Original Article
A Controlled Trial of Plasmapheresis Therapy in Severe Lupus Nephritis
N Engl J Med 1992; 326:1373-1379May 21, 1992
- Abstract
- Abstract
Background.
The prognosis of patients with systemic lupus erythematosus who have glomerulonephritis is poor, despite treatment with immunosuppressive therapy. Plasmapheresis therapy has been used, but there have been few controlled clinical observations of its efficacy.
Methods
We carried out a randomized, controlled trial comparing a standard-therapy regimen of prednisone and cyclophosphamide (standard therapy) with a regimen of standard therapy plus plasmapheresis in 86 patients with severe lupus nephritis in 14 medical centers. The patients underwent plasmapheresis three times weekly for four weeks. Drug therapy was standardized, with strict adherence to nine detailed medical-management protocols.
Results
Forty-six patients received standard therapy, and 40 patients received standard therapy plus plasmapheresis. The mean follow-up was 136 weeks. Six patients (13 percent) in the standard-therapy group and eight patients (20 percent) in the plasmapheresis group died. Renal failure developed in 8 patients (17 percent) in the standard-therapy group, as compared with 10 (25 percent) in the plasmapheresis group. Thirty patients (35 percent) reached stopping points — 14 (30 percent) in the standard-therapy group and 16 (40 percent) in the plasmapheresis group. A similar number of patients in each group had a decrease in both the serum creatinine concentration and urinary protein excretion to approximately normal values. Patients treated with plasmapheresis had a significantly more rapid reduction of serum concentrations of antibodies against double-stranded DNA and cryoglobulins.
Conclusions
Treatment with plasmapheresis plus a standard regimen of prednisone and cyclophosphamide therapy does not improve the clinical outcome in patients with systemic lupus erythematosus and severe nephritis, as compared with the standard regimen alone. (N Engl J Med 1992;326:1373–9.)
Article Activity
- Article
THE mortality rate in patients with systemic lupus erythematosus and severe glomerulonephritis (lupus nephritis) is high.1 2 3 In 1976 plasmapheresis was proposed as a new approach to interrupting the pathogenetic events in systemic lupus erythematosus.4 The initial use of plasmapheresis in systemic lupus erythematosus resulted in several reports of improvement,4 5 6 7 8 but the studies were uncontrolled. We report the results of a controlled clinical trial of plasmapheresis in the treatment of patients with severe lupus nephritis.
Methods
The Lupus Nephritis Collaborative Study was organized to assess the efficacy and safety of plasmapheresis for the treatment of patients with severe lupus nephritis. Study patients meeting defined entry criteria were assigned to initial treatment with prednisone and cyclophosphamide (hereafter referred to as standard therapy) or with plasmapheresis in addition to the standard therapy.
Entry and Exclusion Criteria
Patients 16 years of age or older were eligible for entry into the study if they had systemic lupus erythematosus as defined by criteria modified from those of the American Rheumatism Association9 , 10 and had a qualifying renal biopsy. Exclusion criteria included pregnancy, a serum creatinine concentration above 530 μmol per liter (6 mg per deciliter), previous treatment with plasmapheresis, a history of primary myocardial disease, a history of cancer within the past five years, prednisone-associated psychosis, peptic ulcer disease, and active liver disease. This study was approved by the institutional review committees of each of the participating institutions, and informed consent was obtained from each patient.
Renal Pathological Analysis
Renal-biopsy specimens were evaluated by light, immunofluorescence, and electron microscopy, according to standard methods.11 , 12 Eligibility for entry into the study was based on histologic criteria.13 , 14 A previously published categorization of severe lupus nephritis was used that was derived from the classification developed by the Consensus Conference of the International Study of Kidney Disease in Children (held in Paris in 1980)2 and adopted by the World Health Organization.11 The histologic categories included severe segmental and proliferative lupus nephritis with active or necrotizing lesions in more than 50 percent of glomeruli (category III), diffuse proliferative nephritis (category IV), and membranous nephritis with superimposed severe segmental or diffuse proliferative nephritis (category V). Subsequently, each biopsy specimen was reevaluated by a committee of pathologists who were not aware of treatment assignment. The diagnoses made by this group were used to classify patients for data analysis. The biopsy results for one patient in the standard-therapy group were judged to be nonqualifying by the committee. The renal pathological analyses and the correlation of histologic subclassification with outcome in these patients have been reported elsewhere.13 , 14 The histologic analyses of severe lupus nephritis showed that in the standard-therapy group (n = 45, with the exclusion of the patient with the nonqualifying biopsy result), 15 patients (33 percent) were in category III, 19 (42 percent) were in category IV, and 11 (25 percent) were in category V. In the plasmapheresis group (n = 40), 9 patients (23 percent) were in category III, 16 (40 percent) in category IV, and 15 (37 percent) in category V.
Randomization and Treatment Plan
Randomization of the patients was stratified according to clinic. The randomization sequences were generated by the Biostatistical Coordinating Center, which issued treatment assignments by telephone after confirmation of patient eligibility.
