Fetal development in experimental uremia.
Uremic women on hemodialysis with metabolic bone disease (hyperparathyroidism, osteomalacia resulting from defective vitamin D metabolism) and anemia (erythropoietin deficiency) are known to give birth to infants without bone disease or anemia. Therefore, skeletal development (enchondral and desmal bone formation) and hepatic erythropoiesis were evaluated in fetuses of uremic rats. These fetuses failed to show defective mineralisation or evidence of bone disease. Bolus injection of high doses of exogenous PTH into the maternal or fetal organism did not affect fetal bone histology. In addition, no apparent defect of bone mineralisation or bone formation was found in fetuses of ricketic rats. Normal mineralisation in the offspring of uremic rats may be explained by fetal hyperphosphatemia and/or insensitivity of fetal (woven) bone mineralisation to vitamin D. Absence of fetal anemia (normal hematocrits, normal density of hematopoietic cells in the liver) in the presence of maternal anemia is presumably due to the insensitivity of fetal erythropoiesis to erythropoietin.
D000818:Animals; D001835:Body Weight; D001846:Bone Development / Q000187:drug effects; D004195:Disease Models, Animal; D005260:Female; D005333:Fetus / Q000502:physiology*; D006400:Hematocrit; D006410:Hematopoiesis; D008297:Male; D010281:Parathyroid Hormone / Q000494:pharmacology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D012863:Skeleton / Q000196:embryology; D014511:Uremia / Q000503:physiopathology; D014808:Vitamin D Deficiency / Q000503:physiopathology
D010281:Parathyroid Hormone