An update on the treatment options for focal segmental glomerulosclerosis

Focal segmental glomerulosclerosis (FSGS) is not a disease but a lesion initially affecting the podocyte. Various factors may induce ‘secondary’ FSGS, including defects in molecules that contribute to the podocyte slit diaphragm permselectivity to albumin. They do not represent indications for immunosuppression and require symptomatic treatment only, comprising angiotensin 2 and endothelin antagonists. Primary (idiopathic) FSGS is possibly but not certainly of immunologic origin, owing to an elusive glomerular permeability factor (GPF), explaining relapse on a renal transplant and justifying an immunosuppressive treatment. The best prognostic feature of primary nephrotic FSGS is its response to corticosteroids. Alkylating agents are mostly ineffective in steroid-resistant forms. An association of corticosteroids and cyclosporine A (CsA) remains the mainstay of treatment, with a good tolerability when CsA dosage is low. A definite advantage of tacrolimus on CsA has not yet been established. Sirolimus appears ineffective and potentially harmful. Azathioprine is not indicated. A number of mostly uncontrolled trials indicate that mycophenolate mofetil might find an adjunctive place in the treatment. Plasmapheresis is of no avail outside the special case of relapse in a transplanted kidney. Immunoabsorption of the GPF has not led to practical treatment options. Anecdotal reports on rituximab are as yet too few to determine whether this monoclonal anti-CD20 antibody will find a place in the treatment of primary FSGS.     

Treatment of focal segmental glomerulosclerosis

Focal segmental glomerulosclerosis (FSGS) is not a disease, but a lesion affecting the podocyte. Secondary FSGS may be due to a host of various factors, and patients are rarely nephrotic, requiring symptomatic treatment only. The best prognostic feature of nephrotic FSGS is its response to corticosteroids. Some forms are most likely of immunological origin, relapse in a renal transplant and justify immunosuppressive treatment. In a growing number of cases, genetic profiling of molecules that contribute to the podocyte slit diaphragm permselectivity to albumin has identified defects that do not represent indications for immunosuppression. In the other forms, corticosteroids and cyclosporin A (CsA) remain the mainstay of treatment, with better efficacy when CsA is associated with steroids. The renal tolerability of CsA is reasonably good when the dosage is low. CsA dependency is not constant. Alkylating agents are reluctantly indicated in steroid-sensitive forms, which are rare. They are mostly ineffective in steroid-resistant forms. Tacrolimus seems a promising therapy with low toxicity, but it is usual for dependency on the drug to occur. Sirolimus seems to be ineffective. Azathioprine is not considered indicated, despite rare reports with favourable results, which would deserve further controlled trials. Recent publications indicate that mycophenolate mofetil might usefully find a place in the treatment. Plasmapheresis is of no avail outside the special case of relapse in a transplanted kidney. Immunoabsorption of the elusive substance that causes the nephrotic syndrome and its relapse on a transplant has not led to practical treatment options.     

Treatment of focal segmental glomerulosclerosis

Focal segmental glomerulosclerosis (FSGS) is not a disease, but a lesion affecting the podocyte. Secondary FSGS may be due to a host of various factors, and patients are rarely nephrotic, requiring symptomatic treatment only. The best prognostic feature of nephrotic FSGS is its response to corticosteroids. Some forms are most likely of immunological origin, relapse in a renal transplant and justify immunosuppressive treatment. In a growing number of cases, genetic profiling of molecules that contribute to the podocyte slit diaphragm permselectivity to albumin has identified defects that do not represent indications for immunosuppression. In the other forms, corticosteroids and cyclosporin A (CsA) remain the mainstay of treatment, with better efficacy when CsA is associated with steroids. The renal tolerability of CsA is reasonably good when the dosage is low. CsA dependency is not constant. Alkylating agents are reluctantly indicated in steroid-sensitive forms, which are rare. They are mostly ineffective in steroid-resistant forms. Tacrolimus seems a promising therapy with low toxicity, but it is usual for dependency on the drug to occur. Sirolimus seems to be ineffective. Azathioprine is not considered indicated, despite rare reports with favourable results, which would deserve further controlled trials. Recent publications indicate that mycophenolate mofetil might usefully find a place in the treatment. Plasmapheresis is of no avail outside the special case of relapse in a transplanted kidney. Immunoabsorption of the elusive substance that causes the nephrotic syndrome and its relapse on a transplant has not led to practical treatment options.     

