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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

Computed tomography coronary angiography (CTCA) has a higher negative predictive value (NPV) for coronary artery disease (CAD) than stress echocardiography (SE). CT calcium scoring (CTCS) allows detection and quantification of coronary artery calcification (CAC). The NPV of combined SE and CTCS for CAD is not well defined. Consecutive patients from the executive screening program who underwent exercise SE and concomitant CTCA were retrospectively identified between January 2010 and December 2014. Patients with normal SE and CAC score of zero were determined, and the presence or absence of any CAD (obstructive or non-obstructive plaques) on CTCA was confirmed. The NPV of combined SE and CTCS was then re-tested using a validation cohort of subsequent consecutive patients enrolled between January 2015 and July 2018. The initial cohort consisted of 173 patients (19% age > 65 years, 19% diabetic); 40% had normal CTCA, 48% with non-obstructive CTCA (77 with CAC score > 0), and 12% with obstructive CTCA (all with CAC score > 0). There were 16 (9.2%) patients with inducible ischemia on SE. A normal SE had a 93% NPV to exclude obstructive CAD but only 42% NPV to exclude any CAD. A combined normal SE and CTCS had a 100% NPV for obstructive CAD, and 92% for any CAD. In a validation cohort of 111 patients, a normal SE and CAC score of zero had NPV of 100% for obstructive CAD and 92% for any CAD. The combined cohort consisted of predominately low Framingham risk patients; more than 40% (70/181) had CAC score > 0 and 5/70 had obstructive CAD, with the remaining non-obstructive. A concomitant normal SE and CAC score of zero excluded obstructive CAD (NPV 100%) and any CAD in 92% of the testing and validation cohorts. CTCS seems to add incremental risk stratification, particularly for patients with low Framingham score.