For the first four weeks, all patients received 60 mg of prednisone per day orally (80 mg per day if they weighed more than 80 kg) and 2 mg of cyclophosphamide per kilogram of body weight per day orally (protocol 1), after which therapy was altered according to previously defined schedules (see below). For the purposes of this study, the initial course of prednisone and cyclophosphamide is referred to as standard therapy. In addition, patients randomly assigned to the plasmapheresis group underwent plasmapheresis three times weekly for four weeks. Patients weighing less than 55 kg underwent exchanges of 3 liters, and those weighing more than 55 kg underwent exchanges of 4 liters. The volume of plasma removed was replaced with equal amounts of isotonic saline containing 2.5 g of albumin per liter. All patients were examined weekly for eight weeks, then at weeks 12, 18, and 24 and every eight weeks thereafter. Patients who entered one of the specific medical-management protocols (see below) because of persistent or recurrent activity of systemic lupus erythematosus were seen more frequently. Laboratory studies were performed at each visit. To minimize the effect of plasmapheresis itself on serum protein components, blood samples were collected three days after the last plasmapheresis treatment. Patients were advised to avoid the use of aspirin and nonsteroidal antiinflammatory drugs. There was no significant difference in the use of these drugs, hydroxychloroquine, antihypertensive agents, or diuretics between the two study groups.
Medical-Management Protocols
In view of the variable clinical course of systemic lupus erythematosus, nine medical-management protocols were defined to provide standardized care of individual patients in a manner consistent with generally acceptable medical practice. After the initial four weeks of therapy (protocol 1), patients who improved clinically received cyclophosphamide in gradually decreasing doses for four additional weeks, after which it was discontinued. The dose of prednisone was gradually decreased over a 22-week period to 20 mg on alternate days (protocol 2). Patients whose symptoms of systemic lupus erythematosus persisted, worsened, or reappeared were assigned to other standardized protocols of more intensive drug therapy and were then returned to the withdrawal protocol (protocol 2) after these problems resolved. Clearly defined protocols (3 through 7) were written for the uniform treatment of the various manifestations of systemic lupus erythematosus according to their severity. Patients with persistent or recurrent severe renal manifestations (protocol 7) received a second course of treatment with their initial randomization therapy. Specific clinical stopping points were defined; when patients reached any of these points, randomized therapy was stopped. The length of time that passed before a stopping point was reached was one of the major outcome variables in the study. The medical-management protocols have been described in detail elsewhere.15
Laboratory Analyses
Serum creatinine, C3 and C4 complement components, total IgG, antibody against double-stranded DNA (anti-dsDNA), and cryoglobulin concentrations were determined in a central laboratory according to previously published methods.16 Serum creatinine was measured by a Creatinine Analyzer II (Beckman Instruments, Fullerton, Calif.) with use of a modified alkaline picrate method. Serum IgG, C3, and C4 were measured by radial immunodiffusion (Calbiochem—Behring, La Jolla, Calif.), and anti-dsDNA was measured by radioimmunoassay (Amersham, Arlington Heights, Ill.). Other laboratory studies, including 24-hour urinary protein determinations, were performed in the clinical laboratories of the participating institutions.
Outcome Variables
The major study outcomes were the length of time to death, the length of time to renal failure (defined as an increase in the serum creatinine concentration that was at least 265 μmol per liter [3 mg per deciliter] above the base-line level, or the initiation of dialysis or renal transplantation), the length of time before a stopping point was reached, and changes in the levels of 24-hour urinary protein excretion and serum creatinine, IgG, anti-dsDNA antibody, cryoglobulins, C3, and C4. All patients, including the patient with the nonqualifying biopsy result, those reaching stopping points, and any others failing for any reason to follow their assigned treatment protocol, were followed until the end of the study and were included in the analyses.
All important clinical events, including death, reaching a stopping point, and renal failure, were reviewed in detail by a clinical review committee. There were six stopping points. The first was renal failure and serologic abnormalities, defined as an increase in the serum creatinine concentration that was at least 265 μmol per liter (3 mg per deciliter) above the base-line level, the occurrence of end-stage renal failure (the clinical need for dialysis or transplantation), documentation by repeat renal biopsy of more than 80 percent glomerular sclerosis, a persistent decrease in serum C3 or C4 concentrations, or a doubling of the initial rate of urinary protein excretion. The other stopping points were unresponsiveness to therapy or major extrarenal manifestations of systemic lupus erythematosus, intercurrent illness, serious complication of therapy, unrelated serious clinical events (including unrelated death), and loss of the patient to follow-up.
Statistical Analysis
Data management and statistical analyses were conducted with the Statistical Analysis System (SAS Institute, Cary, N.C.)17 and BMDP statistical software.18 All results with a P value of less than 0.05 (two-sided) are reported, without adjustment for multiple tests of significance. For qualitative variables, the proportions of events were compared with either the chi-square statistic or, when the cell frequencies were small, Fisher's exact test.19 For continuous variables, t-tests20 were used to compare the mean values in the two groups; Wilcoxon rank tests21 were used to compare for laboratory values whose distribution seriously deviated from normal. Survival was described with the product-limit method, and the significance of differences between two survival curves was tested with the logrank statistic.22 Laboratory results were analyzed separately at each time point; analysis of covariance, with adjustment for the base-line value, was used to assess the difference between the two groups.23 The covariate-adjusted values were plotted over time. A smoothed line was fit through the points of each plot with a spline function for ease of visualization and reduction of noise in the results.17
Sample Size and Power
The results of previous studies24 , 25 showed that among cohorts of patients with severe lupus nephritis, mortality was very nearly exponentially distributed, with a rate of 0.30 per year. Death was most often due to renal failure; thus, the rate of renal failure or death in this study was assumed to be 0.30 per year. The study was planned to treat 125 patients in four years, with the study lasting for a total of six years, which would have provided a power of 88 percent to detect a 50 percent reduction in this rate (to 0.15 per year) in the plasmapheresis group.26
Early Termination
In March 1986, after 86 patients had been recruited, statistical analysis of the accrued results showed that there was no difference between groups in the primary outcomes and that there was little chance that plasmapheresis was beneficial.27 , 28 When a clinical trial fails to find a difference between two treatment groups, it is important to assess the likelihood that there could still be a difference of clinical importance. This issue was addressed with assessments of the conditional power27 that the study could have detected a significant difference had it continued. The analysis showed that if the trial were continued, the trend favoring standard treatment would have to be reversed dramatically to provide even a small (50 percent) power to detect a difference.28 On the basis of the recommendation of the study's External Advisory Board-Patient-Safety Monitoring Committee, appointed by the National Institute of Diabetes and Digestive and Kidney Diseases, and after a review of the medical, ethical, and statistical considerations, we decided to terminate the trial.
