Preprints.org
Systemic Lamination of the Retroperitoneal Fascia Driven by Tension-Induced Poisson Compression: In Vivo Evidence from Congenital Renal Agenesis and Mechanical Phase Transition at Around the 20th Gestational Week
By Tokuchi H.
Abstract
For decades, the prevailing interpretation—beginning with Tobin (1944) and supported by Benjamin and Tobin (1951)—dictated that "without the kidney, the renal fascia cannot form." However, this premise was based on specific anatomical specimens lacking both the kidneys and adrenal glands and has never been systematically tested through modern diagnostic imaging. In this study, congenital unilateral renal agenesis was utilized as a natural "subtraction experiment" to re-evaluate the mechanical model of retroperitoneal fascial lamination. In all three adult cases identified from 5,509 unenhanced CT scans, despite the lifelong absence of the kidney, a distinct fascial plane corresponding to the parietal lamina (outer layer) of the renal fascia was invariably preserved. Uniform thinning (mean 1.52 mm vs. 1.85 mm) was observed on the agenesis side, strongly suggesting the selective absence of the organ-dependent "inner lamina" and the autonomous formation of the systemically derived "outer lamina." Integrating fetal embryology, materials science, and mechanical modeling, this framework aligns with the early trunk stiffening (evolutionary front-loading) and extracellular matrix (ECM) material phase transition occurring around 20 gestational weeks. These events induce tension-induced Poisson compression orthogonal to the multiaxial tension field, which may drive the macroscopic lamination of the retroperitoneal fascia. We outline a conceptual "two-stage alignment model" consisting of passive Poisson compression followed by active mechanotransduction, suggesting that retroperitoneal fascial formation is unlikely to be explained solely by organ dependency. Furthermore, we propose a biomechanical "conceptual causal loop" suggesting that the fascial sheet formed during fetal life undergoes functional exaptation, becoming a tensegrity cable that disperses and transmits the gravitational load encountered during postnatal upright bipedalism.