Restless legs syndrome: an update on treatment options

Restless legs syndrome (RLS) was first described in 1672 but it is only recently that this disorder has attracted attention in defining its phenotype, and identifying its aetiology, pathogenesis and pharmacological treatment. RLS can be divided into primary (idiopathic) and secondary forms. RLS is common, affecting 5-15% of the total population and manifesting at any age from childhood to late adulthood. Prevalence tends to increase with patient age and there may be geographic variation. There is a clear genetic contribution to primary RLS and evidence for dopaminergic dysfunction. Although not all patients with RLS require medication, there can be a substantial reduction in the patient's quality of life related to pain, poor sleep and excessive daytime sleepiness. A variety of medications are now available for the symptomatic treatment of RLS. Dopaminergic therapy is currently the treatment of choice, usually initiated with a long-acting dopamine agonist, thereby avoiding some of the complications associated with levodopa. Anticonvulsants may be used as second-line treatment. Levodopa should be reserved for those patients who fail to respond to alternative medications because of the high risk of inducing augmentation. Hypnosedatives also have a role in RLS management. Patients with intractable RLS may require combination treatment. Several systemic disorders can cause RLS, and these should be identified and treated appropriately.     

Cyclosporin therapy for steroid resistant nephrotic focal glomerulosclerosis

A young man with focal glomerulosclerosis and severe steroid resistant nephrotic syndrome was treated with oral cyclosporin for six months without histological evidence of drug induced nephrotoxicity. A marked and sustained partial remission of the degree of proteinuria one year following cessation of treatment was not accompanied by a deterioration in renal function. Cyclosporin may have a role, as yet not fully defined, in the treatment of steroid-resistant or dependent nephrotic syndrome.     

Investigational drugs in development for focal segmental glomerulosclerosis

Introduction: Focal segmental glomerulosclerosis is an important cause of end stage kidney disease and is a paradigm for the study of glomerular scarring. There are no FDA approved treatments for this condition. Current therapies, assessed based on reduction in proteinuria, are generally effective in a subset of patients which suggests that FSGS is a heterogeneous group of glomerular disorders or podocytopathies that converge on a common histopathological phenotype.

Areas covered: We searched for investigational drugs agents that target different pathophysiological pathways using the key words ‘FSGS’ and ‘podocyte’ in American and European clinical trial registers (clinicaltrials.gov; clinicaltrialsregister.eu). Published articles were searched in PubMed, Medline, the Web of Science and the Cochrane Central Register of Controlled Trials Library.

Expert opinion: Progress is being made in defining the mechanism of action of subtypes of FSGS. Current and investigational therapies for FSGS target these different pathways of injury. It is anticipated that advances in systems biology will further refine the classification of FSGS by subdividing the disease based on the primary mechanism of glomerular injury, identify biomarkers to discriminate between different subtypes, and enable appropriate selection of appropriate therapy for each individual in accordance with the goals of precision medicine.     

Cyclosporine-based immunosuppressive therapy for patients with steroid-resistant focal segmental glomerulosclerosis: a meta-analysis

Objective: Focal segmental glomerulosclerosis (FSGS) is a leading cause of end-stage kidney disease that requires immunosuppressive treatment as therapy. Few studies have been specifically designed to assess the efficacy of cyclosporine (CSA) in patients with steroid-resistant FSGS. This study investigated the efficacy of CSA-based therapy in steroid-resistant FSGS.

Methods: Medline, Cochrane, EMBASE, and Google Scholar databases were searched through April 30, 2014 using the keywords “cyclosporine”, “steroid-resistant”, “focal segmental glomerulosclerosis”, and “FSGS”. Studies with an adult and children with steroid-resistant primary FSGS treated with CSA-based therapy with or without steroid use were included. Complete, partial, and overall remission were the primary outcomes. Change in proteinuria, serum creatinine, and estimated glomerular filtration rate (eGFR) following treatment were secondary outcomes.

Results: Seven randomized controlled trials with a total of 373 patients were included. Five studies were included in the meta-analysis to assess complete, partial, and overall remission of FSGS. Compared with other treatments, CSA-based therapy resulted in a significantly greater partial remission rate (p?=?.018), but complete (p?=?.226) or overall remission rate (p?=?.050). CSA-based therapy also resulted in similar change in proteinuria (p?=?.084), serum creatinine (p?=?.772), and eGFR (p?=?.155) compared with other therapy. Study limitations included small sample size and heterogeneity in age and comparative treatments across the studies.

Conclusions: Cyclosporin-based treatments provided a significantly better partial remission rate as compared with other therapies.     

