Background: Shockwave therapy (SWT) is a commonly used intervention for a number of musculoskeletal conditions with varying clinical outcomes. However, the capacity of SWT to influence pathophysiological processes and the morphology of affected tissues remains unclear. The objective of the current review is to evaluate changes in imaging outcomes of musculoskeletal conditions following SWT.Methods: A comprehensive search of Medline, Embase, Cochrane Controlled Trials Register, CINAHL and SportDiscus was conducted from inception to October 2018. Prospective clinical trials evaluating the effectiveness of SWT based on changes in imaging outcomes were eligible for inclusion. Articles were evaluated independently for risk of bias using the Cochrane Risk of Bias list and the Methodological Index for Non-Randomized Studies. Random-effects meta-analysis and meta-regression with a priori determined covariates was conducted for each condition to determine potential predictors of SWT effects.Results: Sixty-three studies were included, with data from 27 studies available for effect size pooling. Meta-analyses and meta-regression on imaging outcomes were performed for rotator cuff calcific tendinitis (n = 11), plantar fasciitis (n = 7) and osteonecrosis of the femoral head (n = 9). There was an overall reduction in the size of measured lesion following SWT (MD 8.44 mm (95%CI 4.30, 12.57),p < 0.001) for calcium deposit diameter, (MD 0.92 mm (95%CI 0.03, 1.81),p = 0.04) for plantar fascia thickness and (MD 4.84% (95%CI -0.06, 9.75),p = 0.05) for lesion size in femoral head osteonecrosis. Meta-regression showed no influence of SWT dosage parameters, however, baseline lesion size was an independent predictor for changes in imaging outcomes.Conclusions: SWT altered the morphology of musculoskeletal conditions, potentially reflecting changes in underlying pathophysiological processes. The parameters of SWT dosage are not significant predictors of changes in imaging outcomes. Lack of adequate reporting of imaging outcomes limited the conclusions that could be drawn from the current review. Registration number: PROSPERO CRD42018091140.

Key Points: Twenty-five percent of those with unexplained kidney failure have a monogenic cause. Whole genome sequencing with broad gene panel analysis is a feasible diagnostic approach in nephrology. Background: The cause of kidney failure is unknown in approximately 10% of patients with stage 5 chronic kidney disease (CKD). For those who first present to nephrology care with kidney failure, standard investigations of serology, imaging, urinalysis, and kidney biopsy are limited differentiators of etiology. We aimed to determine the diagnostic utility of whole genome sequencing (WGS) with analysis of a broad kidney gene panel in patients with kidney failure of unknown cause. Methods: We prospectively recruited 100 participants who reached CKD stage 5 at the age of ≤50 years and had an unknown cause of kidney failure after standard investigation. Clinically accredited WGS was performed in this national cohort after genetic counseling. The primary analysis was targeted to 388 kidney-related genes with second-tier, genome-wide, and mitochondrial analysis. Results: The cohort was 61% male and the average age of participants at stage 5 CKD was 32 years (9 months to 50 years). A genetic diagnosis was made in 25% of participants. Disease-causing variants were identified across autosomal dominant tubulointerstitial kidney disease (6), glomerular disorders (4), ciliopathies (3), tubular disorders (2), Alport syndrome (4), and mitochondrial disease (1). Most diagnoses (80%) were in autosomal dominant, X-linked, or mitochondrial conditions (UMOD; COL4A5; INF2; CLCN5; TRPC6; COL4A4; EYA1; HNF1B; WT1; NBEA; m.3243A>G). Participants with a family history of CKD were more likely to have a positive result (odds ratio, 3.29; 95% confidence interval, 1.10 to 11.29). Thirteen percent of participants without a CKD family history had a positive result. In those who first presented in stage 5 CKD, WGS with broad analysis of a curated kidney disease gene panel was diagnostically more informative than kidney biopsy, with biopsy being inconclusive in 24 of the 25 participants. Conclusions: In this prospectively ascertained Australian cohort, we identified a genetic diagnosis in 25% of patients with kidney failure of unknown cause.

Background: One-third of patients who recover from COVID-19 present with long COVID. Their symptoms are broad, affecting their physical functioning and, ultimately, their quality of life. Many of those individuals who develop long COVID, possibly from a mild COVID-19 infection, are in the 18–65 age group. This prolongation of malaise directly influences national workforce economies. Objectives: To summarise the commonly reported physical symptoms of long COVID in order to inform potential adjustments in healthcare for the employable population. Methods: The Embase, CINAHL, Medline, SCOPUS, and WHO COVID-19 databases were searched. The study selection process was based on the PRISMA guidelines. The extracted data were synthesised and presented narratively. Results: 7403 studies were accessed, comprising 60 cohort studies and 10 case series/studies, representing 289,213 patients who met our criteria. The most frequently reported physical symptoms were fatigue (92%), shortness of breath (SOB) (81.8%), muscle pain (43.6%), and joint pain (34.5%). Conclusions: The range of reported physical symptoms was broad and varied; the main ones being fatigue, breathlessness/SOB, and pain. Similarities observed between long COVID and other post-acute infection syndromes may help formulate protocols to manage and promote recovery for long COVID patients. Inconsistencies were evident, particularly with a lack of adherence to the standardised definitions of long COVID.