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Objective: The study aimed to describe "minimal-touch" technique for primary artificial urinary sphincter placement and evaluate early device outcomes by comparing it with a historical cohort. Materials and methods: We identified patients who underwent primary artificial urinary sphincter placement at our institution from 1983 to 2020. Statistical analysis was performed to identify the rate of postoperative device infection in patients who underwent minimal touch versus those who underwent our traditional technique. Results: 526/2601 total procedures (20%) were performed using our "minimal-touch" approach, including 271/1554 patients (17%) who underwent primary artificial urinary sphincter placement over the study period. Around 2.3% of patients experienced device infection after artificial urinary sphincter procedures. In the "minimal-touch" era, 3/526 patients (0.7%) experienced device infection, including 1/271 (0.4%) of those with primary artificial urinary sphincter placement. In comparison, 46/2075 patients (2.7%) experienced device infection using the historical approach, with 29/1283 (2.3%) of primary artificial urinary sphincter placements resulting in removal for infection. Notably, 90% of device infections occurred within the first 6 months after primary placement. The difference in cumulative incidence of device infections at 12 months did not meet our threshold for statistical significance for either the total cohort of all AUS procedures (primary and revision) or the sub-group of only those patients undergoing primary artificial urinary sphincter placement (Gray K-sample test; P = .13 and .21, respectively). Conclusion: The "minimal-touch" approach for artificial urinary sphincter placement represents an easy-to-implement modification with potential implications on device outcomes. While early results appear promising, longer-term follow-up with greater statistical power is needed to determine whether this approach will lower the infection risk. [ABSTRACT FROM AUTHOR]

Large DNA rearrangements account for about 8% of disease mutations and are more common in duplicated genomic regions, where they are difficult to detect. Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in either PKD1 or PKD2. PKD1 is located in an intrachromosomally duplicated region. A tuberous sclerosis gene, TSC2, lies immediately adjacent to PKD1 and large deletions can result in the PKD1/TSC2 contiguous gene deletion syndrome. To rapidly identify large rearrangements, a multiplex ligation-dependent probe amplification assay was developed employing base-pair differences between PKD1 and the six pseudogenes to generate PKD1-specific probes. All changes in a set of 25 previously defined deletions in PKD1, PKD2 and PKD1/TSC2 were detected by this assay and we also found 14 new mutations at these loci. About 4% of the ADPKD patients in the CRISP study were found to have gross rearrangements, and these accounted for about a third of base-pair mutation negative families. Sensitivity of the assay showed that about 40% of PKD1/TSC contiguous gene deletion syndrome families contained mosaic cases. Characterization of a family found to be mosaic for a PKD1 deletion is discussed here to illustrate family risk and donor selection considerations. Our assay improves detection levels and the reliability of molecular testing of patients with ADPKD.Kidney International (2008) 74, 1468–1479; doi:10.1038/ki.2008.485; published online 24 September 2008 [ABSTRACT FROM AUTHOR]

Background: Autosomal dominant polycystic kidney disease (ADPKD) has phenotypic variability only partially explained by established biomarkers that do not readily assess pathologically important factors of inflammation and kidney fibrosis. We evaluated asymptomatic pyuria (AP), a surrogate marker of inflammation, as a biomarker for disease progression., Methods: We performed a retrospective cohort study of adult patients with ADPKD. Patients were divided into AP and no pyuria (NP) groups. We evaluated the effect of pyuria on kidney function and kidney volume. Longitudinal models evaluating kidney function and kidney volume rate of change with respect to incidences of AP were created., Results: There were 687 included patients (347 AP, 340 NP). The AP group had more women (65% versus 49%). Median ages at kidney failure were 86 and 80 years in the NP and AP groups (log rank, P =0.49), respectively, for patients in Mayo Imaging Class (MIC) 1A-1B as compared with 59 and 55 years for patients in MIC 1C-1D-1E (log rank, P =0.02), respectively. Compared with the NP group, the rate of kidney function (ml/min per 1.73 m 2 per year) decline shifted significantly after detection of AP in the models, including all patients (-1.48; P <0.001), patients in MIC 1A-1B (-1.79; P <0.001), patients in MIC 1C-1D-1E (-1.18; P <0.001), and patients with PKD1 (-1.04; P <0.001). Models evaluating kidney volume rate of growth showed no change after incidence of AP as compared with the NP group., Conclusions: AP is associated with kidney failure and faster kidney function decline irrespective of the ADPKD gene, cystic burden, and cystic growth. These results support AP as an enriching prognostic biomarker for the rate of disease progression., Competing Interests: C. Hanna reports consultancy agreements with Horizon Therapeutics and honoraria from Horizon Therapeutics. P.C. Harris reports consultancy agreements with Mitobridge, Otsuka, Regulus, and Vertex; research funding from Acceleron, Jemincare, Navitor, Otsuka Pharmaceuticals, and Palladio Biosciences; patents and inventions with Amgen, Bayer, Genzyme, GlaxoSmithKline, Millipore, Mitobridge, and Vertex; honoraria from Otsuka Pharmaceuticals and Vertex Pharmaceuticals; and serving on the clinical advisory board of Mironid. P.J. Schulte reports other interests/relationships with OxThera. S.R. Senum reports ownership interest with Marvell Technology Inc. V.E. Torres reports consultancy agreements with Acceleron Pharma, Blueprint Medicines, Mironid, Otsuka Pharmaceuticals, Palladio, Reata, and Sanofi; research funding from Blueprint Medicines, Mironid, Otsuka Pharmaceuticals, Palladio Biosciences, Reata, and Sanofi Genzyme (all preclinical trials, preclinical research, or clinical trials); honoraria from Otsuka Pharmaceuticals (to the institution); and scientific advisor or membership with Mironid, Otsuka Pharmaceuticals, and Sanofi. Z.M. Zoghby reports research funding from Kadmon Corporation. All remaining authors have nothing to disclose., (Copyright © 2022 by the American Society of Nephrology.)

Objective: Artificial urinary sphincter (AUS) device failure or revision can be due to multiple etiologies including erosion, infection, mechanical malfunction, and urethral atrophy. However, few studies have evaluated factors that predispose patients to urethral atrophy. Here, we sought to identify preoperative and perioperative risk factors associated with urethral atrophy in men undergoing primary artificial urinary sphincter (AUS) placement for stress urinary incontinence., Material and Methods: From 1987 to 2013, 1829 AUS procedures were performed at our institution. A total of 1068 patients underwent primary AUS placement and were the focus of our study. Multiple clinical and surgical variables were evaluated for a potential association with revision for atrophy. Those found to be associated with atrophy and relevant competing risks were further evaluated on multivariable analysis., Results: With a median follow-up of 4.2 years (IQR 1.3-8.1), 89 men (8.3%) had urethral atrophy requiring reoperation. Median time to revision was 4.5 years (IQR 1.9-7.6). On univariable analysis, only smaller cuff size (4.0-cm versus 4.5-cm; HR 3.1, p=0.04) was associated with an increased rate of urethral atrophy. Notably, patient age at the time of surgery (p=0.62), body mass index (0.22), and smoking status (p=1.00) were not associated with a risk of atrophy. On multivariable analysis smaller urethral cuff size remained significant (HR 2.8, 95% CI 1.1-7.1; p=0.01)., Conclusion: Revision surgery for urethral atrophy was performed in approximately 8% of men undergoing primary AUS placement. Utilization of a smaller AUS cuff size appears to be an independent factor associated with increased rate of urethral atrophy.