Clinical nephrology最新文献

Volume overload is a frequent complication in critically ill patients. Ultrafiltration (UF) uses a semipermeable membrane for removal of plasma water driven by a transmembrane pressure gradient. Employed outside dialysis, it is referred to as aquapheresis (AQ). This study is a retrospective review of our experience with AQ beyond management for congestive heart failure (CHF). The use of AQ was at the discretion of the nephrologist overseeing the case. The study population was categorized according to hospital unit and specific indications for AQ therapy. A total of 69 patients underwent AQ in various critical units: 23 in the cardiothoracic intensive care unit (ICU); 21 in both the cardiac ICU and medical ICU, and 4 patients in the surgical ICU. All patients had a component of kidney dysfunction and volume overload, ranging from non-oliguric acute kidney injury to end-stage renal disease (ESRD). The average UF volume was 6.4 L per patient, with an UF rate of 82 mL/h. The mean AQ duration was 78 hours per patient. 64% (n = 44), were receiving vasopressor support during AQ. Volume optimization remains a fundamental component of management in critically ill patients. AQ can be employed as an additional resource to accelerate fluid removal in a myriad of clinical settings. This analysis underscores the versatility of AQ as an effective treatment for managing fluid overload across diverse patient populations.

Objectives: The aim of this study was to determine the differential dose response of parathyroid hormone (PTH) and fibroblast growth factor (FGF23) to paricalcitol in patients with secondary hyperparathyroidism and end-stage renal failure on chronic intermittent hemodialysis.

Materials and methods: The multicenter, randomized, double-blind, prospective, crossover study comprised a total of 43 hemodialysis patients (average age 64 years, female 30%) with 31 complete patient data sets, and with PTH levels between 200 and 600 pg/mL, serum calcium < 2.55 mmol/L, phosphorus ≤ 2.1 mmol/L, and 25 OH-vitamin D > 20 ng/mL as inclusion criteria (Eudract 2007-006606-16).

Results: Mean intact PTH at baseline was 319 pg/mL (standard deviation (SD) 141, normal 11.3 - 42.4 pg/mL; ECLIA; Roche, Basel, Switzerland) and FGF23 651.25 RU/mL (SD 1,099.98; normal 21 - 424 RU/mL; c-terminal, 2^nd generation ELISA kit, Immutopics, San Clemente, CA, USA) at baseline. The initial oral dose of paricalcitol was 2 μg/day, adjusted to a mean dosage of 1.9 μg/day at week 6 and 1.5 μg/day at week 12, guided by PTH response. PTH levels remained significantly suppressed at both 6 (189 pg/mL; SD 95) and 12 weeks (164 pg/mL; SD 95), both p < 0.001 as compared to baseline. FGF23 levels showed a significant increase at 6 weeks (1,442.1 RU/mL, SD 1,860.2; p = 0.002) but returned at 12 weeks to levels not significantly different from baseline (1,150.7 RU/mL, SD 1,509.3; p = 0.24).

Conclusion: Treatment with paricalcitol resulted in a significant reduction in PTH levels at both 6 and 12 weeks compared to placebo. The suppression of PTH levels with paricalcitol was possible without elevating FGF23 within the restrictions of this short duration study, at least if over-suppression of PTH is avoided by dose adaption. Our findings suggest a cautious lower oral paricalcitol starting dose to mitigate the initial spike in FGF23 while effectively managing PTH levels.

Objective: This is a single-center retrospective cohort study on the demographics and clinical outcomes including the response to therapy of patients with primary membranous nephropathy (PMN) over the past decade. With the spread of diverse therapeutic agents available today, this study seeks to present an interesting array of varied responses.

Materials and methods: All histology-proven PMN cases diagnosed between 2008 and 2018 were analyzed for their clinical, laboratory, and histological characteristics including treatment that could influence disease progression and renal outcome.

Results: There were two sub-groups of patients, those with nephrotic syndrome and those without nephrotic syndrome. All secondary causes of secondary membranous nephropathy were excluded. The response to therapy including RAS blockers, steroids, and immunosuppressants all showed a consistent reduction of proteinuria with therapy for the whole cohort, nephrotic as well as non-nephrotic syndrome with only 10% of the 102 patients in end-stage renal disease (ESRD) at 10 years.

Conclusion: Our data show that membranous nephropathy is a disease responsive to most forms of therapy with decreasing proteinuria. The progression of the disease is slow with a gradual decline to ESRD.

Objective: Renal survival is crucial in patients with idiopathic membranous nephropathy (IMN). Our aim was to identify baseline clinical and histopathological predictors of long-term renal survival in patients with IMN.

