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To describe patterns of practice of PSA testing and imaging for Ontario men receiving continuous ADT for the treatment of non-metastatic castration-resistant prostate cancer (nmCRPC).This was a retrospective, longitudinal, population-based study of administrative health data from 2008 to 2019. Men 65 years and older receiving continuous androgen deprivation therapy (ADT) with documented CRPC were included. An administrative proxy definition was applied to capture patients with nmCRPC and excluded those with metastatic disease. Patients were indexed upon progression to CRPC and were followed until death or end of study period to assess frequency of monitoring with PSA tests and conventional imaging. A 2-year look-back window was used to assess patterns of care leading up to CRPC as well as baseline covariates.At a median follow-up of 40.1 months, 944 patients with nmCRPC were identified. Their median time from initiation of continuous ADT to CRPC was 26.0 months. 60.7% of patients had their PSA measured twice or fewer in the year prior to index, and 70.7% patients did not receive any imaging in the year following progression to CRPC. Throughout the study period, 921/944 (97.6%) patients with CRPC progressed to high-risk (HR-CRPC) with PSA doubling time ≤ 10 months, of which more than half received fewer than three PSA tests in the year prior to developing HR-CRPC, and 30.9% received no imaging in the subsequent year.PSA testing and imaging studies are underutilized in a real-world setting for the management of nmCRPC, including those at high risk of developing metastatic disease. Infrequent monitoring impedes proper risk stratification, disease staging and detection of treatment failure and/or metastases, thereby delaying the necessary treatment intensification with life-prolonging therapies. Adherence to guideline recommendations and the importance of timely staging should be reinforced to optimize patient outcomes.

Background Sorafenib has been shown to improve survival in patients with advanced hepatocellular carcinoma (HCC), however, full dose can be difficult to tolerate. The aim of this study was to determine whether sorafenib starting dose and mean dose intensity affect survival. Methods Patients treated with sorafenib for HCC from January 2008 to July 2016 in several Canadian provinces were included and retrospectively analyzed. The primary end point was overall survival (OS) of patients starting on sorafenib full dose compared to reduced dose. Secondary analysis compared OS with different mean dose‐intensity groups. Survival outcomes were assessed with Kaplan‐Meier curves and Cox proportional hazards models. A propensity score analysis was performed to account for treatment bias and confounding. Results Of 681 patients included, sorafenib was started at full dose in 289 patients (42%). Median survival for starting full and reduced dose was 9.4 months and 8.9 months (P = .15) respectively. After propensity score matching and adjusting for potential confounders there was still no difference in survival (HR 0.8, 95% CI, 0.61‐1.06, P = .12). Almost half of the patients (45%) received a dose intensity 75%, 50%‐75%, and, Starting dose and dose intensity of sorafenib does not impact mortality in patients with hepatocellular carcinoma. They also do not appear to affect discontinuation rates due to toxicity.

Several systems (tumor‐node‐metastasis [TNM], Barcelona Clinic Liver Cancer [BCLC], Okuda, Cancer of the Liver Italian Program [CLIP], and albumin–bilirubin grade [ALBI]) were developed to estimate the prognosis of patients with hepatocellular carcinoma (HCC) mostly prior to the prevalent use of sorafenib. We aimed to compare the prognostic and discriminatory power of these models in predicting survival for HCC patients treated with sorafenib and to identify independent prognostic factors for survival in this population. Patients who received sorafenib for the treatment of HCC between 1 January 2008 and 30 June 2015 in the provinces of British Columbia and Alberta, and two large cancer centers in Toronto, Ontario, were included. Survival was assessed using the Kaplan–Meier method. Multivariate Cox regression was used to identify predictors of survival. The models were compared with respect to homogeneity, discriminatory ability, monotonicity of gradients, time‐dependent area under the curve, and Akaike information criterion. A total of 681 patients were included. 80% were males, 86% had Child–Pugh class A, and 37% of patients were East Asians. The most common etiology for liver disease was hepatitis B (34%) and C (31%). In all model comparisons, CLIP performed better while BCLC and TNM7 performed less favorably but the differences were small. The utility of each system in allocating patients into different prognostic groups varied, for example, TNM poorly differentiated patients in advanced stages (8.7 months (m) (95% CI 6.5–11.5) versus 8.4 m (95% CI 7.0–9.6) for stages III and IV, respectively) while ALBI had excellent discrimination of early grades (15.6 m [95% CI 13.0–18.4] versus 8.3 m [95% CI 7.0–9.2] for grades 1 and 2, respectively). On multivariate analysis, hepatitis C, alcoholism, and prior hepatic resection were independently prognostic of better survival (P

BACKGROUND The best model of care to retard diabetic kidney disease (DKD) in the clinic is underexplored. In this study we investigated the long-term renal outcomes of a joint endocrinologist-nephrologist clinic. METHODS The present study was a nested case-control study derived from a cohort of patients with type 2 diabetes mellitus (T2DM) seen prospectively at a secondary care diabetes center (DC). Cases ("DKD clinic group") were patients seen at the CKD clinic after being referred by physicians in DCs for management of DKD. Controls ("non-DKD clinic group") were patients from the same DC (i.e. same source population) with the same inclusion criteria of Stages 3-4 chronic kidney disease (CKD) at baseline but not seen at the DKD clinic. The outcome was Stage 5 CKD, defined as an estimated glomerular filtration rate

