International Journal of Nephrology and Renovascular Disease最新文献

Purpose: Despite management advances, accelerated atherosclerotic cardiovascular disease (ACVD) remains a major cause of morbimortality in systemic lupus erythematosus (SLE) patients; that is not fully explained by traditional risk factors. Fibroblast growth factor-23 (FGF23) is a bone-derived phosphaturic hormone with multiple klotho-dependent and independent effects, including promotion of atherosclerosis and vascular calcification, particularly in the context of chronic kidney disease. Increased circulating FGF23 was reported in SLE patients, particularly with lupus nephritis (LN); but its atherogenic role in these disorders was not explored.

Subjects and methods: Three study groups of predominantly middle-aged females were categorized by the 2012 SLE International Collaborating Clinics (SLICC) criteria as SLE (without LN), LN, or controls matching for traditional CVD risk profile. Measures of SLE activity, damage, steroid therapy, and glomerular filtration rate were calculated. Fasting blood samples were checked for serum lipid profile, anti-DNA, urea, creatinine, uric acid, proteins, albumin, calcium, phosphorus, C3, C4, CRP, vitamin-D3, intact parathyroid hormone and FGF23 (iFGF23). By carotid ultrasonography, mean common carotid artery intima-media thickness (CC-IMT), plaque score (PS) and internal carotid resistive index (ICRI) were recorded.

Results: CC-IMT, ICRI and serum iFGF23 differed along the study groups (LN>SLE>controls). In both SLE and LN patients, serum iFGF23 had a significant positive correlation with serum phosphorus, CC-IMT and PS. On multivariate analysis, the strongest predictor of increased CC-IMT was cumulative steroid dose in SLE and serum iFGF23 in LN patients. Most significant independent predictors of increased serum iFGF23 were hyperphosphatemia in SLE and proteinuria in LN patients.

Conclusion: FGF23-phosphate axis has a key role in accelerated ACVD in SLE patients. Serum phosphorus and iFGF23 should be included in ACVD risk profile assessment of these patients. Prospective studies shall define the role of dietary and/or pharmacologic control of hyperphosphatemia and proteinuria in reducing circulating iFGF23 and ACVD in them.

Extracorporeal membrane oxygenation (ECMO) is a temporary life support system used to assist patients with life-threatening severe cardiac and/or respiratory insufficiency. Patients requiring ECMO can be considered the sickest patients admitted to the intensive care unit (ICU). Acute kidney injury (AKI) represents a frequent complication during ECMO, affecting up to 70% of patients, with multifactorial pathophysiology and an independent risk factor for mortality. Severe AKI requiring Continuous Renal Replacement Therapy (CRRT) occurs in 20% of ECMO patients, but multiple indications and different timing may imply a significantly higher application rate in different centers. CRRT can be run in parallel to ECMO through different vascular access, or it can be conducted in series by connecting the circuits. Anticoagulation of ECMO is typically managed with systemic heparin, but several approaches can be applied for the CRRT circuit, from no anticoagulation to the addition of intra-filter heparin or regional citrate anticoagulation. The combination of CRRT and ECMO can be considered a form of multiple organ support therapy, but this approach still requires optimization in timing, set-up, anticoagulation, prescription and delivery. The aim of this report is to review the pathophysiology of AKI, the CRRT delivery, anticoagulation strategies and outcomes of patients with AKI treated with ECMO.

Background: Constipation is a common problem among patients with advanced chronic kidney disease (CKD), leading to a loss of quality of life. Pharmacologic treatments are in common use, but whether lactulose and senna plus ispaghula husk is effecive to treat constipation among patients with pre-dialysis CKD remains unknown.

Objective: The aim of the study was to compare efficacy of lactulose and senna plus ispaghula husk to treat constipation among patients with pre-dialysis CKD.

Methods: A study was conducted among patients with pre-dialysis CKD receiving a diagnosis of constipation by ROME IV criteria. All subjects were randomly assigned to receive either lactulose or senna plus ispaghula husk daily for 14 days. After a 7-day washout period, the patients were switched to the other substance for another 14 days. Primary outcome was complete spontaneous bowel movement (CSBM) weekly, assessed using a stool diary after each laxative. Secondary outcome measure was the change of stool appearance using the Bristol stool form scale (BSFS).

