Clinical Kidney Journal最新文献

Patients with advanced cardiovascular kidney metabolic syndrome generally face a high risk of cardiovascular complications. Guideline-directed medical therapies (GDMT) are critical for mitigating cardiovascular risk and improving prognosis. However, patients with more advanced kidney disease have frequently been excluded from the foundational cardiovascular outcome trials, leaving clinicians with a paucity of evidence with regards to the cardiovascular benefits and potential risks involved in initiating or maintaining GDMT for cardiovascular diseases in patients with chronic kidney disease stages 4 and 5. Numerous studies have demonstrated a systematic underutilization of GDMT among patients with advanced chronic kidney disease (CKD), likely caused by a combination of clinical inertia and a legitimate fear of potential side-effects such as hyperkalemia and rises in creatinine, which may necessitate repeat laboratory monitoring, dose adjustment, and additional potassium-lowering treatment. In this clinical review, we aim to summarize the accumulating evidence with regards to the use of key cardiovascular drugs among patients with advanced CKD, with an emphasis on GDMT in patients with heart failure, and outline the treatment approach used in our integrated heart-nephrology-diabetes clinic. Since the evidence is not always clear and our patients are generally both older, frailer, and have more multimorbidity than those included in clinical trials, sound clinical judgment, individual patient tolerability as well as shared decision-making are key. We also address the need to continuously align treatment goals with patient preferences across different phases of life and adjusting GDMT in the face of increasing frailty.

Background: Hyponatraemia is one of the most common electrolyte disorders. While hyponatraemia can cause severe neurological symptoms, its clinical predictors remain poorly defined. This study aimed to identify factors associated with neurological involvement in patients with severe hyponatraemia.

Methods: This retrospective cohort study included patients with severe hyponatraemia (serum sodium level ≤120 mEq/L) at admission or during hospitalization between January 2014 and June 2024 in two tertiary centres. Neurological symptoms were defined as vomiting, deep somnolence, seizures, coma or cardiopulmonary arrest. Risk factors were evaluated using multivariable logistic regression analysis.

Results: Among 834 patients included in the analysis, the median (interquartile range) age was 73 (62-82) years, 382 (46%) were female and the median serum sodium level was 118 (116-119) mEq/L. Neurological symptoms were observed in 221 (26%). Low serum potassium [<4.0 mEq/L; odds ratio (OR) 1.53; 95% confidence interval (CI) 1.05-2.23] was independently associated with an increased risk of neurological symptoms, together with low serum sodium (<115 mEq/L; OR 2.23; 95% CI 1.49-3.33). Compared with chronic onset, both acute onset (OR 3.92; 95% CI 2.36-6.51) and uncertain onset (OR 2.05; 95% CI 1.40-2.99) also showed significant association with their occurrence.

Conclusion: Low serum potassium, low serum sodium and onset pattern were independent predictors of neurological symptoms in patients with severe hyponatraemia. Particularly in those with these risk factors, careful assessment and individualized management of sodium imbalance may be appropriate to achieve favourable outcomes.

Historically, the management of patients with nephrolithiasis has been primarily delivered by urologists. In recent decades nephrologists have had an increasing role in caring for these patients not only in advanced stages of chronic kidney disease (CKD) but also in the diagnosis and management of underlying systemic disease, and metabolic and genetic risk factors. Globally the burden of kidney stone disease has been increasing, with metabolic disorders strongly associated with nephrolithiasis and stone-promoting urinary risk factors, including hypercalciuria, hyperoxaluria and hypocitraturia. At a healthcare level, kidney stones account for a relatively large number of emergency department visits, while individually the impact of kidney stones and the fear of recurrence often result in loss of work and high levels of psychological distress, in addition to an increased CKD risk. Kidney stones in the context of CKD of unknown cause can be the signature of an inherited disorder such as Dent disease, primary hyperoxaluria or adenine phosphoribosyltransferase deficiency (among others). Diagnosing these diseases is imperative in the current age of new treatments (e.g. small interfering RNA therapies), to avoid further deterioration of kidney function and disease recurrence post-transplantation. We outline 10 practical tips to guide clinicians in the diagnostic evaluation and management of nephrolithiasis in CKD.

