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Renal infection in autosomal dominant polycystic kidney disease. Am J Med 1987; 82: 714-718, doi: 10.1016/0002-9343(87)90005-2.
Morbidity from congenital hepatic fibrosis after renal transplantation for autosomal recessive polycystic kidney disease. Am J Transplant 2002 [http://dx.doi.org/10.1034/j.1600-6143.2002.20412.x]
If there are no other malformations in the fetus the main diagnosis is polycystic kidney disease with recessive or dominant genetic disorder.3 In dominant polycystic kidney disease the fetus shows macro cysts and the amniotic fluid is normal.
Mechanisms of progression in autosomal dominant polycystic kidney disease. Kidney Int Suppl.
Ambulatory blood pressure correlates with renal volume and number of renal cysts in children with autosomal dominant polycystic kidney disease. Blood Press Monit.
This classification represents an expansion on the strategy of Kissane116 and Elkin and Bernstein,118 employing key groupings of genetic disorders, such as the 2 polycystic kidney diseases, and entities with similar morphologic findings, such as metanephric dysgenesis of renal dysplasias, without mixing pathogenetically unrelated entities, such a medullary sponge kidney with the genetic medullary cystic diseases and nephronophthisis
These processes are responsible for cell proliferation, cyst formation, and the inflammation that accounts for progression in all forms of polycystic kidney disease (PKD) (Verghese et al., 2008).
Recent studies from vertebrates have implicated a [Ca.sup.2+]-dependent signaling pathway in normal kidney development, because the loss of function in either of two [Ca.sup.2+]-related proteins is known to result in abnormal kidney development resulting in polycystic kidney disease. We have begun a study to image [Ca.sup.2+] signaling during the formation of the pronephros (the functional embryonic kidney) in both intact zebrafish and Xenopus laevis embryos, as well as in Xenopus animal caps that are isolated at the blastula stage and induced to differentiate into pronephric tubules by incubation with retinoic acid (RA) and activin A (AA).
(Nasdaq:AVII)(Nasdaq:AVIIW)(Nasdaq:AVIIZ), Portland, Ore, has announced that its NEUGENE(R) antisense drug (AVI-4126) has proved safe in adult patients with autosomal dominant Polycystic Kidney Disease (PKD).
Genetic factors involve family history and the presence of certain heritable connective tissue disorders such as Ehlers-Danlos syndrome, Marfan's syndrome, neurofibromatosis, and polycystic kidney disease. Acquired factors include traumatic brain injury, sepsis, smoking, and hypertension.

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