin on ischemia-reperfusion (I/R) injury and the antioxidant effects of curcumin in rats. Methods Thirty rats were randomly divided into five experimental groups (control, sham, curcumin, I/R and I/R + curcumin, n  = 6 each). Curcumin was administered (200 mg kg −1 ) orally to curcumin and I/R + curcumin groups for 7 days. Then, the rats were subjected to bilateral renal ischemia for 45 min and followed by reperfusion for 24 h. All rats were killed and kidney function tests, serum and tissue nitric oxide (NO), protein carbonyl (PC), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels were determined. Histopathological examinations were also performed. Results Curcumin significantly improved the urea and cystatin C levels in I/R + curcumin group compared to I/R group ( p  < 0.05). Reduction of serum GSH-Px was significantly improved by curcumin ( p  < 0.001), but SOD enzyme activity did not alter ( p  > 0.05). Treatment with curcumin also resulted in significant reduction in serum and tissue MDA, NO and PC and for tissue that were increased by renal I/R injury ( p  < 0.001 for serum and p  < 0.05 for tissue, respectively). In histological examination, the rats treated with curcumin had nearly normal morphology of the kidney. Conclusions Based on our results, it can be concluded that curcumin protects the kidneys against I/R injury via its antioxidant effects.

Acute kidney injury (AKI) is an independent risk factor for morbidity and mortality. This review provides essential information for the diagnosis and management of AKI. Blood urea nitrogen and serum creatinine are used for the diagnosis of AKI. The review also focuses on recent studies on the diagnosis of AKI using the RIFLE (R-renal risk, I-injury, F-failure, L-loss of kidney function, E-end stage kidney disease) and Acute Kidney Injury Network criteria, and serum and urine AKI biomarkers. Dialysis is the only Food and Drug Administration-approved therapy for AKI. Recent studies on the dose of dialysis in AKI are reviewed.

Background/aims Vascular access dysfunction caused by stenosis is a major complication for hemodialysis (HD) patients. However, physiopathology of late arteriovenous fistula (AVF) stenosis is still under investigation. The aim of the present study was to evaluate the association between plasma soluble EPCR (sEPCR) with serum soluble E-selectin (sE-selectin) concentration and late AVF stenosis in HD patients. Methods Plasma sEPCR and serum sE-selectin concentrations were measured in 94 HD patients. Using these data, we studied the association of sEPCR and sE-selectin with the presence and degree of AVF stenosis using ultrasonography and fistulogram. Results Fifty-one patients have AVF stenosis, and the others ( n  = 43) have patent AVF. The degree of AVF stenosis was correlated with serum sE-selectin levels ( r  = 0.351, p  = 0.01), but not sEPCR ( r  = 0.075, p  = 0.702). The median level of sE-selectin was statistically higher in the group of AVF stenosis than in the group of patent AVF [463.2 pg/ml (275.4–671.4) vs. 162.5 pg/ml (96.7–285.3), p  = 0.001]. Increased sE-selectin levels [OR (OR) = 6.356, p  = 0.015] and high levels of LDL (OR = 4.321, p  = 0.044) were independent predictors of late AVF stenosis in the multivariate model. Conclusions sE-selectin and the LDL were the most important predictors of late AVF stenosis. In addition, sE-selectin correlated with the degree of AVF stenosis. We suggested that atherosclerosis might be contributing factor for development of late AVF stenosis.

Background Contrast-induced nephropathy (CIN) is a common cause of acute kidney injury. Several preventive therapies for this injury have been tested; however, there is still no consensus on the optimal protocol. Methods We performed a systematic search of the National Library of Medicine and the Cochrane Library databases from January 1985 to November 2008 to identify randomized controlled studies examining sodium bicarbonate as a preventive measure for CIN in humans. We also reviewed conference abstracts from cardiology nephrology and radiology meetings from 2004 to 2008. A change in serum creatinine levels defined by an absolute (≥0.5 mg/dl) or percentage (≥25%) increase in the serum creatinine level is defined as CIN. The primary outcome measure was the incidence of CIN, and the secondary outcome measures were: change in serum creatinine from baseline, requirement for renal replacement therapy and death. Results Seventeen randomized controlled trials have investigated the role of sodium bicarbonate for prophylaxis of CIN. The overall incidence of CIN was 11.3%. Using the results from all 17 studies that compared bicarbonate versus saline, the pooled relative risk of developing CIN was 0.54 (95% CI, 0.36–0.83) in the intervention arm, indicating a significant benefit from sodium bicarbonate. The pooled relative risk of CIN was 0.57 (95% CI, 0.35–0.95) when we analyzed for the studies that compared the effects sodium bicarbonate to NAC on development of CIN. There was no difference in the rates of requirement for renal replacement therapy and death. Conclusions The use of sodium bicarbonate appears to reduce the incidence of CIN when compared to other preventive strategies for CIN without a significant difference in the requirement of renal replacement therapy and mortality. There are study heterogeneity and publication biases. Further adequately powered randomized controlled studies are needed to determine whether sodium bicarbonate will reduce the clinically meaningful outcomes (e.g., need for dialysis or death) and optimal hydration strategy in high-risk patients.

Helicobacter pylori (H. pylori) is one of the frequently encountered micro-organisms in the aerodigestive tract. Although infections caused by H. pylori are this common, the exact mode of transmission has not been fully understood yet. Oral-oral, fecal-oral and gastrointestinal-oral routes are the possible modes of transmission. This infection is usually acquired in childhood and may persist for the whole life of the patient. However, about 80% of the infected humans are asymptomatic. Human stomach was considered to be the only reservoir of H. pylori until bacteria were discovered in human dental plaque, in oral lesions, in saliva, in tonsil and adenoid tissue. It is suggested that H. pylori enters the nasopharyngeal cavity by gastroesophageal reflux and colonize in the dental plaques, adenoid tissues and tonsils. From these localizations, the bacteria ascend to the middle ear and to the paranasal sinuses directly or by the reflux again and may trigger some diseases, including otitis, sinusitis, phyrangitis, laryngitis and glossitis. But still, the exact mechanism remains unclear.