20例儿童局灶节段硬化性肾小球肾炎临床病理分析

探讨儿童局灶节段硬化性肾小球肾炎临床及病理特点。方法对２０例儿童ＦＳＧＳ患者的临床表现,病理改变以及对激素治疗的反应进行观察,并进一步分析三者间关系。结果儿童ＦＳＧＳ的发生率为５％。临床表现以浮肿及蛋白尿为主,肾病综合征占７０％高血压及肾功能不全分别占１０％、５％。     

Emerging therapeutic strategies for minimal change disease and focal and segmental glomerulosclerosis

ABSTRACT

Introduction: Minimal change disease (MCD) and Focal and segmental glomerulosclerosis (FSGS) are two of the major causes of nephrotic syndrome (NS) in children and adults. According to KDIGO (Kidney Disease: Improving Global Outcomes) guidelines, the treatment of adult primary MCD and FSGS should be based on immunosuppressants and antiproteinuric drugs. Recently, Rituximab, a humanized monoclonal antibody (mAb) has emerged as a potential treatment for steroid or calcineurin inhibitor-dependent patients; it has however demonstrated lower efficacy in those with nephrotic syndrome that is resistant to the above indicated drugs.

Area covered: Analysis of ongoing and already completed clinical trials, retrieved from clinicaltrials.gov, clinicaltrialsregister.eu and PubMed involving new therapies for nephrotic syndrome secondary to MCD and FSGS.

Expert opinion: The most promising drugs under investigation for MCD and FSGS are mAbs. We are hopeful that new therapeutic options to treat multi-drug resistant MCD and FSGS will emerge from currently ongoing studies. What appears certain is the difficulty in enrolling patients affected by orphan renal diseases and the selection of valid endpoints in clinical trials, such as kidney failure.     

Treatment with lecinoxoids attenuates focal and segmental glomerulosclerosis development in nephrectomized rats

Focal segmental glomerulosclerosis (FSGS) is a scarring process associated with chronic low‐grade inflammation ascribed to toll‐like receptor (TLR) activation and monocyte migration. We developed synthetic, small‐molecule lecinoxoids, VB‐201 and VB‐703, that differentially inhibit TLR‐2‐ and TLR‐4‐mediated activation and monocyte migration. The efficacy of anti‐inflammatory lecinoxoid treatment on FSGS development was explored using a 5/6 nephrectomy rat model. Five‐sixths of nephrectomized rats were treated with lecinoxoids VB‐201, VB‐703 or PBS, for 7 weeks. Upon sacrifice, albumin/creatinine ratio, glomerulosclerosis, fibrosis‐related gene expression and the number of glomerular and interstitial monocyte were evaluated. Treatment of nephrectomized rats with lecinoxoids ameliorated glomerulosclerosis. The percentage of damaged glomeruli, glomerular sclerosis and glomeruli fibrotic score was significantly reduced following VB‐201 and VB‐703 treatment. VB‐703 attenuated the expression of fibrosis hallmark genes collagen, fibronectin (FN) and transforming growth factor β (TGF‐β) in kidneys and improved albumin/creatinine ratio with higher efficacy than did VB‐201, but only VB‐201 significantly reduced the number of glomerular and interstitial monocytes. These results indicate that treatment with TLR‐2, and more prominently, TLR‐4 antagonizing lecinoxioids, is sufficient to significantly inhibit FSGS. Moreover, inhibiting monocyte migration can also contribute to treatment of FSGS. Our data demonstrate that targeting TLR‐2‐TLR‐4 and/or monocyte migration directly affects the priming phase of fibrosis and may consequently perturb disease parthogenesis.     

Pharmacotherapeutic review and update of idiopathic nephrotic syndrome in children