Results: A total of 22 patients underwent randomization. Baseline CSBM and BSFS were 3.4 ± 1.4 and 2.3 ± 1.2 time/week, respectively. At the end of the study, the mean CSBM weekly increased in the lactulose group (mean difference 1.3 ± 1.6, P < 0.001) and the senna plus ispaghula husk group (mean difference 2.1 ± 2.1, P < 0.001) from baseline. Comparing CSBM between lactulose and senna plus ispaghula husk exhibited no significant difference (95% CI -1.2 to 0.06; P = 0.276). BSFS was significantly changed after using ispaghula husk with senna, the mean ± SD of BSFS changed to 1.7 ± 1.8 (p = 0.001) and after use lactulose, the mean ± SD of BSFS changed to 1.6 ± 1.8 (p = 0.001). No significant BSFS change was observed between groups regarding stool appearance. No serious adverse event in either group was found.

Conclusion: Lactulose and senna plus ispaghula husk were similar in efficacy to treat constipation among patients with pre-dialysis CKD.

Trial registration: Thai Clinical Trials number is TCTR20200818006. Retrospectively Registered 18 August 2020.

Population-based studies have shown that most patients with advanced chronic kidney disease (CKD) do not have optimal phosphate levels. Meta-analyses suggest that there is a morbidity and mortality benefit associated with the lowering of serum phosphate levels. However, to date there is no conclusive evidence from randomized controlled trials (RCTs) that lowering serum phosphate levels reduces the risk of morbidity and mortality. However, hyperphosphatemia may pose a risk to patients and treatment should be considered. We therefore sought to conduct a multidisciplinary review to help guide clinical decision-making pending results of ongoing RCTs. Restricting dietary phosphate intake is frequently the first step in the management of hyperphosphatemia. Important considerations when proposing dietary restriction include the patient's socioeconomic status, lifestyle, dietary preferences, comorbidities, and nutritional status. While dietary phosphate restriction may be a valid strategy in certain patients, serum phosphate reductions achieved solely by limiting dietary intake are modest and should be considered in conjunction with other interventions. Conventional dialysis is also typically insufficient; however phosphate removal may be augmented by increased frequency or duration of dialysis, or through enhanced methods such as hemodiafiltration. Phosphate binders have been shown to reduce absorption of dietary phosphate and lower serum phosphate levels. There are several phosphate binders available, and while they all lower phosphate levels to variable degrees, they differ with respect to their pill burden, potential to induce or exacerbate vascular calcification or ectopic calcification, tissue accumulation, safety, and tolerability. The widespread treatment of hyperphosphatemia requires convincing data from RCTs to ascertain whether lowering serum phosphate levels improves patient-important outcomes, as well as the optimal method and degree of phosphate control. In the interim, the decision and approach used to treat hyperphosphatemia should be based on the best available data, as well as patient needs and clinical judgment.

Background: Musculoskeletal disorders contributed from chronic kidney disease are increasing worldwide. Musculoskeletal disorders had a significant health burden and are leading causes of co-morbidities, disability and low productivity, which potentially affect individual's functional status and quality of life.

Purpose: The aim of this study was to assess the prevalence of musculoskeletal disorders and its associated factors among patients with chronic kidney attending in Saint Paul Hospital, Addis Ababa, Ethiopia.

Patients and methods: An institution-based cross-sectional study was conducted on 302 enrolled study participants through systematic random sampling techniques. Face-to-face interview, physical examination and chart reviews were used to collect data using semi-structured questionnaire adapted from a standard Nordic Musculoskeletal Questionnaire and other literatures. Data were entered into Epi Info version 7 and exported to SPSS version 23 for analysis. Bivariate logistic regression analysis was employed with a p-value less than 0.25. Finally, those variables having a p-value less than 0.05 with 95% CI in multivariate analysis were taken as statistically significant.

Results: The prevalence of musculoskeletal disorders among CKD individuals was found to be 58.6% (95% CI; 53.0, 64.1). Being female (AOR = 0.49; 95% CI 0.26, 0.94), age between 40 and 49 (AOR = 3.34; 95% CI 1.07, 10.44), stage III (AOR = 0.24; 95% CI 0.06, 0.89) and stage IV (AOR = 0.24; 95% CI 0.06, 0.89) chronic kidney disease, having HTN (AOR = 7.47; 95% CI 3.47, 16.06), parathyroid hormone level ≥100 pg/mL (AOR = 0.43; 95% CI 0.21, 0.87), calcium level <8.4 mg/dl (AOR = 5.89; 95% CI 2.66, 13.56) and serum 25 hydroxy vitamin D level <20 ng/mL (AOR = 3.91; 95% CI 1.32, 11.56) were significantly associated with musculoskeletal disorders.

