Fetal serum ß2‐microglobulin and cystatin C in the prediction of post‐natal renal function in bilateral hypoplasia and hyperechogenic enlarged kidneys

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Abstract
Objectives: To evaluate fetal serum ß2‐microglobulin and cystatin C in the prediction of post‐natal renal function in bilateral hypoplasia and hyperechogenic enlarged kidneys. Predicting post‐natal renal function is crucial to the prenatal evaluation of fetal nephropathies. Prenatal ultrasound can identify terminal renal failure, but is not sensitive enough to identify infants whose post‐natal renal function will be impaired. Fetal serum ß2‐microglobulin and cystatin C are potential predictors of post‐natal renal function.Methods: Fifty‐four prenatally diagnosed cases of bilateral nephropathy were retrospectively reviewed. Final diagnosis was established using histological or post‐natal findings: renal hypoplasia (n = 7), cystic dysplasia (n = 9), autosomal dominant polycystic kidney disease (ADPKD; n = 8) or autosomal recessive polycystic kidney disease (ARPKD; n = 22) and transient sonographic abnormalities (n = 8). Fetal serum ß2‐microglobulin and cystatin C were assayed respectively in 54 and 38 cases. The prognostic value of these markers was assessed in terms of the post‐natal outcome.Results: In bilateral kidney hypoplasia and cystic dysplasia, ß2‐microglobulin and cystatin C were significantly (p < 0.0001 and p < 0.02 respectively) higher than in the normal control group. In hyperechogenic fetal kidneys (ARPKD, ADPKD and transient sonographic abnormalities), these markers were not different from controls. However, whereas normal values cannot exclude renal failure, abnormal values predict post‐natal renal failure.Conclusions: In bilateral renal hypoplasia and dysplasia, fetal serum ß2‐microglobulin and cystatin C are good markers for post‐natal renal function. However, in bilateral renal hyperechogenic enlargement, abnormal values are associated with poor post‐natal renal function, but normal values cannot preclude renal failure. Copyright © 2004 John Wiley & Sons, Ltd.