Background: Secondary hyperparathyroidism (sHPT) develops frequently in patients with chronic kidney disease (CKD). However, the burden and long-term impact of sHPT on the risk of adverse health outcomes are not well studied. Methods: We evaluated all adults receiving nephrologist care in Stockholm during 2006–11 who were not undergoing kidney replacement therapy and had not developed sHPT. Incident sHPT was identified by using clinical diagnoses, initiated medications or two consecutive parathyroid hormone (PTH) measurements ≥130 pg/mL. We characterized sHPT incidence by estimated glomerular filtration rate (eGFR) strata, evaluated clinical predictors and quantified the association between incident sHPT (time-varying exposure) and the risk of fractures, CKD progression, major adverse cardiovascular events (MACEs) and death. Results: We identified 2556 adults with CKD Stages 1–5 (mean age 66 years, 38% women), of whom 784 developed sHPT during follow-up. The incidence of sHPT increased with advancing CKD: from 57 cases/1000 person-years in CKD Stage G3 to 230 cases/1000 person-years in Stage G5. In multivariable analyses, low eGFR was the strongest sHPT predictor, followed by young age, male sex and diabetes. Incident sHPT was associated with a 1.3-fold (95% confidence interval 1.1–1.8) increased risk of death, a 2.2-fold (1.42–3.28) higher risk of MACEs, a 5.0-fold (3.5–7.2) higher risk of CKD progression and a 1.3-fold (1.5–2.2) higher risk of fractures. Results were consistent in stratified analyses and after excluding early events. Conclusions: Our findings illustrate the burden of sHPT in advanced CKD and highlight the susceptibility for adverse outcomes of patients developing sHPT. This may inform clinical decisions regarding pre-sHPT risk stratification, PTH monitoring and risk-prevention strategies post-sHPT development.

OBJECTIVE Patients with diabetes and chronic kidney disease (CKD) have increased susceptibility to acute kidney injury (AKI), but mechanisms are unclear. We investigated the association of glycemic control with risk of AKI. RESEARCH DESIGN AND METHODS In two observational cohorts of U.S. (Geisinger Health System, Danville, PA) and Swedish (Stockholm CREAtinine Measurements [SCREAM] project, Stockholm, Sweden) adults with type 2 diabetes and confirmed CKD stages G3–G5 undergoing routine care, we evaluated associations between baseline and time-varying hemoglobin A_1c (HbA_1c) with the incident AKI (defined as increase in creatinine ≥0.3 mg/dL over 48 h or 1.5 times creatinine over 7 days). RESULTS In the U.S. cohort, there were 22,877 patients (55% women) with a median age of 72 years and estimated glomerular filtration rate (eGFR) 52 mL/min/1.73 m². In the Swedish cohort, there were 12,157 patients (50% women) with a median age of 77 years and eGFR 51 mL/min/1.73 m². During 3.1 and 2.3 years of follow-up, 7,060 and 2,619 AKI events were recorded in the U.S. and Swedish cohorts, respectively. The adjusted association between baseline HbA_1c and AKI was similar in both cohorts. Compared with baseline HbA_1c 6–6.9% (42–52 mmol/mol), the hazard ratio for AKI in patients with HbA_1c >9% (75 mmol/mol) was 1.29 (95% CI 1.18–1.41) in Geisinger and 1.33 (95% CI 1.13–1.57) in the Swedish cohort. Results were consistent in stratified analysis, when using death as competing risk, and when using time-varying HbA_1c. CONCLUSIONS Higher HbA_1c was associated with AKI in adults with type 2 diabetes and CKD, suggesting that improving glycemic control may reduce the risk of AKI.

Background: Sepsis affects millions of people and imposes a substantial economic and social burden worldwide. However, the role of human albumin in the management of septic patients remains unclear. Methods: EMBASE, PubMed, and Cochrane Library databases were searched. Randomized controlled trials regarding the use of human albumin in septic patients were eligible. The overall mortality and the intensive care unit (ICU), in-hospital/28-day, and 90-day mortality were pooled, respectively. Subgroup analyses were performed according to target population, type and dose of human albumin, and type of control group. Risk ratios (RRs) was calculated. Results: Twenty-four randomized controlled trials were finally included. Meta-analysis showed that human albumin cannot decrease the overall (RR = 1.02, P = .56), ICU (RR = 1.06, P = .65), in-hospital/28-day (RR = 1.01, P = .68), and 90-day (RR = 1.01, P = .65) mortality of total patients. Subgroup analyses showed that human albumin both cannot significantly decrease the overall, ICU, in-hospital/28-day, and 90-day mortality of sepsis and septic patients. Additionally, 20% human albumin (RR = 0.89, P = .03) and high daily dose of human albumin (RR = 0.90, P = .03) might benefit for the survival of patients with septic shock. Conclusions: Based on the current evidence, the general use of human albumin to improve the survival of septic patients cannot be recommended.

Preclinical studies suggest that acute kidney injury (AKI) results in biochemical and pathologic changes in the brain. We aimed to explore the association between experiencing AKI and subsequent risks of developing dementia. We conducted a study involving individuals aged 65 years and older in Stockholm from 2006 to 2019, who were free from dementia diagnosis and had data on kidney function. The exposure was an episode of AKI (time varying), ascertained by issued clinical diagnoses and transient creatinine elevations according to Kidney Disease Improving Global Outcomes criteria. The outcome was all-cause dementia and specific types of dementia, ascertained by clinically confirmed cases in the Swedish registry of cognitive/dementia disorders, the presence of 2 issued dementia diagnoses in outpatient care, or initiation of specific antidementia medications. We investigated associations with dementia through Cox proportional hazard regression by AKI, severity levels of AKI, AKI recurrence, and setting (community-acquired or hospital-acquired AKI). We included 305,122 individuals with a median age of 75 ± 8 years (56.6% women). During a median follow-up of 12.3 (interquartile range 8.7-13.3) years, there were 79,888 individuals (26%) suffering from at least 1 episode of AKI and 47,938 incident cases (16%) of dementia. The rate of dementia cases was 37.0 per 1,000 person-years (95% CI 36.2-37.8) after developing AKI, which was approximately 2 times higher than the rate observed during the periods before AKI (17.3, 95% CI 17.2-17.5). After multivariable adjustment, developing AKI was associated with a 49% higher rate of subsequent dementia (adjusted hazard ratio hazard ratio [HR] 1.49, 95% CI 1.45-1.53). This pattern was consistent across dementia types, with HRs of 1.88 (95% CI 1.53-2.32), 1.47 (1.38-1.56), and 1.31 (1.25-1.38) for dementia with Lewy bodies and Parkinson disease with dementia, vascular dementia, and Alzheimer dementia, respectively. Risk associations were stronger in magnitude across more severe AKIs and in hospital-acquired vs community-acquired AKI. Individuals who experienced an AKI were at increased risk of receiving a diagnosis of dementia.