Results
Eighty-six patients entered the study between April 1, 1981, and September 30, 1986. Forty-six were randomly assigned to the standard-therapy group and 40 to the plasmapheresis group. One patient in the standard-therapy group was lost to follow-up before the study was terminated. All other patients were followed until death or the termination of the study, and the final status of all surviving patients in terms of stopping points was verified at that time. Follow-up of these patients has continued since the conclusion of the formal study, and the status of all but one surviving patient (other than the one who dropped out) in terms of death and renal failure has been verified as of January 31, 1990. The average (±SD) length of follow-up in the formal study was 133±10 weeks (median, 120) for the standard-therapy group and 139±13 (median, 150) for the plasmapheresis group. The total follow-up (to January 31, 1990) of the patients in the standard-therapy and plasmapheresis groups was 277 and 297 weeks, respectively.
Base-Line Characteristics
The base-line characteristics of the two groups are shown in Table 1.Table 1
Characteristics of Patients at Entry into the Study.* There were no significant differences between the groups. The fact that the patients had both active and severe lupus nephritis is evidenced not only by the histologic findings needed for entry into the study, but by the average serum creatinine concentration of 180 μmol per liter (2 mg per deciliter). Predictably, these patients had low serum levels of C3 and C4 and elevated concentrations of anti-dsDNA antibodies.Clinical Outcomes
The patients assigned to the plasmapheresis group received a mean of 10 of the 12 prescribed plasma exchanges in the first treatment period. Compliance with the prescribed prednisone and cyclophosphamide therapy was excellent overall and was comparable in the two groups. There was no significant difference in any of the clinical-outcome measures (Table 2Table 2
Outcome Events in Patients with Systemic Lupus Erythematosus and Severe Nephritis.* and Fig. 1Figure 1
Clinical Outcomes in Patients with Severe Lupus Nephritis., 2Figure 2
Mean (±SE) Serum Creatinine Concentration and Urinary Protein Excretion in Patients with Lupus Nephritis Treated with Standard Therapy or Standard Therapy and Plasmapheresis., and 3Figure 3
Serum anti-dsDNA, IgG, and Cryoglobulin Concentrations in Patients with Lupus Nephritis Treated with Standard Therapy or Standard Therapy and Plasmapheresis.). There were 14 deaths during the formal study — 6(13 percent) in the standard-therapy group and 8 (20 percent) in the plasmapheresis group (P = 0.39). End-stage renal disease developed in 8 patients (17 percent) in the standard-therapy group and in 10 patients (25 percent) in the plasmapheresis group (P = 0.39). Thirty patients reached stopping points — 14 (30 percent) in the standard-therapy group and 16 (40 percent) in the plasmapheresis group (P = 0.35). The types of stopping points reached were similar in the two groups (Table 2). The attainment of any stopping point proved to be highly predictive of an adverse renal outcome or death. Twenty-five of the 30 patients who reached a stopping point subsequently either died or had renal failure — 11 (24 percent) in the standard-therapy group and 14 (35 percent) in the plasmapheresis group (P = 0.30).The percentage of patients in each group who had a remission of their renal disease, on the basis of a serum creatinine concentration of ≤106 μmol per liter (1.2 mg per deciliter) and a 24-hour urinary protein excretion of ≤0.2 g per day, was also similar: 13 of 46 patients (28 percent) in the standard-therapy group and 12 of 40 patients (30 percent) in the plasmapheresis group (P = 0.86). If the definition of the attainment of remission of renal disease and stabilization of renal function was changed to include a serum creatinine concentration of ≤ 124 μmol per liter (1.4 mg per deciliter) and a 24-hour urinary protein excretion of ≤0.33 g per day, 19 patients (41 percent) in the standard-therapy group and 16 (40 percent) in the plasmapheresis group achieved remission.
Extended Follow-up
During the spring of 1990, all participating centers were contacted to ascertain the status of all surviving patients as of January 31, 1990. The centers were able to locate all but one patient (in the standard-therapy group). Since the last follow-up four patients had died, all in the standard-therapy group. Thus, a total of 10 patients (22 percent) in the standard-therapy group and 8 patients (20 percent) in the plasmapheresis group had died (P = 0.80). During the same period renal failure developed in 4 additional patients in each group, so that a total of 12 patients (26 percent) in the standard-therapy group and 14 patients (35 percent) in the plasmapheresis group had renal failure (P = 0.41). Among the patients who were followed for at least five years, 17 in the standard-therapy group and 18 in the plasmapheresis group died (P = 0.80).
Clinical Management
There were no differences between the two treatment groups in the frequencies with which patients entered various treatment protocols (Table 3Table 3
Clinical-Management Protocols.). Forty-two of the 46 patients (91 percent) in the standard-therapy group were entered into the drug-tapering protocol (protocol 2) at some time in their course, whereas only 32 of the 40 patients (80 percent) treated with plasmapheresis were ever entered into this protocol (P>0.05). Among the patients who reached the withdrawal protocol, the numbers in the two treatment groups who were entered into the exacerbation protocols were similar.Renal Laboratory Outcomes
The changes in serum creatinine concentration and 24-hour urinary protein excretion in the two groups are shown in Figure 2. Although the mean serum creatinine values in the standard-therapy group were lower than those in the plasmapheresis group most of the time, none of the values were significantly different. Similarly, the mean 24-hour urinary protein values were not significantly different at any time, although the rate was higher at week 4 in the standard-therapy group (P<0.05).
