Fetal renal impairment

Abstract

Renal function in utero deals chiefly with urine production rather than the excretion of metabolites, which are cleared by the placenta. Fetal renal impairment (FRI) in bilateral renal disease thus presents as oligohydramnios or anhydramnios; this can lead to lung hypoplasia and early neonatal death. As in the adult, FRI can be divided into prerenal, renal and postrenal causes. Causes of prerenal FRI include intrauterine growth restriction, unbalanced intertwin transfusion in monochorionic twins and maternal drug ingestion. Bilateral renal agenesis, multicystic dysplasia and both the autosomal dominant and recessive forms of polycystic kidney disease are examples of renal causes, whereas postrenal etiologies are usually caused by lower urinary tract obstruction (LUTO). When both kidneys are affected and there is severe mid-trimester oligohydramnios, the prognosis is poor. Although animal studies have shown that prolonged LUTO leads to lung hypoplasia and renal damage, and that decompression of the fetal kidney in early pregnancy restores fetal pulmonary and renal function, the value of fetal therapy such as vesico-amniotic shunting remains controversial, with a high procedure-related complication rate and a high incidence of end-stage renal failure in childhood. Fetal cystoscopic treatment of posterior urethral valves in utero may obviate some of these difficulties but remains an investigational procedure.