Background In the present study, we examined the association between HbA1c variability and renal disease progression based on estimated glomerular filtration rate (eGFR) decline in patients with type 2 diabetes mellitus (T2DM) in Singapore. Methods Glycemic burden and renal function were retrospectively assessed in 1628 patients in 2002–2014. Multivariable logistic regression was used to assess the relationships between HbA1c variability (expressed as HbA1c coefficient of variation [HbA1c-CV] in quartiles), HbA1c intrapersonal mean (HbA1c-IM), and eGFR decline, adjusted for baseline covariates. Results Among patients with relatively good glycemic control (i.e. HbA1c-IM below the median cohort value [8.0%]), HbA1c-CV Quartile 4 was associated with eGFR decline (odds ratio [OR] 1.88; 95% confidence interval [CI] 1.10–3.25). The OR for HbA1c-CV Quartile 4 was 2.20 (95% CI 1.24–3.89) after additional adjustment for HbA1c-IM. Where HbA1c-IM was above the median cohort value, HbA1c-CV Quartiles 3 and 4 were associated with eGFR decline, with ORs of 2.60 (95% CI 1.48–4.55) and 3.29 (95% CI 1.89–5.76) respectively. After further adjusting for HbA1c-IM, the ORs for Quartiles 3 and 4 were 2.69 (95% CI 1.53–4.74) and 3.51 (95% CI 1.98–6.21), respectively. Conclusions Variability in HbA1c is strongly and independently associated with eGFR decline in patients with T2DM independent of mean HbA1c. The findings may highlight the importance of sustained stable glycemic control in management of diabetes mellitus.

Aim To study prospectively the ethnic-specific risks of cardiovascular disease, end-stage renal disease and all-cause mortality in patients with Type 2 diabetes mellitus among native Asian subpopulations. Methods A total of 2337 subjects with Type 2 diabetes (70% Chinese, 17% Malay and 13% Asian Indian) were followed for a median of 4.0 years. Time-to-event analysis was used to study the association of ethnicity with adverse outcomes. Results Age- and gender-adjusted hazard ratios for cardiovascular disease in ethnic Malay and Asian Indian subjects were 2.01 (1.40–2.88; P

Aim Initial heparin locks instilled after tunnelled dialysis catheter (TDC) insertion can leak causing systemic anticoagulation and also promote staphyloccocal biofilm formation, predisposing to catheter-related infection (CRI). The 1000 U/mL concentration is thus advocated as the optimal dose for preventing catheter bleeding and malfunction. The effect of lower heparin concentrations on further lowering these complications is not known. We compared early TDC outcomes between a non-standard ultra-low (500 U/mL) and standard initial heparin locks (1000 and 5000 U/mL). Methods This was a retrospective study on prospectively collected data on 238 de novo internal jugular TDCs placed by nephrologists. Cases were categorized into groups 1, 2 and 3, according to initial heparin lock: 500 [n = 30], 1000 [n = 180] and 5000 U/mL [n = 28] respectively. Bleeding and malfunction within 24 h of TDC insertion, 30 days CRI-free catheter survival and the effects of clinical and laboratory factors on bleeding were evaluated. Results Bleeding events were similar in groups 1, 2 and 3 (7 vs 14 vs 13%, respectively, P = 0.61). Malfunction was only seen in group 2 (3.3%). Thirty-day CRI-free catheter survival was comparable (96 vs 98 vs 97%, respectively, P = 0.22), giving a cumulative CRI rate of 0.76/1000 catheter days. All CRIs were staphylococcal. Univariate analysis did not reveal any significant predictors of catheter bleeding. Conclusion Immediate TDC bleeding, malfunction and CRI rate are not influenced by heparin lock concentrations ≤5000 U/mL in this low-risk cohort. However this needs to be corroborated in higher risk patients.

Over the last number of years, the treatment of metastatic renal cell cancer has evolved tremendously with the advent of targeted therapy. Previously, immunotherapies, such as interferon alpha and interleukin-2, were the only treatment options available for this chemoresistant malignancy. Currently, seven additional agents, including sunitinib, sorafenib, axitinib, pazopanib, bevacizumab, everolimus and temsirolimus, have been approved for use in metastatic renal cell cancer, with several more in development. The efficacy of these agents depends primarily on inhibition of the vascular endothelial growth factor and mammalian target of rapamycin pathways, and have drastically improved the outcomes of patients diagnosed with metastatic renal cell cancer. This article reviews the major treatment advances that have occurred for metastatic renal cell cancer with the advent of targeted treatments, summarizes the evidence to support their use and addresses clinical issues that have arisen with them. To help guide clinicians in their decision-making with these emerging therapeutic choices, the evidence for sequencing and combining these agents, and the need for biomarkers will be addressed. The role of surgical management options, such as cytoreductive nephrectomy and metastectomy, in the era of targeted treatment is also reviewed. Several novel treatments are also on the horizon, which might serve as future avenues for treatment advancement in metastatic renal cell cancer.