***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Recently , our group has shown that a 3-month course of intravenous immunoglobulin ( 2 g/kg/monthly ) followed by 6 months of intramuscular immunoglobulins ( IMIG , 16.5 % , 0.35 ml/kg every 15 days ) was able to slow or to stop the decline in the glomerular filtration rate , to reduce proteinuria , hematuria , leukocyturia and the histological index of activity on renal biopsy in patients with severe forms of IgA nephropathy ( IGAN ) and Henoch-Schönlein purpura ( HSP ) . The aim of this open prospect i ve trial was to evaluate the efficacy and safety of low-dose immunoglobulin therapy in moderate IGAN and HSP with permanent proteinuria . Fourteen patients with moderate IGAN [ idiopathic IGAN : n = 11 ; chronic idiopathic HSP : n = 3 ] and permanent albuminuria were treated with polyvalent IMIG ( 16.5 % ) for 9 months ( 0.35 ml/kg once a week for 1 month , followed by 0.35 ml/kg every 15 days for a further 8 months ) . Eligibility criteria in the study were Lee histological stage I , II or III , albuminuria between 300 and 2,000 mg/day and a glomerular filtration rate > 70 ml/min/1.73 m2 . IMIG were well tolerated and only 1 patient withdrew from the trial . No viral , renal or immunological side effects were observed . IMIG induced a significant decrease in albuminuria as well as in the histological activity index in the 11 cases in which a follow-up biopsy was performed . There was also a decrease in serum IgA , serum beta 2-microglobulin and IgA immune complex levels , and an increase in serum IgG1 levels . Twelve of the 13 evaluable patients improved during treatment Protein trafficking across the glomerular capillary has a pathogenic role in subsequent renal damage . Despite evidence that angiotensin-converting enzyme ( ACE ) inhibitors improve glomerular size-selectivity , whether this effect is solely due to ANG II blocking or if other mediators also play a contributory role is not clear yet . We studied 20 proteinuric patients with IgA nephropathy , who received either enalapril ( 20 mg/day ) or the ANG II receptor blocker irbesartan ( 100 mg/day ) for 28 days in a r and omized double-blind study . Measurements of blood pressure , renal hemodynamics , and fractional clearance of neutral dextran of grade d sizes were performed before and after 28 days of treatment . Both enalapril and irbesartan significantly reduced blood pressure over baseline . This reduction reached the maximum effect 4 - 6 h after drug administration but did not last for the entire 24-h period . Despite transient antihypertensive effect , proteinuria was effectively reduced by both treatments to comparable extents . Neither enalapril nor irbesartan modified the sieving coefficients of small dextran molecules , but both effectively reduced transglomerular passage of large test macromolecules . Theoretical analysis of sieving coefficients showed that neither drug affected significantly the mean pore radius or the spread of the pore-size distribution , but both importantly and comparably reduced the importance of a nonselective shunt pathway . These data suggest that antagonism of ANG II is the key mechanism by which ACE inhibitors exert their beneficial effect on glomerular size-selective function and consequently on glomerular filtration and urinary output of plasma proteins IgA nephropathy is the world 's most common primary glomerulonephropathy . Recent evidence in a rat model implicated excessive production of oxygen-free radicals in the pathogenesis and suggested that vitamin E-treatment ameliorated progression . We studied this antioxidant therapy on the glomerular filtration rate ( GFR ) , proteinuria and hematuria in biopsy-proven IgA nephropathy in children . The duration of treatment or placebo was 2 years , with vitamin E treatment consisting of 400 IU/day in children weighing < 30 kg , and twice that dose for those > 30 kg . We measured GFR at entry , midpoint and exit . At baseline and at 4-month intervals after r and omization , urinary protein/creatinine ratios and urinalysis were examined . The mixed model procedure with log transformation was used in data analysis to test treatment difference as well as the potential time effect . Fifty-five patients were r and omized and 38 completed at least 1 year of follow-up . At entry , the clinical characteristics were not different between the treatment and placebo groups . There was a trend toward better preservation of GFR  in vitamin E-treated versus placebo