Aim of the review The therapeutic management of pediatric idiopathic nephrotic syndrome is still a challenge due to the large number of potentially effective pharmacological alternatives and the insufficient scientific evidence available. A bibliographic review was performed in order to identify the available pharmacological alternatives, as well as their place in therapy, and to analyze whether the treatment algorithm developed by the pediatric nephrology department of our hospital is consistent with the evidence published to date. Method A literature search was carried out on MEDLINE, through PubMed, using the medical subject heading (MeSH) nephrotic syndrome. The search was limited to review papers, meta-analyses, clinical practice guidelines, and randomized controlled trials performed on pediatric populations up to September 2009. Results The treatment algorithm established in our hospital is consistent with the evidence available. Prednisone constitutes the first line treatment with evidence level Ia. When corticosteroids do not achieve remission, there are other therapeutic options that are not clearly positioned yet and further studies that provide more information on their comparative efficacy and safety are needed. These alternative therapeutic options are cyclosporine, mycophenolate mofetil, levamisol, cyclophosphamide and methylprednisolone, as independent strategies or as part of “Mendoza Protocol”, tacrolimus and rituximab. Their sequence of introduction in the therapeutic scheme of NS is classified as evidence level IV and grade D recommendation. Conclusion The wide range of options available for the pharmacotherapeutic management of NS and the lack of evidence about the comparative efficacy and safety of the different therapeutic strategies, make its positioning rather difficult. Therefore each hospital needs to draw up protocols based not only on the small amount of evidence available, but also on the authorized indications, availability of the drugs, clinical experience, associated costs, and patient preferences with regard to the duration of treatment, incidence and type of adverse effects. Development of new randomized controlled trials should be encouraged and setting up national plans for the treatment of this pathology might be a good approach for this problem.     

阿霉素诱发局灶节段性肾小球硬化肾病大鼠模型的建立

目的 建立临床表现和病理特点与人类肾小球疾病相似的阿霉素肾病大鼠模型.方法 将40只SD大鼠完全随机分为造模组(32只)和对照组(8只),造模组完全随机分为首次注射阿霉素后2周组、4周组、8周组、12周组,每组各8只.造模组大鼠尾静脉分2次注射阿霉素,第1次注射按6 mg/kg给药,第2次子1周(7 d)后按4 mg/kg给药;对照组按照造模组方法经大鼠尾静脉2次注射等量生理盐水.检测各组大鼠24h尿蛋白量、血清总蛋白、白蛋白、CH、TG、BUN、Cr的变;双抗体夹心酶联免疫吸附方法检测各组大鼠血清基质金属蛋白酶( MMP)2、MMP-9、转化生长因子(TGF) -β1;免疫组化方法检测各组大鼠纤维连接蛋白(FN)和层粘连蛋白(LN)的表达化;光镜、电镜观察2组大鼠肾脏病理变化.结果 造模组24h尿蛋白定量明显增加,8周末达高峰.造模组大鼠2周、4周、8周和12周组与对照组相比,血清总蛋白、白蛋白明显降低[(50.7±3.6)、(42.2±3.4)、(40.4±3.1)、(41.7±3.3)g/L比(62.8±2.8) g/L、(22.2±1.8)、(16.4±1.7)、(14.8±2.1)、(13.0±2.2)g/L比(29.0±1.3)g/L];TG、CH明显升高[(5.2±1.4)、(6.1±1.5)、(7.3±1.5)、(7.2±1.2)mmol/L比(0.6±0.3)mmol/L,(3.8±1.7)、(5.6±1.9)、(8.6±2.7)、(9.6±1.6) mmol/L比(1.3±0.1)mmol/L];MMP-2、MMP-9降低[(151.4±2.4)、(100.5±3.1)、(76.5±3.6)、(83.7±3.1)μg/L;(73.4±2.7)、(58.9±2.2)、(35.4±2.0)、(33.3±1.5) μg/L],血清TGF-β1含量升高;肾组织FN、LN的表达和分布范围均明显增加.造模12周在可见部分肾小球出现局灶节段性硬化.结论 采用阿霉素首次大剂量(6mg/kg)冲击诱导,1周后小剂量(4mg/kg)给药的方法,大鼠在12周末可见部分肾小球出现局灶节段性硬化.     

黄芪注射液佐治小儿原发性肾病综合征疗效观察

目的 观察黄芪注射液佐治小儿原发性肾病综合征的效果.方法 将57例原发性肾病综合征患儿随机分为对照组和观察组,两组均采用泼尼松中程疗法,观察组在此基础上加用黄芪注射液.观察两组治疗前后24 h尿蛋白定量,血浆白蛋白、总蛋白、总胆固醇、甘油三酯的变化.结果 2组治疗后均见尿蛋白减少,血浆白蛋白、总蛋白升高,总胆固醇和甘油三酯下降,与治疗前比较差异有统计学意义(P<0.01);观察组与对照组治疗后比较,对照组尿蛋白减少,血浆白蛋白、总蛋白升高,总胆固醇和甘油三酯下降更明显,差异有统计学意义(P<0.01).结论 加用黄芪注射液佐治小儿原发性肾病综合征效果良好.     

