Introduction: Hyponatremia is the most common electrolyte imbalance in hospitalized patients, associated with increased morbidity and mortality. Tolvaptan effectively raises serum sodium in SIADH. However, concerns regarding rapid overcorrection and safety persist. This study evaluates the efficacy, safety, and real-world usage patterns of tolvaptan in a tertiary care setting. Methodology: A retrospective single-centre observational study was conducted at Hospital Putrajaya using the electronic records of patients treated with tolvaptan from January 2020 to December 2025. Overcorrection was defined as >10 mmol/L increase within 24 hours, and non-response as <4 mmol/L increment at 24 hours. Results: Twenty-one patients were included, with a mean age of 66.7 years; 57% were male. Most (90.5%) received 7.5 mg initially. Mean baseline sodium was 118.1 ± 4.1 mmol/L. Tolvaptan produced rapid correction, with mean sodium increasing to 127.0 mmol/L at 24 hours (mean increment 8.9 mmol/L). Only one patient (4.8%) was a non-responder at 24 hours. Median time to sodium >130 mmol/L was 1 day, with 60% achieving this within 24 hours. At discharge, mean sodium was 130.4 mmol/L. Median length of stay following initiation was 5.5 days. Overcorrection occurred in 23.8% (n = 5), all in the 7.5 mg group, particularly among those with baseline sodium 115–120 mmol/L. No cases of osmotic demyelination syndrome (ODS) were observed. The mean internal for initiation is approximately 6 days from diagnosis. Tolvaptan usage increased and peaked in the first 3 years, but subsequently dropped and plateaued over the last 2 years. Conclusion Tolvaptan is safe and effective for sodium correction; although overcorrection remains a risk, no long-term sequelae of ODS were observed, underscoring the need for vigilant monitoring. Its use in Hospital Putrajaya remains limited, with delayed initiation possibly due to tolvaptan being considered a secondary treatment after failure of other options
Hyponatremia ; Tolvaptan

INTRODUCTION: We investigated the factors associated with readmission in patients with congestive heart failure (HF) receiving long-term administration of tolvaptan (TLV) to support treatment decisions for HF. METHODS: This retrospective cohort study included 181 patients with congestive HF who received long-term administration of TLV. Long-term administration of TLV was defined as the administration of TLV for 60 days or longer. The outcome was a readmission event for worsening HF within 1 year after discharge. Significant factors associated with readmission were selected using multivariate analysis. To compare the time to readmission using significant factors extracted in a multivariate analysis, readmission curves were constructed using the Kaplan-Meier method and analysed using the log-rank test. RESULTS: The median age was 78 years (range, 38-96 years), 117 patients (64.6%) were males, and 77 patients (42.5%) had a hospitalisation history of HF. Readmission for worsening HF within 1 year after long-term TLV treatment occurred in 62 patients (34.3%). In the multivariate analysis, estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m 2 (odds ratio, 3.22; 95% confidence interval, 1.661-6.249; P = 0.001) was an independent significant factor. When eGFR at discharge was divided into two groups (eGFR < 30 vs. eGFR ≥ 30), readmission rates within 1 year were 53.3% vs. 25.4%, respectively ( P = 0.001). CONCLUSION We revealed that eGFR was strongly associated with readmission in patients with HF who received long-term administration of TLV. Furthermore, we showed that eGFR is an important indicator in guiding treatment of HF in patients receiving TLV.
Humans ; Tolvaptan/therapeutic use* ; Heart Failure/drug therapy* ; Male ; Female ; Patient Readmission/statistics & numerical data* ; Aged ; Retrospective Studies ; Aged, 80 and over ; Middle Aged ; Glomerular Filtration Rate ; Adult ; Antidiuretic Hormone Receptor Antagonists/therapeutic use* ; Risk Factors ; Kaplan-Meier Estimate ; Multivariate Analysis

Humans ; Tolvaptan/therapeutic use* ; Ascites/drug therapy* ; Receptors, Vasopressin ; Liver Cirrhosis/drug therapy* ; Sodium

Autosomal dominant polycystic kidney disease (ADPKD) is a common hereditary disease, mainly caused by polycystic kidney disease 1/2 (PKD1/2) gene mutation. The main manifestation is the formation of multiple progressive enlarged cysts in both kidneys, which can be accompanied by decreased glomerular filtration rate, hypertension, liver cyst and cerebral aneurysm. About 45% of patients will progress to end-stage renal failure before the age of 60. ADPKD gene sequencing can be chosen for suspicious patients with atypical clinical features, no positive family history, and inconspicuous imaging findings. In the ADPKD positive families, imaging examination is the main means of diagnosing ADPKD. Height-adjusted total kidney volume (htTKV) and kidney growth rate are commonly used to monitor ADPKD disease progression and prognosis. There is no effective treatment for ADPKD to stop its progress. Drugs such as tolvaptan and bosutinib can delay the renal disfunction and they have been applied to clinical therapy in Europe and America.
Disease Progression ; Glomerular Filtration Rate ; Humans ; Kidney ; Polycystic Kidney, Autosomal Dominant ; Tolvaptan