patients , 127±50 vs. 112±31 ml/min/1.73 m2 , respectively ( P=0.09 ) . The urinary protein/creatinine ratio was significantly lower in the vitamin E-treated group vs. placebo ; 0.24±0.38 vs. 0.61±1.37 ( P<0.013 ) . However , there was no difference in the prevalence of hematuria between the groups . Vitamin E treatment in our study patients was associated with significantly lower proteinuria , but no effect on hematuria . While there was a trend toward stabilization of GFR in the vitamin E-treated patients , long-term treatment and follow-up are needed to determine whether antioxidant therapy is associated with preservation of renal function in IgA nephropathy This study investigates the ability of low doses of angiotensin-converting-enzyme inhibitors , in combination with angiotensin II receptor blockers , to exert antiproteinuric effects in normotensive and proteinuric out patients with immunoglobulin A ( IgA ) nephropathy confirmed by biopsy . We performed a prospect i ve , r and omized , 6-month study of the effects of temocapril 1 mg ( n=10 ) , losartan 12.5 mg ( n=10 ) , and both ( n=11 ) on mild-to-moderate proteinuria 0.76+/-0.35 g/day ( range , 0.4 to 1.6 g/day ) and renal function . The study subjects comprised 31 normotensive and proteinuric out patients with IgA nephropathy accompanied by normal , or mild-to-moderately reduced but stable renal function ( glomerular filtration rate>50 ml/min ) without steroid or immunosuppressive therapy . We prospect ively evaluated blood pressure , proteinuria , renal function and biochemical parameters before and after 6 months of therapy . The combination therapy significantly reduced proteinuria ( 63.2 % ) compared with either temocapril or losartan alone ( 41.3 % and 36.6 % , respectively , p=0.04 and 0.01 , respectively ) . Blood pressure was most decreased in the group that received combination therapy . The reduced proteinuria did not correlate with reduced systolic or diastolic blood pressure or mean arterial pressure in any of the groups . The glomerular filtration rate fell during the first 3 months of combined therapy , but became reversible after a further 3 months of therapy . The combination significantly decreased angiotensin II ( p < 0.01 ) , and this decrease was greater than that by either drug alone . In conclusion , the effectiveness of the combined therapy may have been at least partly due to the greater inhibition of the action of angiotensin II in patients with IgA nephropathy . This strategy apparently reduced mild-to-moderate proteinuria in patients with normotensive IgA nephropathy Some retrospective studies have suggested a beneficial influence of angiotensin-converting enzyme ( ACE ) inhibitors on the progression of IgA nephropathy ( IgAN ) , but prospect i ve and controlled studies demonstrating this effect are lacking . Forty-four patients with biopsy-proven IgAN , proteinuria > or = 0.5 g/d , and serum creatinine ( SCr ) < or = 1.5 mg/dl were r and omly assigned either to receive enalapril ( n = 23 ) or to a control group ( n = 21 ) in whom BP was controlled with antihypertensives other than ACE inhibitors . Primary outcome was renal survival estimated by a 50 % increase in baseline SCr . Secondary outcomes were the presence of a SCr > 1.5 mg/dl at the last visit and the evolution of proteinuria . Baseline clinical findings were similar at baseline between enalapril-treated and control group , and there were no differences in BP control during follow-up . Mean follow-up was 78 + /- 37 mo in the enalapril group and 74 + /- 36 mo in the control group . Three patients ( 13 % ) in the enalapril group and 12 ( 57 % ) in the control group reached the primary end point ( P < 0.05 ) . Kaplan-Meier renal survival was significantly better in enalapril group than in control group : 100 % versus 70 % after 4 yr and 92 % versus 55 % after 7 yr ( P < 0.05 ) . Three patients in the enalapril group ( 13 % ) and 11 ( 52 % ) in the control group showed SCr > 1.5 mg/dl at the last visit ( P < 0.05 ) . Proteinuria significantly decreased in the enalapril group , whereas it tended to increase in the control group ( P < 0.001 between groups ) . In conclusion , ACE inhibitors significantly improve renal survival in proteinuric IgAN with normal or moderately reduced renal function Twenty children and adolescents with IgA glomerulonephritis were enrolled in a crossover trial . Each received 12 weeks of prednisone therapy and 12 weeks of placebo dosing .  