Conclusion: MSDs were shown to be moderately common in CKD patients. Female gender, age between 40 and 49 yrs, stage III and stage IV CKD, hypertension, higher PTH level, lower calcium level and lower vitamin D level were statistically significant in their association with musculoskeletal disorders.

Retroperitoneal fibrosis (RPF) is a rare disorder consisting of idiopathic and various secondary forms and characterized by chronic inflammatory infiltrates and marked fibrosis in the retroperitoneal space. In idiopathic RPF (IRPF), 35-60% of cases have been reported to be IgG4-related RPF, the retroperitoneal lesions of IgG4-related disease (IgG4-RD). IRPF can frequently lead to renal insufficiency mediated by urinary tract obstruction and hydronephrosis irrespective of being IgG4-related or not. Clinical pictures, laboratory and imaging findings, and location of the urinary tract obstruction are generally similar in IgG4-related and non-IgG4-related IRPF although multiple organ involvement and serum IgG4 elevation may be characteristic of the IgG4-related forms. Periaortic/periarterial lesions are the most frequent cause of renal insufficiency. Although the response to glucocorticoids is generally good, relapse does occur in a considerable proportion of patients, and may require an additional immunosuppressive agent and/or urological intervention in cases with multiple relapses or refractory obstructive uropathy. In general, the prognosis of patients with IRPF is good, but careful attention needs to be paid to chronic kidney disease as a major complication and rupture of the affected aorta/artery as a life-threatening one. Further studies are necessary to better understand the pathogenesis of the disease and to establish the optimal diagnostic and therapeutic strategies for it.

Background: The management of nonviral cryoglobulinemic vasculitis (CV) has not been established yet. Randomized control trials are challenging to perform because of the rarity of the disease. The most promising biological therapy is rituximab (RTX), an anti-CD 20 monoclonal antibody. The aim of the study was to assess rituximab treatment's safety and effectiveness in patients with severe noninfectious cryoglobulinemic vasculitis.

Materials and methods: We retrospectively reviewed 8 courses of RTX treatment in three patients with severe noninfectious CV. In 2 patients, the indication for the start of RTX therapy was the relapse of the disease despite the maintenance treatment, for the third patient, it was the first-line therapy.

Results: Clinical, renal, and immunologic efficacy was observed in all evaluable RTX courses. We found a significant decrease of cryoglobulins in the 3-rd month from RTX treatment. However, 5 clinical relapses occurred and two patients experienced severe adverse events (SAEs) after RTX therapy. Patients with SAEs were relatively older and had a longer duration of disease. Lower levels of hemoglobin, C3 component of complement and eGFR as well as higher rheumatoid factor (RF) concentration were observed before RTX treatments complicated with SAEs.

Conclusion: Data from our observation show the efficacy of rituximab in the refractory, nonviral cryoglobulinemic vasculitis with a severe course of the disease. However, the therapy is associated with the risk of SAEs, especially in elderly patients with kidney failure and significant immunologic alterations.

Purpose: Treatment with low-intensity shockwave therapy (LI-ESWT) is associated with angiogenesis and is suggested as a treatment for different types of vascular diseases. It was hypothesized that LI-ESWT improves the renal filtration barrier and halts the progression of GFR decline in diabetic kidney disease (DKD) potentially through VEGF and NO formation. We present the first data on LI-ESWT in human DKD.

Methods: The study was designed as an interventional, prospective, one-arm, Phase 1 study. We investigated change in GFR and albuminuria in 28 patients with DKD treated with six sessions of LI-ESWT over three weeks. The patients were followed for six months. Urine excretion of kidney injury markers, vascular endothelial growth factor (VEGF) and nitric oxide metabolites (NOx) was studied after LI-ESWT.

