Objectives Dental problems occur widely in patients with chronic kidney disease (CKD) and may increase comorbidities. Root canal therapy (RCT) is a common procedure for advanced decayed caries with pulp inflammation and root canals. However, end-stage renal disease (ESRD) patients are considered to have a higher risk of potentially life-threatening infections after treatment and might fail to receive satisfactory dental care such as RCT. We investigated whether appropriate intervention for dental problems had a potential impact among dialysis patients. Design Men and women who began maintenance dialysis (hemodialysis or peritoneal dialysis) between January 1, 2000, and December 31, 2015, in Taiwan (total 12,454 patients) were enrolled in this study. Participants were followed up from the first reported dialysis date to the date of death or end of dialysis by December 31, 2015. Setting Data collection was conducted in Taiwan. Results A total of 2633 and 9821 patients were classified into the RCT and non-RCT groups, respectively. From the data of Taiwan’s National Health Insurance, a total of 5,092,734 teeth received RCT from 2000 to 2015. Then, a total of 12,454 patients were followed within the 16 years, and 4030 patients passed away. The results showed that members of the non-RCT group (34.93%) had a higher mortality rate than those of the RCT group (22.79%; p = 0.001). The multivariate-adjusted hazard ratio for the risk of death was 0.69 (RCT vs. non-RCT; p = 0.001). Conclusions This study suggested that patients who had received RCT had a relatively lower risk of death among dialysis patients. Infectious diseases had a significant role in mortality among dialysis patients with non-RCT. Appropriate interventions for dental problems may increase survival among dialysis patients. Abbreviations: CKD = chronic kidney disease, ESRD = end-stage renal disease, RCT = root canal therapy.

Vitamin D has been described as an essential nutrient and hormone, which can cause nuclear, non-genomic, and mitochondrial effects. Vitamin D not only controls the transcription of thousands of genes, directly or indirectly through the modulation of calcium fluxes, but it also influences the cell metabolism and maintenance specific nuclear programs. Given its broad spectrum of activity and multiple molecular targets, a deficiency of vitamin D can be involved in many pathologies. Vitamin D deficiency also influences mortality and multiple outcomes in chronic kidney disease (CKD). Active and native vitamin D serum levels are also decreased in critically ill patients and are associated with acute kidney injury (AKI) and in-hospital mortality. In addition to regulating calcium and phosphate homeostasis, vitamin D-related mechanisms regulate adaptive and innate immunity. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections have a role in excessive proinflammatory cell recruitment and cytokine release, which contribute to alveolar and full-body endothelial damage. AKI is one of the most common extrapulmonary manifestations of severe coronavirus disease 2019 (COVID-19). There are also some correlations between the vitamin D level and COVID-19 severity via several pathways. Proper vitamin D supplementation may be an attractive therapeutic strategy for AKI and has the benefits of low cost and low risk of toxicity and side effects.

The catastrophic coronavirus disease 2019 (COVID-19) pandemic is currently a critical global issue. One well-known complication of COVID-19 in severe cases is acute kidney injury, but no research has given a description of its impact on the kidney in patients with mild symptoms. We explore the renal function changes in mild COVID-19 patients. This retrospective, single-center study included 27 participants with laboratory-detected severe acute respiratory syndrome coronavirus two (SARS-CoV-2) infection who were admitted to the Tri-Service General Hospital from 4 February to 26 May 2020 and analyzed their clinical features, radiological findings, and laboratory data. Data collected upon admission and discharge showed a median estimated glomerular filtration rate (eGFR) of 106.7 mL/min/1.732 m² and 112.2 mL/min/1.732 m², respectively, with a p-value of 0.044. A correlation between renal function and the severity of infection was also found and was statistically significant upon admission. Patients with a lower lymphocyte count or higher C-reactive protein, neutrophil count, and neutrophil-to-lymphocyte ratio presented with a decreased eGFR during their early infection phase. The biomarkers (CRP and NLR) may be linked with dynamic changes of renal function in COVID-19 patients who are asymptomatic or have mild symptoms.

Herpes zoster (HZ) has emerged as a post-viral complication in COVID-19 survivors, but its long-term clinical impact remains uncertain. This retrospective cohort study utilized the TriNetX Global Collaborative Network to evaluate whether HZ reactivation after COVID-19 is associated with increased risks of mortality, cardiovascular, and renal outcomes. Adults diagnosed with HZ within one year of COVID-19 were propensity score-matched 1:1 with controls without HZ. A total of 48,442 matched patients were followed for three years. Compared with controls, HZ patients had significantly higher risks of major adverse cardiovascular events (HR: 1.38, 95% CI: 1.30-1.46), acute kidney injury (HR: 1.67, 95% CI: 1.55-1.80), and renal function decline defined by eGFR < 60 mL/min/1.73 m² (HR: 1.28, 95% CI: 1.20-1.37). Although no significant difference in overall all-cause mortality was observed across the full follow-up period, time-stratified analysis revealed a biphasic pattern: patients with HZ had lower mortality risk during the first 90 days but showed significantly higher mortality from day 91 to three years post-COVID-19 (HR: 1.33, 95% CI: 1.24-1.44). Subgroup analyses consistently identified older age, chronic comorbidities, impaired renal function, and systemic inflammation as risk enhancers across outcomes. These findings suggest that HZ reactivation after COVID-19 signals a vulnerable subgroup predisposed to cardiorenal complications. Targeted follow-up and risk-based interventions are warranted in this population.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has become a global pandemic since December 2019. Most of the patients are mild or asymptomatic and recovered well as those suffered from other respiratory viruses. SARS-CoV-2 infection is supposed to demonstrate more sequelae. Acute kidney injury (AKI) is common among COVID-19 patients and is associated with disease severity and outcomes. Only a few studies focused on a detailed analysis of kidney damage in asymptomatic or mildly symptomatic COVID-19 patients. Whether any minor viral infection is likely to exhibit similar minor effect on renal function as COVID-19 is still unclear, and the definite pathophysiology of viral invasion is not fully understood. Currently, the proposed mechanisms of AKI include direct effects of virus on kidney, dysregulated immune response, or as a result of multi-organs failure have been proposed. This study will discuss the difference between COVID-19 and other viruses, focusing on proposed mechanisms, biomarkers and whether it matters with clinical significance.

Hypokalemic paralysis is a clinical syndrome characterized by acute flaccid paralysis with concomitant hypokalemia. Complications, such as acute respiratory failure and cardiac arrhythmias, can be fatal. If treated appropriately, the patient can recover without any sequelae. We present a rare case of life-threatening hypokalemic paralysis following the ingestion of an unknown substance. At presentation, her serum potassium concentration was 1.9 mmol/L. A review of the patient’s history confirmed the ingestion of barium chloride. She was diagnosed with acute barium poisoning characterized by high serum and urine barium levels. Aggressive potassium repletion was administered intravenously and orally. Her serum potassium concentration dropped to 1.5 mmol/L and peaked at 5.4 mmol/L following treatment. The patient achieved a complete recovery and was discharged without sequelae. Barium can competitively block the potassium inward rectifier channels and interfere with the efflux of intracellular potassium, leading to severe hypokalemia. Our report illustrates a rare presentation of acute barium intoxication and a differential diagnosis indicating hypokalemic paralysis. We also discuss the pathophysiological features and compare the clinical findings with cases of rebound hyperkalemia.