Urinary protein and erythrocyte excretion were monitored during both courses . There was no evidence that , under the conditions of the study , corticosteroid therapy was effective in IgA nephropathy BACKGROUND Because humoral immunity is believed to play a pivotal role in the pathogenesis of IgA nephropathy ( IgAN ) , a prospect i ve placebo-controlled r and omized study was started in patients with IgAN using mycophenolate mofetil ( MMF ) .  METHODS A total of 34 patients with IgAN were treated with salt intake restriction , angiotensin-converting enzyme ( ACE ) inhibition and MMF 2 g per day ( N= 21 ) or placebo ( N= 13 ) . After 36 months of follow-up clinical , biochemical , and radiologic data were analyzed using linear mixed models for longitudinal data and Kaplan-Meier survival analysis . RESULTS Therapy had to be stopped prematurely in five patients . Two patients ( MMF group ) evolved to end-stage renal disease ( ESRD ) . There was no difference between groups in the percentage of patients with a decrease of 25 % or more in the inulin clearance or with a serum creatinine increase of 50 % or more over 3 years . There was also no significant difference between groups in annualized rate of change of serum creatinine , computed by linear regression analysis . No significant difference was noted between groups for inulin clearance , serum creatinine , proteinuria , blood pressure , or other parameters of renal function . Hemoglobin and C-reactive protein were significantly lower in the MMF group compared with the placebo group . As a function of time , a significant decline in both groups was noted of proteinuria , parenchymal thickness of the kidneys and C3d . CONCLUSION In patients with IgAN at risk for progressive disease , no beneficial effect of 3-year treatment with MMF 2 g per day could be demonstrated on renal function/ outcome or proteinuria . However , larger r and omized studies are needed to confirm or reject these results The role of immunosuppressive therapy in the management of IgA nephropathy ( IgAN ) remains controversial . No consensushas yet emerged on the specific treatment of IgAN and this ismostly related to the lack of complete underst and ing of themultifactorial pathogenesis of the disease . Choice of appropriatetherapeutic agents is further limited by the difficulty inidentifying patients who would most likely benefit from therapy . Immunosuppressive therapy has not been recommended in patients with isolated hematuria and well preserved renal function becauseof their generally favourable prognosis and there are no clinical trials in this area . Considering that mild IgAN may be an earlystage of the disease and can be reversed by immunosuppressiveagents we have used prednisolone and azathioprine in patients with isolated hematuria in a prospect i ve , r and omized , controlled study since 1988 . In this prospect i ve study we have evaluated theeffect of prednisolone with azathioprine on the clinical courseof IgAN and its impact on histologic parameters and preventionof progression in patients with isolated hematuria . We studied 43biopsy-proven IgAN patients ( 29 males and 14 females , agedbetween 13–63 years , mean age 28 ± 6 ) with isolated hematuria and well-preserved renal function ( Ccr 89.2 ± 10.2 ml/min ) . The patients were assigned to two groups : 21 patients receivedprednisolone ( 40 mg/day ) and azathioprine ( 100 mg/day ) orally forfour months ( group A ) and 22 patients received no specifictreatment for IgAN and served as a control group ( group B ) . InGroup A prednisolone was reduced to 20 mg/day at the end of thesecond month , then slowly tapered over a two-month period and stopped . The median duration of follow-up was 60 months ( range12–12 
    Output:
    
In patients with IgAN and normal or mildly impaired renal function , steroids significantly delay the progression to end stage kidney disease ( evidence from SR ) and improve proteinuria .
Associating steroids and cytotoxic agents ( cyclophosphamide followed by oral azathioprine ) proves effective in patients with rapidly progressive renal disease ( evidence from RCT ) .
Angiotensin converting enzyme inhibitors and angiotensin II receptor blockers significantly improve proteinuria ( evidence from RCT ) , but there are no conclusive data on efficacy on hard patient level endpoints .
There are no conclusive data available on the use of a therapy combining these agents .
In IgAN patients current evidence supports the hypothesis that immunosuppressive agents delay the progression to end stage renal disease .