Histopathological examinations of donor kidney in twin-twin transfusion syndrome

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  • 双胎間輸血症候群供血児剖検例における腎組織学的検討

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Renal tubular dysgenesis (RTD) is a rare lethal clinical disorder that is observed in fetal anuria leading to oligohydramnios and Potter sequence. The histological hallmark is the incomplete development of renal cortical convoluted proximal tubules and crowding of the glomerli. The severity of RTD underlines the importance of a functional rennin-anigotensin system in the maintenance of blood pressure and renal blood flow during fetal development. Recently, a similar feature due to antenatal hypoplasia of renal proximal tubules has been reported in donor fetuses with twin-twin transfusion syndrome (TTTS). In the present paper, we have explored the histopathology findings of the donor kidney in TTTS at autopsy. Our patient, a boy, was the survivor in which the monochorionic monoaminiotic twin partner died in utero. The infant was born at 27 weeks and 2 days of gestation with a birth weight of 984 g, and was diagnosed as a donor twin in TTTS. From day 2 after birth, peritoneal dialysis was started because anuria persisted and serum potassium level was elevated. Although he developed bowel perforation, urine output gradually improved. However, the patient died at 34 days because of intraperitoneal bleeding. An autopsy revealed a paucity of proximal tubules with crowding of glomeruli characteristic of RTD and thrombosis in glomerular capillary. We speculated that the RTD lesions might result from sustained hypoperfusion of the kidney because the donor twin was thought to suffer from chronic hypovolemia by an unbalanced blood supply through the placental vascular shunts. Furthermore, severe hypotension and anemia developed as a consequence of acute hemodynamic change due to feto-fetal hemorrhage at the time of death of the co-twin. As a result, he was associated with irreversible renal damage by further reducing the renal blood flow. We support that donors in TTTS are at risk for the development of RTD, resulting in persistent tissue hypoperfusion leading to kidney ischemia in the fetal period.

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