The current study aimed to validate the child and parent pain catastrophizing scale in a large chronic pain sample and to identify child pain catastrophizing clinical reference points. Patients and parents (n= 697) evaluated at a pediatric pain program completed the Pain Catastrophizing Scale, child (PCS-C) and parent (PCS-P) report, along with additional measures of psychological functioning. The measure’s psychometric properties were examined, as well as relations across demographic, pain, and psychological characteristics and pain catastrophizing. Clinical reference points were identified for the PCS-C from differences in pain catastrophizing across levels of disability, depressive symptoms, and anxiety. Overall, we did not find support for the hypothesized three-dimension structure and recommend potentially removing items 7 and 8 for both the PCS-P and PCS-C due to floor/ceiling effects. The 11-item PCS-C is most parsimonious as a unitary construct, while the 11 item PCS-P is comprised of two factors. Although parent catastrophizing was significantly associated with child outcomes after controlling for pain level, it was no longer significant when accounting for child catastrophizing. When comparing PCS-C scores based on child outcomes, significant differences emerged for low, moderate, and high catastrophizing levels. It appears that the influence of parent catastrophizing on outcomes can be explained through its impact on child catastrophizing levels. Lastly, PCS-C reference points derived from this large sample can aid clinicians in assessment and treatment planning, in turn increasing the utility of the PCS-C for both clinical and research purposes.
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Background Computer‐assisted scoring is gaining prominence in the evaluation of renal histology; however, much of the focus has been on identifying larger objects such as glomeruli. Total inflammation impacts graft outcome, and its quantification requires tools to identify objects at the cellular level or smaller. The goal of the current study was to use CD45 stained slides coupled with image analysis tools to quantify the amount of non‐glomerular inflammation within the cortex. Methods Sixty renal transplant whole slide images were used for digital image analysis. Multiple thresholding methods using pixel intensity and object size were used to identify inflammation in the cortex. Additionally, convolutional neural networks were used to separate glomeruli from other objects in the cortex. This combined measure of inflammation was then correlated with rescored Banff total inflammation classification and outcomes. Results Identification of glomeruli on biopsies had high fidelity (mean pixelwise dice coefficient of .858). Continuous total inflammation scores correlated well with Banff rescoring (maximum Pearson correlation .824). A separate set of thresholds resulted in a significant correlation with alloimmune graft loss. Conclusions Automated scoring of inflammation showed a high correlation with Banff scoring. Digital image analysis provides a powerful tool for analysis of renal pathology, not only because it is reproducible and can be automated, but also because it provides much more granular data for studies.
<b><i>Introduction:</i></b> Current knowledge of risk factors and renal histologic patterns of oxalate nephropathy (ON) not due to primary hyperoxaluria (PH) has been limited to small case series and case reports. Thus, we analyzed and compared clinical risk factors, histologic characteristics, and renal outcomes of patients with biopsy-confirmed ON among a cohort of patients with enteric and nonenteric risk factors. <b><i>Methods:</i></b> A clinical data repository of native kidney pathology reports from 2009 to 2020 at all Mayo Clinic sites was used to identify 421 ON cases. <b><i>Results:</i></b> After excluding cases in transplanted kidneys or due to PH, 64 cases remained. Enteric risk factors were present in 30 and nonenteric in 34. Roux-en-Y gastric bypass (17) and pancreatic insufficiency (6) were most common in the enteric hyperoxaluria group. In the nonenteric group, vitamin C (7) and dietary oxalate (7) were common, while no apparent risk was noted in 16. Acute kidney injury (AKI) stage III at the time of diagnosis was present in 60%, and 40.6% required dialysis. Patients in the nonenteric group had more interstitial inflammation (<i>p</i> = 0.01), and a greater number of tubules contained intratubular calcium oxalate (CaOx) crystals (<i>p</i> = 0.001) than the nonenteric group. Patients in the enteric group were more likely to have baseline chronic kidney disease (CKD) (<i>p</i> = 0.02) and moderate-to-severe tubulointerstitial fibrosis and atrophy (IFTA) (OR 3.49, <i>p</i> = 0.02). After a median follow-up of 10 months, 39% were dialysis dependent, 11% received a kidney transplant, and 32% died. On univariate analysis, >10 tubules with CaOx crystals, baseline CKD, and AKI requiring dialysis correlated with the risk of dialysis, transplant, or death. On multivariate analysis, only AKI requiring dialysis correlated with adverse renal outcomes. <b><i>Conclusion:</i></b> This is the largest cohort study of ON not due to PH. Histologic features differ in patients with enteric versus nonenteric risks. Patients in the enteric group are more likely to have baseline CKD and significant IFTA, while patients in the nonenteric group were more likely to have a greater number of tubules with CaOx crystals and corresponding interstitial inflammation. AKI requiring dialysis at the time of diagnosis was the single most significant predictor of adverse renal outcome.
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