Immunologic Outcomes
A possible explanation for the lack of benefit of plasmapheresis could have been the failure to achieve the stated goal of reducing the serum concentrations of anti-dsDNA antibodies and cryoglobulins, the latter being a measure of circulating immune complexes. Figure 3 shows the average serum concentrations of anti-dsDNA antibodies, total IgG, and cryoglobulins during the first 24 weeks of the study. During the initial weeks of therapy, the serum concentrations of anti-dsDNA antibodies, total IgG, and cryoglobulins decreased more rapidly in the patients in the plasmapheresis group than in the patients in the standard-therapy group.
The serum C4 and C3 concentrations were similar at base line (Table 1), but the levels of these components changed differently during initial therapy. Whereas the serum C3 and C4 concentrations in the standard-therapy group increased, with C4 levels reaching the normal range at week 3 and C3 levels reaching normal by week 5, the concentrations of both components decreased by 20 percent after two weeks of therapy in the plasmapheresis group (P<0.05). The C3 and C4 concentrations then increased, reaching normal values at weeks 6 and 4, respectively. The concentrations of both remained normal thereafter in both groups.
Discussion
The addition of plasmapheresis therapy did not improve the prognosis of patients with severe lupus nephritis who received a standard program of prednisone and cyclophosphamide therapy in this clinical trial. Randomization resulted in virtually identical base-line characteristics for demographic, clinical, laboratory, and histopathological variables in the two groups when the patients began therapy. Both positive and negative clinical outcomes were similar in the two groups. Thirty to 40 percent of the patients in each group had a remission of their lupus nephritis. In addition, the frequency of negative outcomes such as death or renal failure was the same in both groups. Of the patients whose conditions initially stabilized or improved, allowing them to be entered into the drug-withdrawal protocol, an equal proportion had a subsequent exacerbation (Table 3). There were no differences of any kind between the groups throughout the course of the follow-up.
In contrast to the similarity in clinical responses found during the study, the serologic responses to therapy differed in the two groups. Serum concentrations of anti-dsDNA antibodies and cryoglobulins decreased more rapidly and to a greater degree in patients treated with plasmapheresis (Fig. 3). The decreases in the serum C4 and C3 concentrations in the plasmapheresis group correlated with the decreases in serum IgG concentrations that were observed during the first two weeks of therapy. The earlier response of the complement components suggests increased synthesis of these components and a possible decreased consumption due to rapidly decreasing levels of immune complexes. These results confirm that the plasmapheresis protocol indeed achieved the goal of rapidly removing anti-dsDNA antibodies and cryoprecipitable immune complexes from the circulation of these patients. The serologic changes are in accord with the results of previous studies.4 5 6 7 8 , 29 , 30 Early experience with plasmapheresis provided a number of instances of increased antibody synthesis in response to the rapid removal of immunoglobulins and other substances from the circulation31; cyclophosphamide was included in the initial treatment protocol to prevent increased synthesis of antibodies. The marked decrease in the serum concentrations of IgG and anti-dsDNA antibodies in the patients in the standard-therapy protocol indicates that IgG-antibody secretion was depressed by prednisone and cyclophosphamide.
Although a therapeutic benefit has been ascribed to plasmapheresis in a variety of disorders, the use of concomitant immunosuppressive therapy made the true efficacy of therapy impossible to determine. An earlier controlled trial in patients with lupus nephritis was designed to determine whether a prolonged period of once-monthly plasmapheresis could change the course of the illness. The results suggested that plasmapheresis was beneficial.32 , 33 However, the patients in that study had less severe renal disease than did the patients we studied; their serum creatinine concentrations were 97 to 106 μmol per liter (1.1 to 1.2 mg per deciliter).
The need to exclude patients with a lesser degree of glomerular involvement in any study of the treatment of severe lupus nephritis deserves emphasis. Patients with histologically less severe glomerular involvement have a much better prognosis irrespective of the type of therapy given.10 Actuarial analysis of death or renal failure in this study revealed that the overall survival rate for all patients was 85 percent at one year and 72 percent at two years. The mortality rate and the rate of development of renal failure in these patients did not differ from the rates reported in other patients with severe lupus nephritis.2 , 34 35 36 The rigid definition of severe lupus nephritis by an external pathology reading committee provides assurance of adherence to the definitions required for our study.
Another variable that must be considered is the protocol we used for the administration of cyclophosphamide. We gave all patients cyclophosphamide for only eight weeks. Because of differences in patient selection and protocol, we cannot directly compare the results with the longer trials of cyclophosphamide therapy undertaken by other investigators.37 , 38 Nonetheless, our results are similar to those reported in other studies of comparable patients.34 35 36 Whether prolonged parenteral or oral cyclophosphamide therapy in patients with systemic lupus erythematosus is associated with a better clinical outcome is not known.
Our results indicate that the combination of prednisone and short-term cyclophosphamide therapy was associated with improvement and even resolution of the renal disease in a substantial proportion of patients with severe lupus nephritis. The addition of plasmapheresis therapy to this regimen did not improve the outcome. On the basis of these results we cannot recommend treatment of patients with severe lupus nephritis with plasmapheresis.
Supported by grants (R01-AM-27769 and R01-AM-27770) from the Public Health Service.
*See the Appendix for a list of additional members of the study group.
