Introduction
Amniotic fluid is essential for maintaining the life of the foetus during the prenatal period. It protects against physical trauma and ascending infections, and contributes to the development of the foetal lungs. Foetal resorption and secretion should be in balance for the normal amniotic fluid index (AFI). The amniotic fluid is produced mainly by the placenta and amniotic membrane during the first trimester, and the main source of the amniotic fluid is foetal urine during the second trimester. The foetal urogenital and pulmonary systems contribute to the amniotic fluid balance in the later stages of the pregnancy. Increased amniotic fluid is associated with diminished swallowing or increased foetal excretion [1], and minor changes in the foetal urine production or absorption may cause substantial alterations in the AFI. If the value of the amniotic fluid is between 80-99 mm, it is defined as mild polyhydramnios, and 100-120 mm is considered to be medium polyhydramnios. A value for amniotic fluid >120 mm is accepted as severe polyhydramnios [1]. The etiology of polyhydramnios includes maternal, foetal, and placental abnormalities; additionally, 60% of the cases are idiopathic [1, 2]. Maternal reasons for polyhydramnios are diabetes mellitus (DM) and infections such as TORCH, and the incidence of occurrence with DM was 7.5% in 2004. Foetal causes of polyhydramnios are foetal malformations and tumours, musculoskeletal disorders, chromosomal disorders, immunological and non-immunological hydrops fetalis, and multiple gestations. The incidence of foetal malformations was 24.1% in 2004, and included cerebral, pulmonary, gastrointestinal, cardiac, and urogenital system malformations. Foetal urogenital malformations include increased urine production, diminished urine concentration, and renal tumours [1, 3]. The degree of polyhydramnios is associated with foetal morbidity and mortality, and severe polyhydramnios may cause poor foetal and neonatal prognoses, with a mortality ratio of up to 30% [1, 4]. In this study, we evaluated the foetal renal blood flow, which can affect the production of foetal urine, with colour Doppler ultrasonography (US). Patients with polyhydramnios were investigated for the foetal renal artery pulsatility index (PI) at the beginning of the treatment, and after the conservative treatment in those who reached a normal AFI. Also, statistically significant differences between the values of the foetal renal artery PIs were investigated.