BMC Nephrology最新文献

Background: Acute kidney injury (AKI) is common in cardiogenic shock (CS) and increases mortality, but the prognostic impact of onset timing in infarct-related CS is unclear. We examined whether early versus late AKI onset is associated with differences in patient characteristics and outcomes.

Methods: In this retrospective observational study, 369 patients with infarct-related CS were classified by AKI timing within the first 96 h of admission: early (≤ 48 h) or late (> 48 h), according to KDIGO criteria. Clinical, hemodynamic, and inflammatory parameters and outcomes were compared. Multivariable logistic regression identified independent predictors of early AKI and in-hospital mortality.

Results: AKI occurred in 143 patients (38.8%), with 56.6% early-onset. In-hospital mortality was higher with early AKI than late AKI (71.6% vs. 54.8%; absolute difference 16.8%, 95% CI 3.1-30.5; p = 0.018). Early AKI patients had higher lactate at admission (median 4.3 vs. 3.1 mmol/L; p = 0.028), greater norepinephrine requirements (0.34 vs. 0.21 µg/kg/min; p = 0.044), and more frequent mechanical ventilation (81.5% vs. 61.3%; p = 0.011). In multivariable analysis, early AKI independently predicted in-hospital mortality (adjusted OR 2.12, 95% CI 1.16-3.87; p = 0.015), and was associated with baseline creatinine (OR 5.68 per 1 mg/dL, p = 0.008) and 24-h lactate (OR 2.67 per mmol/L, p < 0.001).

Conclusions: In infarct-related CS, AKI within 48 h marks a high-risk hemodynamic phenotype with markedly increased mortality, driven by renal vulnerability and early hypoperfusion. Incorporating AKI timing into risk stratification may help target early renoprotective interventions.

Routine monitoring of haematological and biochemical parameters is essential in managing people with kidney failure on maintenance haemodialysis (HD), guiding assessment of HD adequacy and kidney failure-associated complications, including anaemia, chronic kidney disease-mineral and bone disorder, and electrolyte disturbances. Currently, however, there is no consensus on optimal testing frequency of key parameters, with variations across clinical guidelines and limited robust evidence. This narrative review synthesises current guideline recommendations and empirical research on the frequency and scope of routine laboratory testing of people on maintenance HD, focusing on areas of consensus, controversy, and future research needs. Key laboratory parameters were established to standardise the evaluation of foundational and region-specific guidelines, and direct literature searches for research within the last decade. Given the paucity of randomised controlled trials (RCTs), this narrative review is derived primarily from observational research and clinical guidelines. Guideline recommendations varied from flexible, clinician-driven frequencies in foundational guidelines, to prescriptive schedules in region-specific guidelines, though with consistencies across specific parameters. Empirical evidence indicated benefits of reduced testing frequency broadly when addressing medical over-testing. However, limited evidence exists to link parameter-specific testing intervals with outcomes such as hospitalisation, sustaining international variation in guidelines. Future research should pair patient-reported outcome measures with parameter target levels longitudinally in pragmatic RCTs to clarify causal links between optimal monitoring intervals and patient outcomes to develop risk-stratified monitoring frameworks for sustainable HD care.

Background: Activated leukocyte cell adhesion molecule (ALCAM) serves as an important effector that activates and traffics lymphocytes into tissues. The expression and role of ALCAM in IgA nephropathy (IgAN) remain unclear. Here, we aim to evaluate the expression and effect of ALCAM in IgAN patients.

Methods: We performed a prospective study including 71 IgAN patients, and 41 controls. Serum and uALCAM levels were evaluated. Renal expression of ALCAM and its ligand S100B were measured. The correlation of serum ALCAM with clinical data, renal pathology, and prognosis was analyzed. Cox regression analysis was conducted to identify independent factors associated with prognosis. Kaplan-Meier survival analysis was performed to explore the role of serum ALCAM.

