The creatinine- and cystatin C-based rapid progressions were associated with increased risk of ESRD (HR = 2.22 [1.57-3.13], HR = 2.03 [1.44-2.86], respectively; all p < 0.001).
A neonatal CysC >3.0 mg/L predicted progression to ESRD while a nadir SCr >0.6 mg/dL predicted progression to CKD 3-5 with the highest specificity and sensitivity by ROC-AUC analysis (<i>P</i> < 0.0001).
Laboratory blood tests including serum creatinine, serum urea, cystatin-C, serum parathyroid hormone (PTH), calcium and phosphorus levels, hemoglobin and hematocrit were performed in all ESRD patients close to the time of the MR examination.
According to our results, although serum KIM-1, NGAL, OPN, MMP-9, and urine MMP-9, urine KIM-1 do not appear to be ideal markers to evaluate renal injury in the early period of obesity, the serum levels of cystatin C and urine NGAL, urine OPN can be used as a good marker for assessing the renal effect of obesity which can lead end stage renal disease in pediatric population.
Using a cross-sectional analysis from the eGFR Study of 654 Indigenous Australians at high risk of ESKD, eGFR was calculated using the CKD-EPI equations for serum creatinine (eGFRcr), cystatin C (eGFRcysC) and combined creatinine and cystatin C (eGFRcysC+cr).
In the Atherosclerosis Risk in Communities Study (n = 13,277 from 4 US communities), we used structural equation modeling to estimate the association between serum 1,5-AG levels and end-stage renal disease (ESRD) from baseline (1990-1992) through 2013 with adjustment for demographics, risk factors, a latent variable for glycemia (diabetes status, fasting glucose, glycated hemoglobin (HbA1c), fructosamine, glycated albumin), and a latent variable for kidney function (creatinine, cystatin C, β2-microglobulin).
Declines in mGFR, eGFR<sub>cr</sub>, eGFR<sub>BTP</sub>, and the average of 4 filtration markers (creatinine, cystatin C, BTP, and B2M) were consistently associated with progression to ESRD.