Source Information
From the Department of Medicine, Rush–Presbyterian–St. Luke's Medical Center, Chicago (E.J.L., R.D.R.); the Biostatistics Center, George Washington University, Washington, D.C. (S.-P.L., J.M.L.); and the Department of Medicine, University of Iowa, Iowa City (L.G.H.). Address reprint requests to Dr. Lewis at the Section of Nephrology, 1653 W. Congress Pkwy., Chicago, IL 60615.
Appendix
The Lupus Nephritis Collaborative Study Group included the following: Rush–Presbyterian–St. Luke's Medical Center, Chicago—J.L. Roberts, M.M. Schwartz, R.A. Rodby, and H.L. Corwin; George Washington University, Washington, D.C. — P. Cleary; William Beaumont Hospital, Royal Oak, Mich. — J. Bernstein, H. Shapiro, and B.F. Rosenberg; Francis Scott Key Medical Center, Baltimore — G.S. Hill; Mayo Clinic, Rochester, Minn. — K. Holley; Cleveland Clinic, Cleveland — M.A. Pohl, J. Clough, and G. Gephardt; University of Colorado, Denver — T. Berl; Henry Ford Hospital, Detroit — N. Levin; University of Iowa, Iowa City — S. Bonsib; Evanston Hospital, Evanston, Ill. — N. Simon and H. Friederici; Northwestern University, Chicago — F. del Greco and F.A. Carone; Ohio State University, Columbus —L. Hebert and H.M. Sharma; University of Pennsylvania, Philadelphia — E. Nielson and J. Tomazewski; Tufts-New England Medical Center, Boston — A. Levey and A. Ucci; Medical College of Wisconsin, Milwaukee—J. Lemann and J. Garancis; New York Medical College, Valhalla — K. Shapiro and P. Chander; West Virginia University, Morgantown — F. Whittier, J.W. Graves, J. Bathon, and R. Riley.
- References
References
1
Appel
CrossRef | Web of Science | Medline2
Lewis
Web of Science | Medline3
Magil
Web of Science | Medline4
Jones
CrossRef | Web of Science | Medline5
Jones
Web of Science | Medline6
Jones
Medline7
Jones
CrossRef | Web of Science | Medline8
Jones
Medline9
Tan
CrossRef | Web of Science | Medline10
Pohl
Web of Science11
Churg J, Sobin LH, eds. Renal disease: classification and atlas of glomerular diseases. Tokyo: Igaku-Shoin, 1982:127–49
12
Balow
CrossRef | Medline13
Schwartz
Web of Science | Medline14
Schwartz
CrossRef | Web of Science | Medline15
Clough JD, Lewis EJ, Lachin JM, et al. Treatment protocols of the lupus nephritis collaborative study of plasmapheresis in severe lupus nephritis. In: Rock G, ed. Apheresis: proceedings of the Second International Congress of the World Apheresis Association, Ottawa, Ontario, May 18–20, 1988. New York: Wiley-Liss, 1990:301–7
16
Roberts
CrossRef | Web of Science | Medline17
SAS user's guide: statistics/graph, version 5 ed. Cary, N.C.: SAS Institute, 1985
18
Dixon WJ, ed. BMDP statistical software. Berkeley: University of California Press, 1988
19
Fleiss JL. Statistical methods for rates and proportions. 2nd ed. New York: John Wiley, 1981
20
Snedecor GW, Cochran WG. Statistical methods. 7th ed. Ames: Iowa State University Press, 1980
21
Randies RH, Wolfe DA. Introduction to the theory of nonparametric statistics. New York: John Wiley, 1979
22
Kalbfleisch JD, Prentice RL. The statistical analysis of failure time data. New York: John Wiley, 1980
23
Searle SR. Linear models. New York: John Wiley, 1971
24
Pollak
Medline25
Baldwin
Web of Science | Medline26
Lachin
CrossRef | Medline27
Halperin
CrossRef | Medline28
Lachin
CrossRef | Medline29
Lewis
Web of Science | Medline30
Frank
Full Text | Web of Science | Medline31
Wysenbeek 32
Clark 33
Clark
Web of Science | Medline34
Donadio
Full Text | Web of Science | Medline35
Morel-Maroger
Medline36
Correia
CrossRef | Web of Science | Medline37
Balow
Full Text | Web of Science | Medline38
Austin
Full Text | Web of Science | Medline
- Citing Articles (130)
Citing Articles
1
M. Haubitz. (2012) Lupusnephritis. Der Nephrologe 7:1, 63-74
CrossRef2
John S. Hayes, Rasheed A. Balogun, Jamison Chang, Emaad M. Abdel Rahman. (2012) Therapeutic Plasma Exchange for Renal-Related Conditions in the Elderly: Ten Years Experience in One Center. Seminars in Dialysisno-no
CrossRef3
Stuart L. Goldstein. (2012) Therapeutic Apheresis in Children: Special Considerations. Seminars in Dialysisno-no
CrossRef4
Charles D. Pusey, Jeremy B. Levy. (2012) Plasmapheresis in Immunologic Renal Disease. Blood Purification 33:1-3, 190-198
CrossRef5
William L. Whittier, Edmund J. Lewis. 2012. Lupus nephritis. , 244-250.
