Ketamine-associated diseases have been increasing with the rise in ketamine abuse. Ketamine-associated uropathy is one of the most common complications. We investigated the effects of ketamine-associated uropathy on renal health and determined predictors of renal function decline in chronic ketamine abusers. This retrospective cohort study analyzed 51 patients (22 with ketamine-associated hydronephrosis and 29 with ketamine cystitis) from Kaohsiung Veterans General Hospital in Taiwan. Primary renal outcome was end-stage renal disease or estimated glomerular filtration rate decline >30% from baseline. Compared with the ketamine cystitis group, the hydronephrosis group had lower initial and final estimated glomerular filtration rates and higher alkaline phosphatase and gamma-glutamyl transferase levels (p < 0.05). Elevated cholestatic liver enzyme levels correlated with renal dysfunction in ketamine-associated uropathy. The hydronephrosis group had a higher proportion of patients reaching endpoints than the ketamine cystitis group (50% and 7%, respectively, p < 0.001). After adjusting for age, sex, and initial serum creatinine level, hydronephrosis remained an independent risk factor for renal function deterioration. Ketamine-associated hydronephrosis was a poor renal outcome and strong predictor of renal function decline in chronic ketamine abusers. Elevated cholestatic liver enzyme levels correlated with the severity of ketamine-associated uropathy. Ultrasonography screening of these high-risk groups and regular renal function follow-ups are necessary.

Background: Hypokalemic periodic paralysis (HPP) is a rare channelopathy characterized by episodic attacks of acute muscle weakness concomitant with hypokalemia. The etiology of hypokalemia is the shift of potassium into the cells, and the clinical symptoms resolve when potassium starts to leak back to the serum. Most of the time, the underlying ion channel defects are well compensated, and an additional trigger is often required to initiate an attack. Well-known trigger factors include carbohydrate-rich meals, exercise followed by rest, stress, cold weather, and alcohol consumption. Case presentation: Here, we present the case of a 26-year-old Asian man who suffered from an acute onset of bilateral lower limb weakness with hypokalemia following dexamethasone injection. He was diagnosed with HPP. Conclusions: We would like to remind physicians to think of steroids as an unusual precipitating factor while managing patients with HPP, per results of this case study.

Background: The relationship between urokinase-type plasminogen activator (uPA) and the development of type 2 diabetes mellitus (T2DM) was investigated in the study by using mice and cell models, as well as patients with T2DM. Methods: In mice models, wild-type and uPA knockout (uPA-/-) BALB/c mice were used for induction of T2DM. In cell models, insulin secretion rate and β cell proliferation were assessed in normal and high glucose after treating uPA siRNA, uPA, or anti-uPA antibody. In our clinical study, patients with T2DM received an oral glucose-tolerance test, and the relationship between uPA and insulin secretion was assessed. Results: Insulin particles and insulin secretion were mildly restored one month after induction in wild-type mice, but not in uPA-/- mice. In cell models, insulin secretion rate and cell proliferation declined in high glucose after uPA silencing either by siRNA or by anti-uPA antibody. After treatment with uPA, β cell proliferation increased in normal glucose. In clinical study, patients with T2DM and higher uPA levels had better ability of insulin secretion than those with lower uPA levels. Conclusion: uPA may play a substantial role in insulin secretion, β cell regeneration, and progressive development of T2DM. Supplementation of uPA might be a novel approach for prevention and treatment of T2DM in the future.

Adverse renal effects of systemic vascular endothelial growth factor (VEGF) inhibitor treatment are well documented. We aimed to identify associations between intravitreal VEGF inhibitor use and renal function decline in patients with diabetic retinopathy. We included 625 patients with diabetic retinopathy for regular renal function follow-ups and grouped them according to intravitreal therapy (67 with and 558 without treatment). We used a generalized estimating equation model to identify renal function decline risk factors. Increased age (p = 0.02), insulin use (p = 0.01), hypertension (p < 0.01), and ischemic heart disease (p < 0.01) were associated with significantly decreased estimated glomerular filtration rates (eGFRs) in patients with diabetic retinopathy after 1-year follow-up. Compared to the control group, patients who received intravitreal VEGF inhibitor injections showed a declining eGFR trend in the repeated measurement model without statistical significance (p = 0.06). In subgroup analysis, patients with initial eGFR ≤ 30 mL/min/1.73 m² who received intravitreal VEGF inhibitors had significantly decreased renal function (p < 0.01) compared to those without treatment. Intravitreal VEGF inhibitor injection was associated with renal function deterioration among patients with diabetic retinopathy and advanced chronic kidney disease. Strategies to monitor renal function after treatment should be considered in these high-risk populations.

Patients with end-stage renal disease have a higher risk of cardiovascular morbidity and mortality. In this study, we investigated the predictive ability of a combination of cardiothoracic ratio (CTR) and aortic arch calcification (AoAC) for overall and cardiovascular mortality in patients receiving hemodialysis. We also evaluated the predictive power of AoAC and CTR for clinical outcomes. A total of 365 maintenance hemodialysis patients were included, and AoAC and CTR were measured using chest radiography at enrollment. We stratified the patients into four groups according to a median AoAC score of three and CTR of 50%. Multivariable Cox proportional hazards analysis was used to identify the risk factors of mortality. The predictive performance of the model for clinical outcomes was assessed using the χ2 test. Multivariable analysis showed that, compared to the AoAC < 3 and CTR < 50% group, the AoAC ≥ 3 and CTR < 50% group (hazard ratio [HR], 4.576; p < 0.001), and AoAC ≥ 3 and CTR ≥ 50% group (HR, 5.912; p < 0.001) were significantly associated with increased overall mortality. In addition, the AoAC < 3 and CTR ≥ 50% (HR, 3.806; p = 0.017), AoAC ≥ 3 and CTR < 50% (HR, 4.993; p = 0.002), and AoAC ≥ 3 and CTR ≥ 50% (HR, 8.614; p < 0.001) groups were significantly associated with increased cardiovascular mortality. Furthermore, adding AoAC and CTR to the basic model improved the predictive ability for overall and cardiovascular mortality. The patients who had a high AoAC score and cardiomegaly had the highest overall and cardiovascular mortality among the four groups. Furthermore, adding AoAC and CTR improved the predictive ability for overall and cardiovascular mortality in the hemodialysis patients.

The association between gout and injury remains unclear. This study aimed to investigate the injury risk in patients with gout. Using the Longitudinal Health Insurance Database (LHID) from 2000 to 2010 in Taiwan, patients with gout (group CFG) and those without gout (group C) were enrolled for further analysis. The CFG group was separated into two subgroups (with and without medication) to determine whether the risk of injury was reduced with drug intervention. The follow-up period was defined as the time from the initial diagnosis of gout to the date of injury. A total of 257,442 individuals were enrolled in this study, with 85,814 people in group CFG and 171,628 people in group C. Using Cox regression analysis, group CFG showed a significant increase in the risk of injury. Traffic injuries, poisoning, falls, crushing/cutting/piercing injury, and suicides were prominent among these injuries. Furthermore, when urate-lowing drugs were used to treat the CFG group, there were no significant differences in the occurrence of injury. Patients with gout had an increased risk of injury overall, and drug intervention did not lower the risk of injury in these patients.