Results: Circulating ALCAM levels were higher in IgAN patients than in controls. Serum ALCAM levels showed a positive correlation with proteinuria and renal pathology. Renal ALCAM expression was also elevated in IgAN patients. IgAN patients were divided into low and high ALCAM groups (< 4.76, and ≥ 4.76 ng/mL) based on the optimal cut-off value for predicting renal progression. The high ALCAM group exhibited more severe clinical parameters and renal pathology. High serum ALCAM level was an independent risk factor for IgAN progression. IgAN patients with high ALCAM level exhibited a lower cumulative renal survival rate compared to the low-level group.

Conclusions: In summary, serum ALCAM level in IgAN patients was elevated, which was consistent with clinical and pathological severity, and served as an independent risk factor and a promising novel predictor for the progression of IgAN.

Clinical trial number: Not applicable.

Background: Autosomal dominant tubulointerstitial kidney disease caused by uromodulin mutation (ADTKD-UMOD) is a hereditary condition characterized by progressive renal dysfunction, often requiring renal replacement therapy by middle age. A notable feature is a strong family history of chronic kidney disease (CKD) and hyperuricemia; however, the absence of urinary abnormalities often delays diagnosis. To facilitate early CKD management, a diagnostic method that is simpler than genetic analysis yet strongly indicative of ADTKD-UMOD is needed.

Methods: Serum and urinary UMOD levels were measured in patients with ADTKD-UMOD, healthy controls, and patients with other diseases. We investigated whether reduced UMOD levels are a distinctive feature of ADTKD-UMOD.

Results: In 13 cases of ADTKD-UMOD, the serum UMOD (sUMOD) was 24.5 ± 13.9 ng/ml, the serum UMOD/GFR (sUMOD/GFR) was 1.23 ± 0.96, and the urinary UMOD/Cr (uUMOD/Cr) was 1.8 ± 0.9 mg/gcr. In the ADTKD-UMOD dataset, the sUMOD values were significantly lower than those in the other disease datasets. The UMOD/Cr and sUMOD/eGFR values also tended to be lower, although statistically significant differences were observed only in limited comparisons. The ROC analysis revealed that a serum UMOD concentration of < 56.4 ng/ml or sUMOD/GFR of < 1.71 is strongly suggestive of ADTKD-UMOD.

Conclusions: Measurement of UMOD protein levels is a useful tool for the diagnosis of　ADTKD-UMOD. Considering the stability of the procedure, serum UMOD may be more reliable than urinary UMOD measurement.

Background: Monocyte chemoattractant protein-1 (MCP-1) has been implicated in the pathogenesis of chronic kidney disease (CKD); however, its clinical significance in CKD remains unclear. This study investigated the association between plasma MCP-1 levels and kidney and cardiovascular outcomes in patients with CKD.

Methods: This multicenter, prospective, observational analysis used data from the BRIGHTEN study. Participants with anemia and CKD (eGFR < 60 mL/min/1.73 m²) were classified into four groups based on quartiles of their baseline plasma MCP-1 levels. The primary outcomes included kidney outcomes (a composite of initiation of maintenance dialysis, kidney transplantation, 50% decline in eGFR, or eGFR ≤ 6 mL/min/1.73 m²), the annual rate of eGFR decline, cardiovascular outcomes, and all-cause mortality. Associations were assessed using Cox proportional hazard and linear mixed-effects models.

Results: This study included 1,447 participants with advanced CKD (median eGFR 17.9 mL/min/1.73 m²). The group with the lowest MCP-1 level (< 324.5 pg/mL) had the highest baseline eGFR. In the univariable analyses, higher MCP-1 levels were associated with an increased risk of kidney and cardiovascular outcomes (log-rank p < 0.01 and p = 0.03, respectively), although these associations were not significant after multivariable adjustment. Analysis of the annual eGFR decline using a multivariable linear mixed-effects model revealed that higher MCP-1 levels were associated with an additional eGFR decline of approximately 1.0 mL/min/1.73 m² per year compared to the lowest MCP-1 group. MCP-1 levels were not associated with mortality.

Conclusions: In patients with CKD, higher plasma MCP-1 levels are associated with a more rapid decline in kidney function but not with the composite outcome of kidney failure. MCP-1 was not associated with cardiovascular outcomes or mortality in this population cohort.