Relationship between lymphocyte and clinical steroid responsiveness in focal segmental glomerulosclerosis

A remission in nephrotic proteinuria with steroid treatment appears to favorably alter the natural history of focal segmental glomerulosclerosis (FSGS). It is not known why some patients have a favorable response to steroid treatment whereas others do not. Considering the possibility that differences in the pharmacodynamic responsiveness to steroids among patients might be one factor, the authors examined the relationship between the pretreatment suppressive effect of steroids on lymphocyte proliferation (% inhibition) in vitro and the short- and intermediate-term responses of creatinine clearance (Clcr) and/or nephrotic proteinuria (urine protein/creatinine ratio = Up/c) in 13 patients with FSGS. There were significant correlations between % inhibition and the changes in Clcr at 3 (r = 0.92, p < 0.001) and 6 (r = 0.86, p < 0.01) months and the changes in Up/c at 3 months (r = -0.74, p = 0.02). Thus, the greater the pretreatment lymphocyte steroid sensitivity, the greater the increase in Clcr or decrease in Up/c. The changes in these parameters could not be accounted for on the basis of steroid dose or histopathology. The in vitro sensitivity of FSGS patients' lymphocytes to steroids may be of value in anticipating their clinical response to treatment.     

Restless legs syndrome in children: a review and update on pharmacological options

Restless legs syndrome (RLS), formally identified and described by Ekbom in the 1940s, is a common clinical disorder, characterized by an overwhelming urge to move the legs, often accompanied by uncomfortable and unpleasant sensations. This impulse can also be present in the upper limbs or other parts of the body. Well recognized in the adult population, the symptoms associated with this condition have commonly been reported to originate in childhood. However, identifying prospectively children suffering from RLS is still a challenging issue. Iron deficiency has been recognized as a feature frequently associated with RLS. Some authors also make a connection with the deficiency, RLS and other common problems encountered in children, such as attention deficit disorder with hyperactivity (ADHD). Linkage to different chromosomal loci has been achieved in recent genetic studies of large kindred, as well as identification of specific genes. Therapeutic considerations in children range from providing sound sleep hygiene to intervening pharmacologically. In that regard, use of iron supplements, dopaminergic stimulation, anticonvulsants, opiates, and benzodiazepines will be assessed along with newer options, such as rotigotine and gabapentin enacarbil. Considerations specific to childhood do apply, as no pharmacological therapy for restless legs syndrome have been approved by the Federal Drug Administration (FDA) in individuals of the pediatric age group.     

阿霉素诱导小鼠局灶节段性肾小球硬化肾病模型的研究

目的观察阿霉素诱导小鼠局灶节段性肾小球硬化发生的过程,为未来研究奠定基础。方法给BALB/c小鼠尾静脉一次性注射阿霉素,按10 mg/kg给予,动态观察阿霉素注射后1、2、4、6周尿蛋白、血生化及光镜、电镜下肾组织病理改变。结果从第1周开始尿蛋白增加,第2周达高峰,4、6周与2周相比稍有下降;血清白蛋白(ALB)于第1周开始下降(P<0.01),2周达最低值,4、6周较2周稍升高。光镜下,第1周肾小球无明显变化,肾小管可见蛋白管型;第2周部分肾小球可见节段性硬化,肾小管蛋白管型增多,较易见到;第4、6周可见50%以上肾小球中出现节段性硬化,肾小管扩张明显,可见大量蛋白管型及局部间质纤维化。电镜下,第1周偶可见足突融合,第2周足突融合更广泛,第4、6周出现足突融合变形,体积变大,胞质中微丝增多,并出现囊泡及包涵体,毛细血管袢闭塞,充血,大量红细胞填塞,内皮细胞孔消失,基底膜正常。结论单次BALB/c小鼠鼠尾静脉注射10 mg/kg阿霉素,可成功诱导局灶节段性肾小球硬化模型。     

Second-line options for refractory steroid-sensitive and -resistant nephrotic syndrome

