Recent advances in understanding mechanisms and natural history of XXXX .

@entity1 @entity644 @entity8 @entity101 @entity6 @entity66 @entity2316 @entity1723 @entity413 @entity454
A large subset of individuals with @entity1723 ( @entity1723 ) develops clinical @entity8 that progresses to @entity454 . Identification of clinically proteinuric @entity1 has limited impact on management of the condition. No treatment strategy has succeeded in permanently arresting the evolution of clinical @entity8 . However, important advances have been made in slowing its progress, and these are reviewed in this study. Treatment of raised blood pressure early in the course of @entity2316 has emerged as the most effective therapeutic measure. Susceptible individuals can be detected before persistent @entity644 becomes manifest by screening @entity1723 @entity1 for microalbuminuria, which has proved predictive of persistent @entity644 in approximately 80% of cases. Microalbuminuria can be associated with a raised glomerular filtration rate and is often accompanied by subclinical @entity101 . The independent predictive significance of the two latter variables remains to be established in @entity1 . Unfortunately, microalbuminuria is not apparent until 5 yr after stabilization of newly diagnosed @entity6 , suggesting that it is a marker of @entity66 rather than an indicator of susceptibility. However, many therapeutic interventions, ranging from blood @entity413 control to low-protein diet and angiotensin-converting enzyme inhibition, are effective in reducing or even normalizing microalbuminuria. If current controlled trials show that treatment of microalbuminuric @entity1 prevents progression to clinical @entity8 , the diagnostic criteria for @entity2316 will require radical revision.