CrossRef6
S. M. Korbet, E. J. Lewis, . (2011) Complete remission in severe lupus nephritis: assessing the rate of loss in proteinuria. Nephrology Dialysis Transplantation
CrossRef7
2011. Therapeutic Apheresis. , 521-553.
CrossRef8
Keiko Uchida, Kosaku Nitta. (2011) Recent advances in the treatment of lupus nephritis. Clinical and Experimental Nephrology
CrossRef9
Guillermo J. Pons-Estel, Gabriel E. Salerni, Rosa M. Serrano, José A. Gomez-Puerta, Miguel A. Plasin, Edelweiss Aldasoro, Miguel Lozano, Joan Cid, Ricard Cervera, Gerard Espinosa. (2011) Therapeutic plasma exchange for the management of refractory systemic autoimmune diseases: Report of 31 cases and review of the literature. Autoimmunity Reviews 10:11, 679-684
CrossRef10
Katrina Shum, Anca Askanase. (2011) Treatment of Lupus Nephritis. Current Rheumatology Reports 13:4, 283-290
CrossRef11
2011. References. , 593-616.
CrossRef12
Hala Alshayeb, Barry M. Wall, Elvira O. Gosmanova. (2011) Treatment of Proliferative and Membranous Lupus Nephritis: Review of Key Clinical Trials. The American Journal of the Medical Sciences1
CrossRef13
L.P. Kihm, V. Schwenger. (2011) Plasmapherese und Immunadsorption auf der Intensivstation. Der Nephrologe 6:2, 149-154
CrossRef14
N. Stoycheff, K. Pandya, A. Okparavero, A. Schiff, A. S. Levey, T. Greene, L. A. Stevens. (2011) Early change in proteinuria as a surrogate outcome in kidney disease progression: a systematic review of previous analyses and creation of a patient-level pooled dataset. Nephrology Dialysis Transplantation 26:3, 848-857
CrossRef15
Sanjeev Baweja, Kate Wiggins, Darren Lee, Susan Blair, Margaret Fraenkel, Lawrence P. McMahon. (2011) Benefits and limitations of plasmapheresis in renal diseases: an evidence-based approach. Journal of Artificial Organs 14:1, 9-22
CrossRef16
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CrossRef17
Rasheed A. Balogun, Emaad M. Abdel-Rahman. (2011) Therapeutic plasma exchange and renal related vasculitis: Therapeutic apheresis academy 2010. Journal of Clinical Apheresis 26:5, 291-296
CrossRef18
Earl Silverman, Allison Eddy. 2011. SYSTEMIC LUPUS ERYTHEMATOSUS. , 315-343.
CrossRef19
Brad H. Rovin, Isaac E. Stillman. 2011. Kidney. , 769-814.
CrossRef20
Noam Jacob, William Stohl. (2010) Autoantibody-dependent and autoantibody-independent roles for B cells in systemic lupus erythematosus: Past, present, and future. Autoimmunity 43:1, 84-97
CrossRef21
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CrossRef22
Sandra V. Navarra, Oscar D. Naidas. 2010. Management of Systemic Lupus Erythematosus Renal Disease. , 108-123.
CrossRef23
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Eun Mi Yang, Dong Kyun Han, Hee Jo Baek, Myung Geun Shin, Young Ok Kim, Hoon Kook, Tai Ju Hwang. (2010) Thrombotic thrombocytopenic purpura with decreased level of ADAMTS-13 activity and increased level of ADAMTS-13 inhibitor in an adolescent. Korean Journal of Pediatrics 53:3, 428
CrossRef25
Zbigniew M. Szczepiorkowski, Jeffrey L. Winters, Nicholas Bandarenko, Haewon C. Kim, Michael L. Linenberger, Marisa B. Marques, Ravindra Sarode, Joseph Schwartz, Robert Weinstein, Beth H. Shaz. (2010) Guidelines on the use of therapeutic apheresis in clinical practice-Evidence-based approach from the apheresis applications committee of the American Society for Apheresis. Journal of Clinical Apheresis 25:3, 83-177
CrossRef26
Emily von Scheven, Aysin Bakkaloglu. (2009) What's new in paediatric SLE?. Best Practice & Research Clinical Rheumatology 23:5, 699-708
CrossRef27
Sandeep Singh, Ramesh Saxena. (2009) Lupus Nephritis. The American Journal of the Medical Sciences 337:6, 451-460
CrossRef28
Andre A. Kaplan. (2009) Why nephrologists should perform therapeutic plasma exchange. Dialysis & Transplantation 38:2, 65-70
CrossRef29
David Jayne. 2008. Plasmapheresis in Renal Diseases. , 125-139.
CrossRef30
James E. Balow, Meryl Waldman, Howard A. Austin. 2008. Lupus Nephritis. , 157-171.
