Renal function was assessed using serum creatinine concentration [creat](sr)

and eGFR (Cockcroft Gault, CG). The primary endpoint was a combination of hospitalization due to cardiovascular disease and all-cause mortality.

Results: Two hundred eighty-four subjects (210 men, 74 women, mean age 62 years) were followed-up for a mean of 1.5 years. PWV was negatively associated with eGFR (r(2) 0.09, P 0.001), even in patients with an eGFR 60 ml/min/m(2) (r(2) 0.04, P 0.01). PWV selleck kinase inhibitor was determined by age, heart rate, systolic blood pressure, body mass index and [creat](sr) (r(2) 0.38, P 0.001). A lower eGFR (P 0.01), PWV above the median (P 0.05) and degree of CAD (P 0.001) predicted a shorter time to the primary endpoint. eGFR and degree of CAD remained independent determinants of outcomes (P 0.01), even in patients with normal renal function (P 0.01).

Conclusions:

This study suggests that check details even minor reductions in eGFR, within the normal range, are an additional independent risk marker in patients with CAD.”
“Congenital abnormalities of the kidney and urinary tract (CAKUT) are the most frequent cause of chronic kidney disease in children, accounting for about half of all cases. Although many forms of CAKUT are likely caused by single-gene defects, mutations in only a few genes have been identified. In order to detect new contributing genes we pooled DNA from 20 individuals to amplify all 313 exons of 30 CAKUT candidate genes by PCR analysis and massively parallel exon resequencing. Mutation carriers were identified by Sanger sequencing. We repeated the analysis with 20 new patients to give a total of 29 with unilateral renal agenesis and 11 with other CAKUT phenotypes. Five heterozygous missense mutations were detected in 2 candidate genes (4 mutations in FRAS1 and 1 in FREM2) not previously implicated in non-syndromic CAKUT in humans. All of these mutations were absent from 96 healthy control individuals and had a PolyPhen score over 1.4, predicting

possible damaging effects of the mutation on protein function. Chlormezanone Recessive truncating mutations in FRAS1 and FREM2 were known to cause Fraser syndrome in humans and mice; however, a phenotype in heterozygous carriers has not been described. Thus, heterozygous missense mutations in FRAS1 and FREM2 cause non-syndromic CAKUT in humans. Kidney International (2012) 81, 196-200; doi:10.1038/ki.2011.315; published online 7 September 2011″
“BACKGROUND: En bloc resection of primary sacral tumors has a demonstrated survival benefit. Total and high sacral amputations are traditionally performed by using a staged anterior and subsequent posterior approach. However, we have found that en bloc resection and biomechanical reconstruction of the spinal column is possible from a posterior-only approach in many cases.