Consequences in the donor twin

Consequences in the donor twin

Net blood loss in the donor twin presumably actives the renin–angiotensin system (RAS). Mahieu-Caputo et al have performed immunohistochemical studies with renin antiserum and with in-situ hybridization using riboprobes complementary to renin mRNA, and reninsecreting cells (RSCs) to assess the renin production in twin pairs affected by transfusion syndrome.8 The overall maturation of the renal cortex, as determined by the percentage of immature glomeruli, was simultaneously assessed. Although donor twin kidneys were smaller than those of recipients, the maturation of the renal cortex was not significantly different (28.2% immature glomeruli in the donor and 24.4% in the recipient kidney). 

The donor kidney showed increased renin gene expression with hyperplastic juxtaglomerular apparatuses (JGAs) that contained excess RSCs (median 20.02 [25th–75th centiles, 5.4, 25.1 RSCs per 100 glomeruli]). In contrast, the recipient kidney is virtually devoid of these cells (0.04 [0, 0.36] RSCs per 100 glomeruli; p <0.05). Increased renin release in the kidney of the donor may act locally and result in renal vasoconstriction and oliguria. As a consequence, the fetal bladder is either small or nonvisible on ultrasound, and the fetus develops oligoanhydramnios. 

The donor twin is presumably hypotensive in utero as a result of the net blood loss to the recipient. Postnatally, it is not uncommon for the donor twin to require inotropic support. In-utero hypotension of the donor, however, has never been documented. 

Spontaneous in-utero demise of the donor twin may result from hypotension, chronic hypoxia, severe growth restriction, or anemia.