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.

Autosomal dominant polycystic kidney disease (ADPKD) is a complex, multisystemic disorder exhibiting notable sex-related differences in clinical presentation, progression and complications. While the disease affects both sexes, disease expression and complications differ significantly between men and women. This review explores the biological, hormonal and psychosocial sex differences in ADPKD across multiple clinical domains. Men tend to experience faster kidney growth, earlier onset of hypertension and slightly younger age at kidney replacement therapy. Women, in contrast, are more susceptible to polycystic liver disease (PLD), often exacerbated by oestrogen exposure, especially during pregnancy or hormonal treatments. Although urinary tract infections are more prevalent among women, cyst infections show no major sex-based difference in incidence, although men may respond less favourably to antibiotic therapy. Cardiovascular complications, intracranial aneurysms and reproductive health risks also show sex-related patterns. Fertility and reproductive counselling must be individualized, as reproductive challenges and risks differ markedly between men and women. Pregnancy in women with ADPKD, especially those with reduced renal function or PLD, carries increased risks and requires specialized care. Fertility in men with ADPKD is usually preserved, although sometimes it may be impaired due to seminal vesicle cysts and sperm morphological abnormalities. However, assisted reproductive techniques generally achieve outcomes comparable to those of unaffected individuals. Psychosocial aspects such as pain, emotional burden and quality of life are also influenced by sex and require integrated management strategies. While tolvaptan slows disease progression in both sexes, pharmacodynamic responses may differ slightly. Incorporating sex-specific insights into ADPKD care, including hormonal and reproductive considerations, is critical to advancing personalized medicine. Understanding these differences will optimize management and improve quality of life for individuals living with ADPKD.

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: Hypertension (HTN) is a leading risk factor for cardiovascular disease, and dietary sodium reduction is a cornerstone strategy for blood pressure (BP) control, particularly in vulnerable populations such as individuals with chronic kidney disease (CKD), who often present with HTN. This study aims to quantify the dose-response relationship between changes in sodium intake and changes in BP, through a meta-analysis of recent randomized controlled trials (RCTs) in individuals with CKD and with or without HTN.

Methods: A systematic literature search was conducted in PubMed, Cochrane Central and Embase databases to identify RCTs published since 2000 that evaluated the isolated effect of sodium intake modification on systolic and diastolic. Only trials estimating sodium intake via 24-h urinary sodium excretion were included to ensure accurate measurement of dietary intervention. A random-effects model was used to pool effect sizes, accounting for between-study heterogeneity. Linear, quadratic and cubic dose-response models were fitted and compared with identify the best-fitting relationship between sodium change and BP change.

Results: The analysis included 43 RCTs with 51 distinct population groups, involving 1759 subjects. The linear model best described the dose-response relationship in subjects with CKD, with or without HTN. A reduction in sodium intake of 40 mmol/day (approximately 2.4 g of salt) was associated with a mean systolic BP/diastolic BP reduction of -4.5 mmHg (95% confidence interval -5.8, -3.1)/-2.2 mmHg (-3.0, -1.3) in patients with CKD, -2.3 mmHg (-3.0, -1.6)/-1.1 mmHg (-1.5, -0.6) in patients with HTN and -0.3 mmHg (-0.5, -0.1)/-0.1 mmHg (-0.2, -0.1) in patients without HTN.

Conclusion: Reducing sodium intake has a pronounced antihypertensive effect in patients with CKD and/or HTN. Regardless of the variability in effect according to BP status, adopting a low-salt diet represents good clinical practice and should be considered a standard prescription, particularly for individuals with CKD, as it supports better BP control and helps reduce cardiovascular risk.

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.

The transition from paediatric to adult renal care is a challenging time for children and young people (CYP). For them, this is a period of seismic change overall and a key step during their journey from parental support to independence. Improving outcomes in paediatric care is resulting in a growing population of CYP who require transition and individualised care planning. The point of transfer to adult services is also a risk escalator to long-term health and it is important to avoid disengagement. Awareness of neurodevelopmental biology and its effects on decision-making is a cornerstone to understanding the behaviour of CYP during this time. There is good evidence to suggest that a holistic approach to transition, rather than simply a formal transfer of care, improves patients' understanding and ability to self-care, and in so doing reduces morbidity and mortality. A coordinated process of transition involves empowerment and shared decision-making and starts in paediatric care aided by transition toolkits. In the absence of a structured transition, CYP often present to adult services unplanned and in a crisis situation. CYP presenting directly to adult services are a particularly vulnerable group with unmet needs due to missing out on a formal transition process. Local innovation, regional initiatives and national policy can help reduce variation and ensure access to good-quality transition care and clinics. Setting up such transition clinics requires careful planning, a multidisciplinary approach and adequate long-term funding. We provide a brief toolkit to set up, run and develop a structured transition service.

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.