Materials and methods: In this retrospective, single-center cohort study, we reviewed 50 adults with biopsy-proven IMN (January 2009 - February 2019) who completed at least 60 months of follow-up. We recorded baseline age, sex, serum creatinine, serum albumin, 24-hour proteinuria, and the total renal chronicity score (Mayo Clinic Chronicity Score). Chronicity was classified as minimal (score 0 - 1) or non-minimal (score ≥ 2). The renal endpoint was defined as a ≥ two-fold increase in serum creatinine from baseline or the initiation of renal replacement therapy (RRT). Predictors of renal survival were assessed using univariate and multivariate Cox regression; renal survival probability was illustrated with Kaplan-Meier analysis.

Results: During the 5-year follow-up, 20 out of 50 patients (40%) reached the renal endpoint. Kaplan-Meier curves demonstrated a significant divergence: only 1 out of 30 patients (3.3%) in the minimal-chronicity group progressed, while 19 out of 20 patients (95%) with non-minimal chronicity experienced either a doubling of creatinine or required RRT (log-rank p < 0.001). In univariate analysis, older age, higher serum creatinine, lower serum albumin, albumin levels below 3 g/dL, and non-minimal chronicity were associated with poor outcomes. Multivariate Cox regression confirmed three independent predictors: baseline serum creatinine (HR 2.38, 95% CI 1.37 - 4.11, p = 0.02), serum albumin (HR 0.43, 95% CI 0.23 - 0.80, p = 0.008), and non-minimal chronicity score (HR 14.4, 95% CI 3.2 - 64.6, p < 0.001).

Conclusion: In IMN, a high total renal chronicity score on biopsy, elevated baseline serum creatinine, and hypoalbuminemia (< 3 g/dL) independently predict poor 5-year renal survival. Early recognition of non-minimal chronicity may facilitate timely therapeutic intervention and closer monitoring to mitigate progression to end-stage kidney disease.

Objective: The association between the atherogenic index of plasma (AIP) and chronic kidney disease (CKD) among individuals with different metabolic syndromes remains inadequately characterized. The aim of this study is to assess the correlations between AIP and the risk of CKD among individuals diagnosed with hypertension (HTN), diabetes mellitus (DM), and hyperuricemia (HUA).

Materials and methods: Data from the National Health and Nutrition Examination Survey, collected between 2009 and March 2020, were used to categorize eligible participants into HTN, DM, and HUA groups. Weighted logistic regression models and restricted cubic splines were employed to examine the correlations between AIP and CKD. The incremental predictive value of AIP, compared with conventional CKD risk factors, was assessed using the area under the curve, net reclassification improvement index, and integrated discrimination improvement.

Results: Among individuals in the HTN and DM groups, an increase of one unit in AIP was associated with a 17% increase in the risk of CKD (odds ratio (OR): 1.17, 95% confidence interval (CI): 1.10 - 1.25) and a 29% increase (OR: 1.29, 95% CI: 1.18 - 1.40), respectively. Conversely, within the HUA group, neither persistent AIP nor any of the three AIP levels demonstrated a statistically significant correlation with CKD.

Conclusion: The findings demonstrated a significant association between AIP and CKD in individuals with HTN and DM, indicating a potential link between dyslipidemia and CKD risk within these populations. In contrast, AIP did not exhibit a significant association with CKD among individuals with HUA.

Background: Double-positive patients exhibit both anti-glomerular basement membrane antibody and anti-neutrophil cytoplasmic antibody. Its initial treatment includes induction cyclophosphamide, glucocorticoids, and plasmapheresis, followed by maintenance therapy similar to that for anti-neutrophil cytoplasmic antibody-associated vasculitis. However, some patients suffer from refractoriness and intolerance to cyclophosphamide, creating an unmet need for second-line therapy. Moreover, no guidance has been provided on the choice of immunosuppressant agents for maintenance therapy.

Case presentation: A 55-year-old Asian woman presented with post-prandial vomiting and a persistent high fever for 1 month. She was diagnosed as a double-positive patient after developing rapidly progressive glomerulonephritis, with a creatinine level of 332 μmol/L. She received induction therapy with cyclophosphamide, glucocorticoids, and plasmapheresis soon after diagnosis. However, worsening renal function and severe nausea and vomiting occurred after 3 monthly doses of cyclophosphamide. Four weekly doses of re-induction rituximab at 375 mg/m², followed by maintenance rituximab 500 mg every 6 months, were administered. The patient had a stable creatinine level of 208 μmol/L 17 months after diagnosis.

Conclusion: Rituximab may be a viable alternative as an induction therapy for double-positive patients when first-line cyclophosphamide is not effective or is not tolerated. Moreover, rituximab may be an effective maintenance therapy for double-positive patients. This case study demonstrates not only the efficacy of rituximab in double-positive patients but also reports the first Asian case of the disorder treated successfully with rituximab.

Background: Studies have suggested that colorectal cancer (CRC) and membranous nephropathy (MN) could be associated with each other. However, the existing conventional research methods fail to establish a conclusive relationship between the two conditions.

