PubMed · 6618321
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R R Zimlichman, C Chaimovitz. 1983-03-15. [Idiopathic edema].. https://pubmed.ncbi.nlm.nih.gov/6618321/
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To our knowledge this is the first report of Schneckenbecken dysplasia with the development of hydrops early in the second trimester. The radiological findings showed the typical hypoplastic iliac bones with medial extension and very flattened, on lateral view, oval-shaped vertebral bodies and short long bones. The histology showed hypercellular and hypervascular cartilage with chondrocytes with centrally located nucleus. The absence of the lacunar space as described before was also observed in some chondrocytes in our case. This male fetus was the product of consanguineous parents of Mediterranean origin compatible with autosomal recessive inheritance.
Cyclic idiopathic edema is a nonlife-threatening syndrome of excessive weight gain. Although the cause is not clear, a number of hormones are postulated to be involved. Altered vascular permeability and increased lymph formation may also be part of the disorder. This article reviews some relevant data as to the pathogenesis of this noninflammatory disorder, concluding with an approach to diagnosis and therapy.
Nephritic edema results from the primary retention of salt. Acute glomerulonephritis is the prototypical form of the disorder. The stimulus for the salt retention arises within the kidney by an unknown mechanism. As effective arterial blood volume (EABV) was normal at the start of the disease process, it becomes expanded as salt and water are added to it. The pathophysiological sequelae of this process are compared with those which follow the salt retention of congestive heart failure (CHF). The latter is a syndrome in which salt retention is secondary, driven by the contraction of EABV which is at the heart of CHF. Finally, mechanisms responsible for the salt retention of nephrosis are considered. It is possible, and even likely, that most patients with nephrotic edema have primary salt retention, rather than secondary edema. If this view is correct, salt is retained not because of urinary protein loss and its consequent hypoalbuminemia, but rather because of the glomerulopathy which caused the syndrome in the first place.