Comparison of outcomes for two cardiovascular risk factors provides some evidence that clinical coding mediates performance for QOF P4P indicators. Uncoded stages 3�C5 CKD patients had worse blood pressure control but similar cholesterol levels in comparison to miscoded stages 3�C5 CKD patients. This also suggests an inappropriate targeting of resources away from individuals in need which could be reversed by better identification of stages 3�C5 CKD without increasing workload. In the sensitivity analysis where patients with either two lab eGFRs or two calculated eGFRs were included the prevalence in 2009 YS-49 varied from 4% to 4.7%. This suggests a further potential cause of misclassification where laboratory reported eGFR is not available. Coronary heart disease is a complex disease with high morbidity and mortality. Very little is known about its genetic etiology. Heat shock protein 70, as a dominant chaperone in the HSPs families, can help in the assembly of newly synthesized proteins, in protein transport, and in the removal of damaged proteins. In humans, the HSP70kDa family comprises 13 members, some of which show constitutive expression while others are stress inducible. These isoforms have highly homogenous structure. They are all composed of a conserved ATPase domain, a peptide-binding domain, a middle region with protease sensitive sites, and a C-terminal domain. For instance, HSPA8, previously referred to as HSP73 or HSC70, shares 86% amino acid homology to inducible HSPA1A. Consistent with their homogenous structure, these proteins have distinct but overlap ping functions. Thus both stress-inducible Hsp70 and constitutively expressed HSPA8 can perform some similar functions and are capable of protecting cardiac muscle cells against injuries like an oxidative Hederacoside C challenge. There is much evidence indicating that Hsp70 can take part in the progress of CHD. A previous study from our laboratory also demonstrated that genetic variants in the HSPA1A gene may be novel genetic risk markers for CHD.We then selected 4 tagging SNPs to identify potential genetic markers of this gene for CHD susceptibility in a case-control study comprised of 1,003 CHD cases and 1,003 age frequency matched controls in a Chinese population.