“
“In response to the increase in Chronic Kidney Disease (CKD) worldwide, several professional organizations have developed clinical practice guidelines to manage and prevent its progression. This study aims to compare the scope, content and consistency of published guidelines on CKD stages I–III. Electronic databases of the medical literature, guideline organizations, and the websites of nephrology societies were searched to November 2011. The Appraisal of Guidelines for Research and Evaluation (AGREE) II instrument and textual synthesis was used to appraise and compare recommendations. One consensus statement and 15 guidelines were identified and included. Methodological

rigour across guidelines was variable, with average domain scores ranging from 24% to 95%. For detection of CKD, all guidelines selleck chemical recommended estimated glomerular filtration rate measurement, some also recommended selleck compound serum creatinine and dipstick urinalysis. The recommended protein and albumin creatinine ratios and proteinuria definition thresholds varied (>150–300 mg/day to >500 mg/day). Blood pressure targets ranged (<125/75 to <140/90 mmHg). Angiotensin converting enzyme inhibitor and angiotensin receptor blockers were recommended for hypertension, as combined or as monotherapy. Protein intake

recommendations varied (no restriction or 0.75 g/kg per day−1.0 g/kg per day). Salt intake of 6 g/day was recommended by most. Psychosocial support and education were recommended by few but specific strategies were absent. CKD guidelines were consistent in scope but were variable with respect to Calpain their recommendations, coverage and methodological quality. To promote effective primary and secondary prevention of CKD, regularly updated guidelines that are based on the best available evidence and augmented with healthcare context-specific strategies

for implementation are warranted. “
“Interstitial infiltrates, consisting of macrophages and other inflammatory cells, have been consistently reported in human and animal models of polycystic kidney diseases (PKD). However, the mechanisms underlying this inflammation are not well defined. Evidence suggests that interstitial inflammation in PKD is driven by pro-inflammatory chemoattractants such as monocyte chemoattractant protein-1 (MCP-1), and cytokines such as tumour necrosis factor (TNF)-α. Putative upregulated inflammatory pathways include JAK-STAT and nuclear factor (NF)-κB signalling. In addition, the genetic mutations of PKD may further complicate the relationship between inflammation and cystic disease, by increasing the susceptibility to inflammatory injury, and facilitating interactions between the genetically determined cystoproteins and biological mediators of inflammation.