CrossRef31
Jennifer K. King, Bevra H. Hahn. (2007) Systemic lupus erythematosus: modern strategies for management – a moving target. Best Practice & Research Clinical Rheumatology 21:6, 971-987
CrossRef32
Yoe Kie Onno Teng, Jacob M van Laar. (2007) Anticyclic citrullinated peptide antibodies: the footprint of autoreactive plasma cells in synovium?. Future Rheumatology 2:6, 577-586
CrossRef33
Hitoshi Yokoyama, Takashi Wada, Wei Zhang, Hideki Yamaya, Mitsuhiro Asaka. (2007) Advances in apheresis therapy for glomerular diseases. Clinical and Experimental Nephrology 11:2, 122-127
CrossRef34
Beth H. Shaz, Michael L. Linenberger, Nicholas Bandarenko, Jeffrey L. Winters, Haewon C. Kim, Marisa B. Marques, Ravindra Sarode, Joseph Schwartz, Robert Weinstein, Ashka Wirk, Zbigniew M. Szczepiorkowski. (2007) Category IV indications for therapeutic apheresis—ASFA fourth special issue. Journal of Clinical Apheresis 22:3, 176-180
CrossRef35
János Jákó, Sámuel Komoly, Pál Soltész. (2007) Plazmaferézis kezelés szisztémás autoimmun betegségekben. Orvosi Hetilap 148:0, 72-76
CrossRef36
Irina Buhaescu, Adrian Covic, Gilbert Deray. (2007) Treatment of Proliferative Lupus Nephritis—A Critical Approach. Seminars in Arthritis and Rheumatism 36:4, 224-237
CrossRef37
Melvin M. Schwartz. (2007) The Pathology of Lupus Nephritis. Seminars in Nephrology 27:1, 22-34
CrossRef38
Atsuhiro Kanno, Osamu Hotta, Naoko Yusa, Yoshio Taguma. (2007) Predictive Factors of Clinical Outcome in Patients with Diffuse Proliferative Lupus Nephritis Treated Early by Intravenous Methylprednisolone Pulse Therapy. Renal Failure 29:1, 41-47
CrossRef39
Anne Davidson, Cynthia Aranow. (2006) Pathogenesis and treatment of systemic lupus erythematosus nephritis. Current Opinion in Internal Medicine 5:6, 631-638
CrossRef40
Chi Chiu Mok. (2006) Therapeutic Options for Resistant Lupus Nephritis. Seminars in Arthritis and Rheumatism 36:2, 71-81
CrossRef41
C Grootscholten, G Ligtenberg, E C Hagen, A W L van den Wall Bake, J W de Glas-Vos, M Bijl, K J Assmann, J A Bruijn, J J Weening, H C van Houwelingen, R H W M Derksen, J H M Berden. (2006) Azathioprine/methylprednisolone versus cyclophosphamide in proliferative lupus nephritis. A randomized controlled trial. Kidney International 70:4, 732-742
CrossRef42
Helmut Soerensen, Jana-Maria Schneidewind-Mueller, Doris Lange, Nobuhito Kashiwagi, Marita Franz, Takashi Yokoyama, Wolfgang Ramlow. (2006) Pilot clinical study of Adacolumn cytapheresis in patients with systemic lupus erythematosus. Rheumatology International 26:5, 409-415
CrossRef43
, Matthew H. Liang, Peter H. Schur, Paul Fortin, E. William St.Clair, James E. Balow, Karen Costenbader, Leslie Crofford, Paola de Pablo, Mary Anne Dooley, Axel Finckh, Caroline P. Gordon, Ingrid E. Lundberg, Alain Meyrier, Ola Nived, Claudio Ponticelli, Matthias K. Schneider, Ajay Singh, Daniel J. Wallace. (2006) The American college of rheumatology response criteria for proliferative and membranous renal disease in systemic lupus erythematosus clinical trials. Arthritis & Rheumatism 54:2, 421-432
CrossRef44
Sylvia Dold, Ranju Singh, Haroon Sarwar, Yamini Menon, Liliana Candia, Luis R. Espinoza. (2005) Frequency of microangiopathic hemolytic anemia in patients with systemic lupus erythematosus exacerbation: Distinction from thrombotic thrombocytopenic purpura, prognosis, and outcome. Arthritis & Rheumatism 53:6, 982-985
CrossRef45
BRAD H ROVIN, HUIJUAN SONG, LEE A HEBERT, TIBOR NADASDY, GYONGYI NADASDY, DANIEL J BIRMINGHAM, CHACK YUNG YU, HAIKADY N NAGARAJA. (2005) Plasma, urine, and renal expression of adiponectin in human systemic lupus erythematosus. Kidney International 68:4, 1825-1833
CrossRef46
Anna-Christine Hauser, Lorenz Hauser, Ingrid Pabinger-Fasching, Peter Quehenberger, Kurt Derfler, Walter Hermann Hörl. (2005) The Course of Anticardiolipin Antibody Levels Under Immunoadsorption Therapy. American Journal of Kidney Diseases 46:3, 446-454
CrossRef47
Carmen T. Narciso. (2005) Apheresis in the Philippines. Journal of Clinical Apheresis 20:2, 107-112
CrossRef48
SJ Chadban, RC Atkins. (2005) Glomerulonephritis. The Lancet 365:9473, 1797-1806
CrossRef49
BRAD H ROVIN, YUXIAO TANG, JUNFENG SUN, HAIKADY N NAGARAJA, KEVIN V HACKSHAW, LINDA GRAY, ROBERT RICE, DANIEL J BIRMINGHAM, CHACK-YUNG YU, DAN N SPETIE, AMY AZIZ, LEE A HEBERT. (2005) Clinical significance of fever in the systemic lupus erythematosus patient receiving steroid therapy. Kidney International 68:2, 747
CrossRef50
KASPER ROSSING, PER K CHRISTENSEN, PETER HOVIND, LISE TARNOW, PETER ROSSING, HANS-HENRIK PARVING. (2004) Progression of nephropathy in type 2 diabetic patients. Kidney International 66:4, 1596-1605
CrossRef51
Harold R. Collard, Marvin I. Schwarz. (2004) Diffuse alveolar hemorrhage. Clinics in Chest Medicine 25:3, 583-592
CrossRef52
MARTIJN A VERKADE, JACQUELINE VAN DE WETERING, MARISKA KLEPPER, LEONARD M B VAESSEN, WILLEM WEIMAR, MICHIEL G H BETJES. (2004) Peripheral blood dendritic cells and GM-CSF as an adjuvantfor hepatitis B vaccination in hemodialysis patients. Kidney International 66:2, 614-621
CrossRef53
Contreras, Gabriel, Pardo, Victoriano, Leclercq, Baudouin, Lenz, Oliver, Tozman, Elaine, O'Nan, Patricia, Roth, David, . (2004) Sequential Therapies for Proliferative Lupus Nephritis. New England Journal of Medicine 350:10, 971-980
Full Text54
Robert S Flanc, Matthew A Roberts, Giovanni F.M Strippoli, Steven J Chadban, Peter G Kerr, Robert C Atkins. (2004) Treatment of diffuse proliferative lupus nephritis: a meta-analysis of randomized controlled trials 1 1This review is excerpted from a Cochrane Review in The Cochrane Library 2004, Issue 1 (“Treatment for Lupus Nephritis”; http://www.update-software.com/cochrane/). Cochrane Reviews are regularly updated as new evidence emerges and in response to comments and criticisms, and The Cochrane Library should be consulted for the most recent version of the Review.. American Journal of Kidney Diseases 43:2, 197-208
CrossRef55
Robert S Flanc, Matthew A Roberts, Giovanni FM Strippoli, Steven J Chadban, Peter G Kerr, Robert C Atkins, Robert S Flanc. 2004. Treatment for lupus nephritis. .
