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ABSTRACT.Purpose: To examine if central corneal thickness (CCT) is different in emmetropia and high myopia. Methods: 57 emmetropic subjects (0 to + 1.5 D) and 48 high myopes (all more than -6 D in spherical equivalent refraction) were studied. CCT was measured by a Haag-Streit Optical Low-Coherence Reflectometry (OLCR) pachymeter, a recently developed high precision pachymeter with a standard deviation (SD) for repeated measurements of 1 mm. Results: Mean CCT for the emmetropic group was 538.6 mm (SD = 32.1), and for the myopic group 527.7 mm (SD = 35.0). Neither the mean CCT nor the variance from the two groups showed a statistically significant different (p > 0.05). Conclusion: CCT is not systematically altered in myopia. The process by which the myopia progresses does not to a measurable degree influence the central cornea.

Diffusion kurtosis imaging (DKI) is sensitive to tissue microstructure and may therefore be useful in the diagnosis and monitoring of disease in brain and body organs. Generally, diffusion MRI (dMRI) in the body is challenging due to heterogeneous body composition that can cause image artifacts due to chemical shifts and susceptibility differences. Additionally, the abdomen has a strong presence of physiological factors (e.g. breath, heartbeat, blood flow), which may severely reduce image quality, especially when echo-planar imaging is employed as is typical in dMRI. Collectively, these challenging measurement conditions impede the use and exploration of DKI in the body. This impediment is further exacerbated by the traditionally large amount of data required for DKI and low signal-to-noise ratio at the b-values needed to effectively probe the kurtosis regime. Recently introduced fast DKI techniques reduce the challenge of DKI in the body by lowering the data requirement substantially so that e.g. triggering and breath hold techniques may be applied for the entire DKI acquisition without causing unfeasible scan times. One common pathologic condition where body DKI may be of immediate clinical value is kidney fibrosis, which causes a progressing change in organ microstructure. With its sensitivity to microstructure, DKI is an obvious candidate for a non-invasive evaluation method. We present preclinical evidence that the rapidly obtainable tensor-derived mean kurtosis (W̄) distinguishes moderately fibrotic kidneys from healthy controls. The presence and degree of fibrosis are confirmed by histology, which also indicates fibrosis as the main driver behind the DKI differences observed between groups. We therefore conclude that fast kurtosis is a likely candidate for an MRI based method for detection and monitoring of renal fibrosis. We provide protocol recommendations for fast renal DKI in humans based on a b-value optimization performed using data acquired at 3T in normal human kidney.

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Obstruction-induced fibrosis is a leading cause of end-stage renal failure in children. The pathophysiological mechanisms may involve apoptosis and the renin-angiotensin system. We studied apoptosis and fibrosis in a well-established neonatal pig model with unilateral partial ureteral obstruction (PUUO) induced during ongoing nephrogenesis in 2-day-old piglets. The role of angiotensin II (ANG II) was studied using the AT(1) receptor blocker CV-11974 (0.12 mg/h candesartan from age 23 to 30 days). At day 30 the kidneys were perfusion fixed and fibrosis, apoptosis, and tubular lengths were quantitated using stereological methods, picro Sirius red staining, and immunohistochemical techniques identifying activated caspase 3, aquaporin-2 (AQP2), and von Willebrand factor. The collagen content was assessed by hydroxyproline density. Neonatal induced PUUO increased interstitial and glomerular cell apoptosis and fibrosis. At this stage, PUUO did not increase tubular cell apoptosis or decrease tubular length and cell number. AT(1) receptor blockade prevented the PUUO-induced interstitial and glomerular cell apoptosis but did not attenuate fibrosis. In conclusion, AT(1) receptor blockade after the end of nephrogenesis may prevent interstitial and glomerular cell apoptosis but not fibrosis, suggesting that pathways not involving AT(1) receptor stimulation contribute to neonatal obstruction-induced fibrosis or that prevention of interstitial cell apoptosis counteracts a potential antifibrotic effect of AT(1) receptor blockade in this pig model of congenital obstructive nephropathy. Our results demonstrate that ANG II plays a role in PUUO-induced glomerular cell apoptosis.