Although initially, many children with idiopathic nephrotic syndrome respond to steroid therapy, a repeated course for patients with relapses often causes significant steroid toxicity. Patients with frequent relapses or steroid dependency thus require alternative treatment, and so far, cyclophosphamide or levamisole have been regarded as first-choice options, although the latter is no longer available in many countries. Data are accumulating that mycophenolic acid may be an alternative for these patients. Calcineurin inhibitors (cyclosporine A or tacrolimus) are usually effective and are often used after cytotoxic treatment, but long-term treatment is necessary, raising concerns regarding the accumulation of side effects. Still, some patients show a tendency to relapse even on this maintenance regimen and some even have a refractory course that creates a medical dilemma. For this situation, recent data have demonstrated an effect of monoclonal antibodies directed to B cells – rituximab, a drug that may also prove to be a therapeutic option in less complicated cases. Patients that do not respond to initial steroid treatment need genetic testing and a renal biopsy, since focal segmental glomerulosclerosis may be present. Treatment options include pulse methylprednisolone, often in addition to calcineurin inhibitors (mainly cyclosporine but also, recently, tacrolimus). Cyctotoxic treatment, especially intravenous cyclophosphamide, has been found to be effective in steroid-resistant nephrotic syndrome by some studies but is inferior to calcineurin inhibitors. In addition, mycophenolic acid and rituximab have been used in children with primary focal segmental glomerulosclerosis; however, response seems to be inferior in comparison with patients with steroid-sensitive nephrotic syndrome. Taken together, idiopathic nephrotic syndrome, including steroid-sensitive as well as steroid-resistant patients, is a potentially serious disorder. Although much progress has been made in recent years and a wide arsenal of immunological interventions is available, some patients have a treatment refractory course. Prospective studies or at least standardization of treatment for complicated cases is urgently needed.     

Second-line options for refractory steroid-sensitive and -resistant nephrotic syndrome

Although initially, many children with idiopathic nephrotic syndrome respond to steroid therapy, a repeated course for patients with relapses often causes significant steroid toxicity. Patients with frequent relapses or steroid dependency thus require alternative treatment, and so far, cyclophosphamide or levamisole have been regarded as first-choice options, although the latter is no longer available in many countries. Data are accumulating that mycophenolic acid may be an alternative for these patients. Calcineurin inhibitors (cyclosporine A or tacrolimus) are usually effective and are often used after cytotoxic treatment, but long-term treatment is necessary, raising concerns regarding the accumulation of side effects. Still, some patients show a tendency to relapse even on this maintenance regimen and some even have a refractory course that creates a medical dilemma. For this situation, recent data have demonstrated an effect of monoclonal antibodies directed to B cells - rituximab, a drug that may also prove to be a therapeutic option in less complicated cases. Patients that do not respond to initial steroid treatment need genetic testing and a renal biopsy, since focal segmental glomerulosclerosis may be present. Treatment options include pulse methylprednisolone, often in addition to calcineurin inhibitors (mainly cyclosporine but also, recently, tacrolimus). Cyctotoxic treatment, especially intravenous cyclophosphamide, has been found to be effective in steroid-resistant nephrotic syndrome by some studies but is inferior to calcineurin inhibitors. In addition, mycophenolic acid and rituximab have been used in children with primary focal segmental glomerulosclerosis; however, response seems to be inferior in comparison with patients with steroid-sensitive nephrotic syndrome. Taken together, idiopathic nephrotic syndrome, including steroid-sensitive as well as steroid-resistant patients, is a potentially serious disorder. Although much progress has been made in recent years and a wide arsenal of immunological interventions is available, some patients have a treatment refractory course. Prospective studies or at least standardization of treatment for complicated cases is urgently needed.     

小儿原发性肾病综合征诊治体会

肾病综合征是一组由多种原因引起的肾小球基底膜通透性增加,导致血浆内大量蛋白质从尿中丢失的临床综合征。结合数十例患儿诊治经过,将诊治体会报告如下:     

贝那普利联合泼尼松治疗小儿肾病综合征的临床效果

目的 观察贝那普利联合泼尼松治疗小儿肾病综合征的临床效果.方法 选取本院2016年9月至2017年3月住院部收治的小儿肾病综合征患者58例,将其按照随机抽取的方式分为观察组(贝那普利联合泼尼松治疗)和对照组(泼尼松治疗),各29例;观察两组临床总有效率、不良反应发生率、临床症状评分、24 h蛋白尿、血浆白蛋白、胆固醇.结果 观察组临床总有效率96.55％,高于对照组(P＜0.05);观察组临床症状评分[蛋白尿(0.38±0.02)分、水肿(0.36±0.03)分、高脂血症(0.24±0.02)分)]、24 h蛋白尿[(0.97±0.48) g/24 h]、胆固醇[(4.66±0.25) mmol/L]低于对照组(均P＜0.05);观察组血浆白蛋白(30.15±3.33)g/L,优于对照组(P＜0.05);两组总不良反应发生率比较,差异无统计学意义(P＞0.05).结论 小儿肾病综合征患者应用贝那普利联合泼尼松治疗疗效显著,能有效改善患者临床症状以及生活质量,临床上值得推广及应用.