Materials and methods: The genome-wide association data for CRC and MN were obtained from previously published genome-wide association studies (GWAS). Inverse variance weighted (IVW), weighted median, weighted mode, and Mendelian randomization (MR)-Egger regression, were employed to analyze the data. Sensitivity analyses were conducted using the heterogeneity test, pleiotropic test, and leave-one-out test. Additionally, a reverse MR analysis was conducted to evaluate any potential reverse causal effects.

Results: The IVW analysis provided strong evidence supporting a causal link between CRC and MN (odds ratio (OR), 1.485; 95% confidence interval (CI), 1.131 - 1.951, p = 0.004). Similar findings were obtained from the weighted median analysis (OR, 1.515; 95% CI, 1.120 - 2.051, p = 0.007) and the weighted mode (OR, 1.572; 95% CI, 0.996 - 2.480, p = 0.084). The MR-Egger regression results indicated that the presence of horizontal pleiotropy was unlikely to bias the findings (intercept, -0.047; p = 0.611). MR-Egger regression did not show any causal association between CRC and MN (OR, 2.075; 95% CI, 0.584 - 7.373, p = 0.292). Reverse MR analysis suggested that MN is not a causative factor for CRC. Cochran's Q test, the funnel plot, and leave-one-out sensitivity analysis demonstrated the robustness of the MR study.

Conclusion: Based on the genetic evidence obtained from this MR study, it can be concluded that CRC may serve as a risk factor for the development of MN. These findings will facilitate a future understanding of the mechanisms underlying MN.

Background: In India, 50% of patients with chronic kidney disease (CKD) present with end-stage renal disease (ESRD) and undergo hemodialysis (HD) primarily via an HD catheter (HDC). CKD is a risk factor for catheter-related thrombosis (CRT), which is well described in the literature, whereas deep venous thrombosis (DVT) is not. The real-world scenario in developing countries is that patients often use temporary HDCs, even for prevalent HD.

Materials and methods: We aimed to determine the incidence rates of DVT and its contributing factors. Patients with temporary non-tunneled HDCs placed for maintenance HD (on an emergency basis or until the maturation of arteriovenous fistula (AVF)) were followed-up for 3 months. Those already undergoing HD elsewhere were excluded. The incidence rates of DVT per 1,000 catheter days were calculated.

Results: The mean age was 46.6 ± 13.47 years; 190/278 were males. 140 patients had CKD for < 6 months. 103 patients had at least 1 risk factor. 24/278 (8.6%) developed DVT, giving an incidence rate of 0.95/1,000 catheter days. A median of 7 HD sessions and a mean of 19.8 ± 6.4 days before the development of DVT was seen. The odds ratios for developing DVT in the right internal jugular vein (IJV), left IJV, right femoral, and left femoral veins were 0.2, 5.0, 1.1, and 4.3, respectively. 31 developed catheter-related bloodstream infection (CRBSI); 6 had both coexisting DVT and CRBSI.

Conclusion: DVT incidence was low. CKD requires early diagnosis and HD planning. CRT is common; patient education and sonographic screening in patients with HDCs may enable a quicker diagnosis and therapy of DVT since many are asymptomatic.

Background: Sodium glucose cotransporter 2 (SGLT2) inhibitor is a standard treatment for kidney and cardiovascular protection in chronic kidney disease (CKD). Recent evidence suggests that SGLT2 inhibitor may enhance erythropoiesis, but data are limited in advanced kidney disease.

Materials and methods: We reviewed 670 CKD patients with diabetes started on SGLT2 inhibitor. Their hemoglobin level and estimated glomerular filtration rate (eGFR) 6 months before the use of SGLT2 inhibitor, immediately before, and 6 months after the use of SGLT2 inhibitor were reviewed.

Results: The hemoglobin level had a small but significant increase 6 months after SGLT2 inhibitor treatment from 12.89 ± 1.75 to 13.08 ± 1.94 g/dL (p < 0.0001). The absolute increase in hemoglobin was 0.19 ± 1.06 g/dL; 117 patients (17.5%) had an increase ≥ 1.0 g/dL. In contrast, the average hemoglobin level was 13.01 ± 1.75 g/dL 6 months before SGLT2 inhibitor, which showed a significant decline to the pre-treatment level (p = 0.001). The increase in hemoglobin after SGLT2 inhibitor was most marked in CKD stage 3b (12.26 ± 1.81 to 12.68 ± 1.98 g/dL, p < 0.0001). There was no significant correlation between the change in hemoglobin level and the severity of pre-treatment albuminuria, eGFR, or HbA1c level, but it had significant correlations with the change in eGFR (r = -0.172, p < 0.0001) and HbA1c (r = 0.120, p = 0.004) during the same period.

Conclusion: SGLT2 inhibitor therapy leads to a small but significant increase in hemoglobin level in patients with diabetes, including those with moderate to severe CKD.