As a result of the enlarging uterus, gestational hydronephrosis occurs by the third trimester in up to 90% and 67% in the right and left side, respectively [
11]. Indeed, it can occur as early as the 6th week of pregnancy and persist until 6 weeks after delivery [
12]. Even when not caused by KSD, hydronephrosis in pregnancy can be painful for the patient and therefore may itself be a cause for the patient’s acute presentation. Dilatation is not usually observed below the pelvic brim and therefore an obstruction below this level raises the suspicion of intraluminal obstruction secondary to KSD. This dilatation also serves to increase the risk of stone migration and subsequent obstruction [
13]. Stones are twice as likely to be located in the ureter than kidney when diagnosed during pregnancy [
5]. Prolonged dilation results in urinary stasis, which, together with elevated progesterone levels, reduces ureteral peristalsis and promotes formation of urinary crystals. This is further accelerated by the gestational increase in glomerular filtration rate (GFR) and plasma flow (up to 50%), which leads to increased excretion of uric acid, oxalate and sodium [
14]. Other lithogenic factors related to pregnancy include elevated urine pH and hypercalciuria. The latter occurs as a result of increased GFR and placental production of 1,25-dihydroxycholecalciferol to meet requirements of the foetus [
15]. However, excretion of inhibitors to stone formation such as glycoprotein, nephrocalcin and urate is believed to compensate for the aforementioned lithogenic properties [
3]. Calcium phosphate is the commonest stone composition type in contrast to calcium oxalate in general population [
13].