Background: Intradialytic hypotension and hypertension significantly increase cardiovascular risk in hemodialysis patients, highlighting the need for effective monitoring systems. By predicting systolic blood pressure (SBP) values, monitoring capabilities can be improved beyond traditional event classification. Despite this potential advantage, current predictive models report a consistent error range (11-13 mmHg) and operate as black boxes. This study aims to develop a transparent SBP prediction model and evaluate its generalizability.

Methods: This retrospective study analyzed data from 524 patients across metropolitan and suburban hospital branches (2016-19), collecting hemodialysis parameters, vital signs and predialytic measurements. The Explainable Boosting Machine (EBM) was used as the primary model to predict SBP changes. Cross-branch validation was implemented to evaluate model generalizability and perform feature selection. The EBM model was then compared with five other common machine learning methods.

Results: EBM with 16 dynamic features achieved competitive performance compared with other machine learning methods (mean absolute error: 10.57-11.33 mmHg, Pearson's r: 0.80-0.83) in cross-validation between branches. A waterfall plot visualized the model's additive scoring process, showing how each feature quantitatively contributes to the final SBP prediction. Error analysis of the models revealed strong positive correlations (Pearson's r: 0.81-0.87) between patients' blood pressure variability and prediction errors.

Conclusions: The EBM models demonstrated excellent cross-branch generalizability while providing feature-level transparency that reflects clinical understanding of dialysis physiology, unlike black-box models that require additional post-hoc explanation methods such as SHapley Additive exPlanations (SHAP). These findings provide a foundation for developing patient-specific solutions for individuals with highly variable blood pressure patterns.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter 2 inhibitors (SGLT-2is) have been shown to provide extra-glycemic advantages, such as cardiovascular and renal protection, in the treatment of type 2 diabetic mellitus (T2DM). Recent data points to the possibility that gut microbiota modification may contribute to their beneficial impact. This review examines changes in microbial composition, metabolite synthesis (such as short-chain fatty acids (SCFA), bile acids, and endotoxins), and their systemic implications by integrating clinical and preclinical data on the interactions between various drug types and the gut microbiota. GLP-1RAs may favor certain taxa that synthesize SCFA and Akkermansia muciniphila. This may improve insulin sensitivity and lower inflammation. Likewise, SGLT-2is may favor a eubiotic state, which is associated with better renal and metabolic outcomes. We also discuss the use of baseline microbial profiles to predict therapy responses in a microbiota-informed precision medicine approach. Larger human investigations are required to explore causality and therapeutic efficacy, as mechanistic insights are still limited despite early encouraging findings. This narrative review synthesizes both clinical and preclinical data identified through PubMed, Scopus, Web of Science, Embase, and Google Scholar up to May 2025. Personalized holistic T2DM therapy plans that integrate both host and microbial pathways may be made possible by gut microbiota studies.

Sodium-glucose cotransporter-2 inhibitors (SGLT2i) reduce the risk of end-stage kidney disease (ESKD), cardiovascular events, and all-cause mortality in chronic kidney disease (CKD), regardless of diabetes or baseline renal function. However, patients with severely impaired kidney function or on dialysis have been excluded from landmark randomized clinical trials (RCTs). Several off-target mechanisms of SGLT2i could be involved in the cardiac protection of patients with ESKD in which the reduced nephron mass strongly diminishes the tubular effects of SGLT2i. However, available evidence in patients undergoing hemodialysis (HD) and peritoneal dialysis (PD) is limited thus leaving efficacy and safety in this population uncertain. Pharmacokinetic studies confirm that dapagliflozin is not dialyzable and shows no significant accumulation in dialysis patients. Small exploratory trials reported favorable cardiovascular and electrophysiological effects of SGLT2i in HD, while retrospective studies suggest they may preserve residual kidney function in incremental dialysis and improve volume status without major safety concerns. Large retrospective cohort analyses of patients starting dialysis showed lower risks of cardiovascular events and mortality in SGLT2i users compared with non-users. When treated with PD, no study has reported outcome data, and findings on efficacy were mixed with some studies showing increased ultrafiltration and lower blood pressure, while others showed no effect on peritoneal glucose transport. The theoretic protection against cardiovascular and mortality risk of SGLT2i must be confirmed by ongoing large-scale trials that will clarify the role of this class of drugs in dialysis populations.

