Pseudohyponatremia remains a problem for clinical laboratories. In this study, we analyzed the mechanisms, diagnosis, clinical consequences, and conditions associated with pseudohyponatremia, and future developments for its elimination. The two methods involved assess the serum sodium concentration ([Na]_S) using sodium ion-specific electrodes: (a) a direct ion-specific electrode (ISE), and (b) an indirect ISE. A direct ISE does not require dilution of a sample prior to its measurement, whereas an indirect ISE needs pre-measurement sample dilution. [Na]_S measurements using an indirect ISE are influenced by abnormal concentrations of serum proteins or lipids. Pseudohyponatremia occurs when the [Na]_S is measured with an indirect ISE and the serum solid content concentrations are elevated, resulting in reciprocal depressions in serum water and [Na]_S values. Pseudonormonatremia or pseudohypernatremia are encountered in hypoproteinemic patients who have a decreased plasma solids content. Three mechanisms are responsible for pseudohyponatremia: (a) a reduction in the [Na]_S due to lower serum water and sodium concentrations, the electrolyte exclusion effect; (b) an increase in the measured sample’s water concentration post-dilution to a greater extent when compared to normal serum, lowering the [Na] in this sample; (c) when serum hyperviscosity reduces serum delivery to the device that apportions serum and diluent. Patients with pseudohyponatremia and a normal [Na]_S do not develop water movement across cell membranes and clinical manifestations of hypotonic hyponatremia. Pseudohyponatremia does not require treatment to address the [Na]_S, making any inadvertent correction treatment potentially detrimental.

Diabetes mellitus (DM) and chronic kidney disease (CKD) are common in middle aged and older adult individuals. DM may accelerate the aging process, and the age-related declines in the estimated glomerular filtration rate (eGFR) can pose a challenge to diagnosing diabetic kidney disease (DKD) using standard diagnostic criteria especially with the absence of severe albuminuria among older adults. In the presence of CKD and DM, older adult patients may need multidisciplinary care due to susceptibility to various health issues, e.g., cognitive decline, auditory or visual impairment, various comorbidities, complex medical regimens, and increased sensitivity to medication adverse effects. As a result, it can be challenging to apply recent therapeutic advancements for the general population to older adults. We review the evidence that the benefits from these newer therapies apply equally to older and younger patients with CKD and diabetes type 2 and propose a comprehensive management. This framework will address nonpharmacological measures and pharmacological management with renin angiotensin system inhibitors (RASi), sodium glucose co-transporter 2 inhibitors (SGLT2i), non-steroidal mineralocorticoids receptor antagonists (MRAs), and glucagon like peptide 1 receptor agonists (GLP1-RAs).

Chronic insomnia is common in patients undergoing in-center hemodialysis, yet there is limited evidence on effective treatments for this population. To compare the effectiveness of cognitive behavioral therapy for insomnia (CBT-I), trazodone, and placebo for insomnia in patients undergoing long-term hemodialysis. Randomized, multicenter, double-blinded, placebo-controlled trial. (ClinicalTrials.gov: NCT03534284). 26 dialysis units in Albuquerque, New Mexico, and Seattle, Washington. Patients with Insomnia Severity Index (ISI) score of 10 or greater, with sleep disturbances on 3 or more nights per week for 3 or more months. Participants were randomly assigned to 6 weeks of CBT-I, trazodone, or placebo. The primary outcome was the ISI score at 7 and 25 weeks from randomization. A total of 923 patients were prescreened, and of the 411 patients with chronic insomnia, 126 were randomly assigned to CBT-I (n = 43), trazodone (n = 42), or placebo (n = 41). The change in ISI scores from baseline to 7 weeks with CBT-I or trazodone was no different from placebo: CBT-I, -3.7 (95% CI, -5.5 to -1.9); trazodone, -4.2 (CI, -5.9 to -2.4); and placebo, -3.1 (CI, -4.9 to -1.3). There was no meaningful change in ISI scores from baseline to 25 weeks: CBT-I, -4.8 (CI, -7.0 to -2.7); trazodone, -4.0 (CI, -6.0 to -1.9); and placebo, -4.3 (CI, -6.4 to -2.2). Serious adverse events (SAEs), particularly serious cardiovascular events, were more frequent with trazodone (annualized cardiovascular SAE incidence rates: CBT-I, 0.05 [CI, 0.00 to 0.29]; trazodone, 0.64 [CI, 0.34 to 1.10]; and placebo, 0.21 [CI, 0.06 to 0.53]). Modest sample size and most participants had mild or moderate insomnia. In patients undergoing hemodialysis with mild or moderate chronic insomnia, there was no difference in the effectiveness of 6 weeks of CBT-I or trazodone compared with placebo. The incidence of SAEs was higher with trazodone. National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases.

Background: Automated peritoneal dialysis (APD) is one of the fastest growing dialysis modalities. It is unknown whether sleep and mood are disturbed while performing repeated overnight exchanges. Objectives: In this report, we aim to describe and compare the prevalence of sleep-disordered breathing (SDB), periodic limb movements (PLMS), poor sleep quality (SQ), and depression among APD patients compared with stages 3b–5 (estimated glomerular filtration rate ≤44 ml/min/1.73 m2) chronic kidney disease (CKD) and hemodialysis (HD) patients. Design: This is a cross-sectional, descriptive study. Setting: Study participants were recruited from outpatient nephrology clinics, local dialysis centers, and the Thomas E. Starzl Transplant Institute in Western Pennsylvania between April 2004 and July 2009. Patients: There were 186 participants in this study including 22 APD patients, 89 CKD patients, and 75 HD patients. Measurements: In-home polysomnography was performed and two questionnaires were completed, the Pittsburgh Sleep Quality Index (PSQI) and the Patient Health Questionnaire-9 (PHQ-9). Methods: SDB and PLMS were quantified by in-home unattended polysomnography; poor SQ was defined by a score >5 on the PSQI, and the presence of moderate to severe depression was defined by a score >5 on the PHQ-9. Results: The APD patients had a median age of 37.5 years, were predominantly female (72.7 %), and had a median body mass index (BMI) of 23.8 kg/m2. In univariate analyses, APD patients had significantly lower apnea-hypopnea index compared to HD patients by 12.2 points (likelihood ratio test p = 0.008) and revealed the least percent of TST with nocturnal hypoxemia compared to CKD patients by 2.7 points, respectively (likelihood ratio test p = 0.01). The APD group had also significantly greater stages 3 to 4 sleep compared to the CKD patients by 8.6 points (likelihood ratio test p = 0.009). In multivariate analyses and after adjustment for age, gender, race, and BMI, both APD and HD patients had higher average PSQI scores than CKD patients by 2.54 and 2.22 points, respectively (likelihood ratio test p = 0.005). No other comparisons of sleep parameters among groups reached statistical significance. Limitations: The limitations of this study are the small sample size of the APD population and the demographic and clinical differences among the three study groups. Conclusions: Despite differences in univariate analyses, after multivariate adjustment, APD patients had similar sleep parameters and sleep architecture and as poor SQ and symptoms of depression as HD patients. Future studies with larger APD cohorts are needed.