Results: There were no significant changes in GFR and albuminuria up to six months after LI-ESWT compared to baseline. Urine VEGF was transiently reduced one month after LI-ESWT, but there were no other significant changes in urine VEGF or NOx after LI-ESWT. Secondary analysis showed that NOx increased after LI-ESWT in patients who had low levels of NOx at baseline. Kidney injury marker trefoil factor 3 (TFF3) increased acutely after the first session of LI-ESWT indicating transient endothelial repair. Other markers of kidney injury were stable in relation to LI-ESWT.

Conclusion: LI-ESWT treatment did not significantly improve kidney function and albumin excretion. It is concluded that LI-ESWT is not harmful. A randomized blinded study should be performed to clarify whether adjunctive treatment with LI-ESWT is superior to standard treatment of DKD.

Acute kidney injury (AKI) is emerging as a complication of increasing clinical importance associated with substantial morbidity and mortality in African children with severe malaria. Using the Kidney Disease: Improving Global Outcomes (KDIGO) criteria to define AKI, an estimated 24-59% of African children with severe malaria have AKI with most AKI community-acquired. AKI is a risk factor for mortality in pediatric severe malaria with a stepwise increase in mortality across AKI stages. AKI is also a risk factor for post-discharge mortality and is associated with increased long-term risk of neurocognitive impairment and behavioral problems in survivors. Following injury, the kidney undergoes a process of recovery and repair. AKI is an established risk factor for chronic kidney disease and hypertension in survivors and is associated with an increased risk of chronic kidney disease in severe malaria survivors. The magnitude of the risk and contribution of malaria-associated AKI to chronic kidney disease in malaria-endemic areas remains undetermined. Pathways associated with AKI pathogenesis in the context of pediatric severe malaria are not well understood, but there is emerging evidence that immune activation, endothelial dysfunction, and hemolysis-mediated oxidative stress all directly contribute to kidney injury. In this review, we outline the KDIGO bundle of care and highlight how this could be applied in the context of severe malaria to improve kidney perfusion, reduce AKI progression, and improve survival. With increased recognition that AKI in severe malaria is associated with substantial post-discharge morbidity and long-term risk of chronic kidney disease, there is a need to increase AKI recognition through enhanced access to creatinine-based and next-generation biomarker diagnostics. Long-term studies to assess severe malaria-associated AKI's impact on long-term health in malaria-endemic areas are urgently needed.

Background: There is only limited information on the utility of urinary biomarkers in predicting long-term kidney function following acute kidney injury (AKI). The current study assessed whether urinary beta 2 microglobulin/creatinine (B2M/creat) and kidney injury molecule-1/creatinine (KIM-1/creat) ratios, measured in the early recovery phase of AKI, are predictive of kidney function at one year.

Methods: This is a prospective study done in a tertiary care centre in South India, from March 2017 to December 2018. Adult patients who survived an episode of AKI were followed up for one year (n=125). B2M/creat and KIM-1/creat ratio were measured at two weeks and three months following AKI.

Results: In the AKI survivors, the B2M/creat ratio at 2 weeks [18.3mg/g (IQR 2.3, 52.9)] and KIM-1/creat ratio [1.1 µg/g (IQR 0.5, 4.0) at two weeks were higher compared to healthy controls [B2M/creat ratio 0.35 mg/g (0.17,0.58) and KIM-1/creat ratio 0.40 µg/g (0.23,1.00); P=<0.001]. After adjusting for covariates, the eGFR and urinary B2M/creat ratio at two weeks following AKI were predictive of eGFR at one year (P<0.001). KIM-1/ creat ratios were not predictive of eGFR at one year. A urinary B2M/creat ratio of 10.85 at two weeks following AKI had an 85.5% sensitivity (95% CI 74, 93) and 64.3% (95% CI 53, 75) specificity to predict CKD at one year. An eGFR cutoff of 60 mL/min/1.73 m² at two weeks had a sensitivity of 81.8% (95% CI 69, 90) and specificity of 71.4% (95% CI 60, 81) for predicting CKD. The presence of either one criteria (urinary B2M/creat ratio >10.85 (mg/g) or eGFR <60 mL at two weeks) had a sensitivity of 100% (95% CI 94%, 100%) in predicting CKD at one year.

Conclusion: An eGFR <60 mL/min/1.73m² and elevated urinary B2M/creat ratio at two weeks following AKI is predictive of low eGFR at one year. Urinary KIM-1/creat ratios do not predict CKD progression.