Background: This study aimed to investigate the significance of persistent haematuria in lupus nephritis (LN).

Methods: A total of 178 patients with LN were enrolled and regularly followed up from December 2016 to September 2022. Follow-up duration was from LN diagnosis to the patient's latest visit or terminated at the onset of endpoint events if they occurred. Their clinical and laboratory data as well as outcomes were monitored and analysed from the enrolment point until the final visit.

Results: A total of 138 of 178 (77.5%) patients with LN presented with haematuria at the initial diagnosis. During follow-up, 34 patients (19.1%) had no haematuria, 72 (40.4%) patients initially diagnosed but later resolved and 66 (37.1%) exhibited persistent haematuria. Furthermore, patients with persistent haematuria showed higher Systemic Lupus Erythematosus Disease Activity Index scores (12.3 ± 2.9 versus 10.7 ± 3.6; P = .002), lower haemoglobin (92.7 ± 25.4 g/l versus 102.0 ± 21.1; P = .010), albumin (24.9 ± 6.8 g/l versus 27.5 ± 7.6; P = .024) and decreased C3 {median 0.4 g/l [interquartile range (IQR) 0.3-0.5]} versus 0.5 [0.3-0.6]; P = .009} and C4 [median 0.1 g/l (IQR 0.0-0.1) versus 0.1 (0-0.1); P = .012] and elevated blood urea nitrogen and serum creatinine [median 8.9 mmol/l (IQR 6.7-14.8) versus 5.7 (4.4-8.8) and median 90.0 μmol/l (IQR 64.5-132.3) versus 62.0 (48.0-80.0); all P < .001, respectively] compared with those without persistent haematuria (n = 106). In time-dependent Cox proportional hazards regression models, persistent haematuria exhibited a significant overall time-averaged effect on composite clinical endpoints, with an adjusted hazard ratio of 3.40 (95% CI 1.06-10.90; P = .039). Notably, this risk effect was not fixed but showed an increasing trend over time-at 1 months of follow-up, the risk of adverse outcomes in patients with persistent haematuria had increased to 10.37-fold.

Conclusions: Almost 37.1% of patients exhibited persistent haematuria in LN. Furthermore, persistent haematuria independently predicted adverse outcomes, with significantly higher risks for all-cause mortality and progression to renal replacement therapy.

Background: Contrast-associated acute kidney injury (CA-AKI) has been reported to occur in a significant proportion of patients undergoing percutaneous coronary intervention (PCI). The role of remote ischemic preconditioning (RIPC) in CA-AKI prevention remains unclear.

Methods: In this single-center double-blind randomized controlled trial, 420 eligible patients with high risk of CA-AKI admitted for PCI were randomized into two groups: RIPC and sham RIPC (control group). RIPC was performed by repeated cycles of inflation and deflation of an upper limb blood pressure cuff prior to PCI. Serum neutrophil gelatinase-associated lipocalin (NGAL) levels were measured at 2- and 6-h, and serum creatinine at 24- and 48-h post-PCI. The primary endpoint was the incidence of CA-AKI. Secondary endpoints were change in serum creatinine at 48 h, incidence of subclinical AKI (defined as an increase in NGAL values by 25% or more from baseline), change in NGAL at 2- and 6-h (delta NGAL), in-hospital mortality and major adverse cardiovascular events (MACE) at Day 30.

Results: CA-AKI occurred in 11.4% (n = 48), with AKI stage 1 in 10.2% (n = 42). The incidence of CA-AKI was significantly lower in the RIPC group, compared with control group [8.1% vs 15.0%, risk ratio (RR) 0.54, 95% confidence interval (CI) 0.31-0.94; P = .027]. There was no significant difference in change in creatinine at 48 h in both the groups (P = .158). The incidence of subclinical AKI was also numerically lower in the RIPC group; however, this was not statistically significant (36.2% vs 40.5%, RR 0.89, 95% CI 0.66-1.22; P = .158). Dialysis-requiring AKI, in-hospital mortality and 30-day MACE were similar in both groups. There were no RIPC-related adverse events.

