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The presence of hyperechoic kidneys during a prenatal ultrasound evaluation can be indicative of a wide variety of renal diseases, ranging from clinically insignificant transient involvement to diseases with progressive deterioration of renal function. This hyperechogenicity is frequently a manifestation of renal cystic disease. There are many conditions that manifest with renal cysts, both genetic and acquired (Table 1), and they may have onset from intrauterine life through adulthood. The most frequent ones are autosomal dominant polycystic kidney disease, autosomal recessive polycystic kidney disease, nephronophthisis and those recently reclassified as autosomal dominant tubulointerstitial kidney disease. The differential diagnosis must take into account the ultrasound findings, the family history and the presence of extrarenal abnormalities. We present the case of a family with renal cystic disease of a genetic aetiology in which the index case that led to diagnosis was a newborn in whom prenatal ultrasound had detected increased echogenicity in both kidneys. The patient underwent an evaluation at 1-month post birth for assessment of the prenatal bilateral renal hyperechogenicity. The postnatal ultrasound examination confirmed increased echogenicity in the renal cortex with presence of microcysts (Fig. 1). The personal history was: product of a twin pregnancy achieved by in vitro fertilization due to primary infertility (fallopian tube obstruction). Maternal gestational diabetes treated with insulin. The prenatal ultrasound examination at week 20 revealed increased echogenicity in the kidneys that persisted until birth, with diminished corticomedullary differentiation, normal kidney size and absence of cysts. This was associated with polyhydramnios from week 26. There were signs of preterm labour at 32 weeks that required treatment with tocolytics and steroids to promote lung maturation. The patient was delivered by caesarean section at 37 weeks’ gestation with a birth weight of 2095 g. He was admitted to the neonatal ward due to transient feeding intolerance. The family history was: healthy father, mother with history of spondylodiscitis in L4-L5 treated with a graft, tuberculous pleural effusion at age 20 years and allergic rhinitis. No history of urologic disease, chronic renal disease

Estudio de hiperecogenicidad renal: del fenotipo al genotipo en la mutación del gen del factor nuclear hepático1β