or apoptosis. As p53 is stabilised in both situations, additionalfactors must determine which response prevails. UlrichMaurer (Freiburg, Germany) showed that in response toDNA damage, glycogen syn

or for the development of CKD.Assessment of NonHDLc/HDLc ratio may help identify hi

w-onset CKD [defined as an estimated glomerular filtration rate (eGFR) of < 60 ml/min/1.73 m2 (low eGFR) and/or proteinuria (defined as urinary protein ≥ 1 + on dipstick testing)] or low eGFR. Cox proportional hazards models were used to examine the independent relationship between the plasma NonHDLc/HDLc ratio and new-onset CKD.During a median follow-up period of 2.8 years, 3% (n = 57) of participants developed new-onset CKD. Compared with patients in the lowest tertile, patients with NonHDLc/HDLc ratios in the highest tertile had a 1.45-fold higher risk of new-onset CKD (hazard ratio [HR], 2.45

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