Conclusions: In patients at high risk of developing CA-AKI after PCI, RIPC is an effective and safe preventive measure.

Introduction: In patients with incident end-stage kidney disease (ESKD), hyperkalemia (HyperK) is a common indication for initiating kidney replacement therapy (KRT). Hemodialysis (HD) and peritoneal dialysis (PD) both effectively reduce serum potassium, but HD is often considered superior due to its perceived faster efficiency. However, evidence supporting this perception remains limited. We hypothesized that HD and PD would be equally effective for the management of severe HyperK during hospitalization.

Methods: We conducted a prospective cohort study at the Nephrology Department of Hospital Civil de Guadalajara. Consecutive, dialysis-naïve patients hospitalized with ESKD and severe HyperK (serum potassium >6.5 mEq/L at admission) between 2022 and 2024 were included. The modality of KRT (HD vs PD) was determined by the treating nephrology team. The primary outcome was the trajectory of serum potassium reduction between groups. Secondary outcomes included daily potassium trajectory, catheter dysfunction, length of stay and mortality.

Results: Eighty-two patients were included: 34 initiated PD, 37 HD and 11 received conservative management. Baseline demographic and clinical characteristics were similar across groups (P > .05). Median age was 65 years [interquartile range (IQR) 53-74], with diabetes in 33% and hypertension in 53%. Median admission potassium was 6.99 mEq/L (6.7-7.6), serum creatinine 15.9 mg/dL (11.5-23.1) and estimated glomerular filtration rate 2.91 mL/min/1.73 m² (1.80-4.09). The PD group underwent a mean of 45 (±15) exchanges during hospitalization, and the HD group received 4.6 (±1) sessions. Serum potassium decreased similarly in both groups (P > .05), with substantial reductions on Day 1 (PD 6.03 mEq/L; HD 5.90 mEq/L) and stabilization by Day 5 through Day 15. Catheter dysfunction occurred in 11% of patients, with similar rates between groups, hospitalization median was 5 days (IQR 3-8) and 12-month mortality was 26.8%, without differences between modalities.

Conclusions: In this prospective cohort of ESKD patients with severe HyperK, both PD and HD achieved comparable potassium reduction and clinical outcomes, supporting PD as an effective alternative for urgent-start KRT.

Background: Increased tissue sodium (Na⁺) concentration is associated with adverse clinical outcomes in people with chronic kidney disease (CKD) including hypertension, inflammation and increased cardiovascular disease (CVD). 23-Sodium magnetic resonance imaging (²³Na-MRI) can non-invasively quantify tissue Na⁺ concentration. However, in the CKD population, few studies have evaluated relationships between ²³Na-MRI-derived tissue Na⁺ concentrations and measures of Na⁺ metabolism, surrogate markers of CVD and other CKD-related health complications.

Methods: We conducted a cross-sectional cohort study, involving 51 participants with CKD (28 with non-dialysis CKD, 23 on dialysis), to explore relationships between ²³Na-MRI-derived tissue Na⁺ concentrations (including skin, bone, muscle and whole leg-tissue), measures of Na⁺ metabolism and CKD-related health outcomes. Multivariable regression and correlation analyses were used to assess associations.

Results: Skin and whole leg-tissue Na⁺ concentrations were positively associated with surrogate cardiovascular markers of troponin I and brain natriuretic peptide (P < .05). Bone and whole leg-tissue Na⁺ concentrations were negatively associated with bone mineral density. Higher muscle Na⁺ concentration was associated with lower levels of physical well-being. Tissue Na⁺ concentration was positively correlated with extracellular fluid volume as measured by proton (¹H) MRI (P ≤ .001) and body composition monitor (P < .05).

Conclusion: Whole leg-tissue Na⁺ in addition to skin Na⁺ concentration may be a useful clinical marker of body Na⁺ with related health outcomes. Tissue Na⁺ may play a role in CVD, bone health and quality of life in people with CKD, representing a potential therapeutic target to improve clinical outcomes.