CrossRef56
Radovan Bogdanović, Vesna Nikolić, Srdjan Pašić, Jovan Dimitrijević, Jasmina Lipkovska-Marković, Jelena Erić-Marinković, Miloš Ognjanović, Aleksandra Minić, Nataša Stajić. (2004) Lupus nephritis in childhood: a review of 53 patients followed at a single center. Pediatric Nephrology 19:1, 36-44
CrossRef57
Hitoshi Yokoyama, Takashi Wada, Kengo Furuichi. (2003) Immunomodulation Effects and Clinical Evidence of Apheresis in Renal Diseases. Therapeutic Apheresis and Dialysis 7:6, 513-519
CrossRef58
Yolanda Braun-Moscovici, Daniel E. Furst. (2003) Plasmapheresis for rheumatic diseases in the twenty-first century. Current Opinion in Rheumatology 15:3, 197-204
CrossRef59
Andre A. Kaplan. (2003) The Use of Apheresis in Immune Renal Disorders. Therapeutic Apheresis and Dialysis 7:2, 165-172
CrossRef60
Richard J. Benjamin, W. Hallowell Churchill. 2003. Therapeutic Plasma Exchange. , 238-243.
CrossRef61
G SAYDAIN, L GEORGE, S RAOOF. (2002) New therapies: plasmapheresis, intravenous immunoglobulin, and monoclonal antibodies. Critical Care Clinics 18:4, 957-975
CrossRef62
F MADORE. (2002) PlasmapheresisTechnical aspects and indications. Critical Care Clinics 18:2, 375-392
CrossRef63
Monika Graninger, Sabine Schmaldienst, K. Derfler, W. B. Graninger. (2002) Immunoadsorption Therapy (Therasorb) in Patients with Severe Lupus Erythematosus. Acta Medica Austriaca 29:1, 26-29
CrossRef64
Luis Carre??o, Francisco Javier L??pez-Longo, Carlos Manuel Gonz??lez, Indalecio Monteagudo. (2002) Treatment Options for Juvenile-Onset Systemic Lupus Erythematosus. Pediatric Drugs 4:4, 241-256
CrossRef65
Bruce C. McLeod. (2002) An approach to evidence-based therapeutic apheresis. Journal of Clinical Apheresis 17:3, 124-132
CrossRef66
Nouhad Mistry-Burchardi, Ulf Schönermarck, Walter Samtleben. (2001) Apheresis in Lupus Nephritis. Therapeutic Apheresis 5:3, 161-170
CrossRef67
Christopher C. Najafi, Stephen M. Korbet, Edmund J. Lewis, Melvin M. Schwartz, Morris Reichlin, Joni Evans, for the Collaborative Study Group. (2001) Significance of histologic patterns of glomerular injury upon long-term prognosis in severe lupus glomerulonephritis. Kidney International 59:6, 2156-2163
CrossRef68
Peter G Kerr, Steven J Chadban, Robert C Atkins. (2001) Is there a role for plasma exchange in rapidly progressive glomerulonephritis?. Nephrology 6:3, 141-143
CrossRef69
Nouhad Mistry-Burchardi, Ulf Schonermarck, Walter Samtleben. (2001) Apheresis in Lupus Nephritis. Therapeutic Apheresis and Dialysis 5:3, 161-170
CrossRef70
Andre A. Kaplan. (2001) Apheresis for Renal Disease. Therapeutic Apheresis and Dialysis 5:2, 134-141
CrossRef71
(2001) Efficacy of Mycophenolate Mofetil in Patients with Diffuse Proliferative Lupus Nephritis. New England Journal of Medicine 344:5, 382-383
Full Text72
Robert W. McMurray. (2001) Nonstandard and adjunctive medical therapies for systemic lupus erythematosus. Arthritis & Rheumatism 45:1, 86-100
CrossRef73
Robert Zimmerman, Jai Radhakrishnan, Anthony Valeri, Gerald Appel. (2001) A
DVANCES IN THE TREATMENT OF LUPUS NEPHRITIS . Annual Review of Medicine 52:1, 63-78
CrossRef74
Margaret A. Lindorfer, Theodore A. Schuman, Maria L. Craig, Edward N. Martin, Ronald P. Taylor. (2001) A bispecific dsDNA×monoclonal antibody construct for clearance of anti-dsDNA IgG in systemic lupus erythematosus. Journal of Immunological Methods 248:1-2, 125-138
CrossRef75
Rolf Bambauer, Ulrike Schwarze, Ralf Schiel. (2000) Cyclosporin A and Therapeutic Plasma Exchange in the Treatment of Severe Systemic Lupus Erythematosus. Artificial Organs 24:11, 852-856
CrossRef76
Chan, Tak Mao, Li, Fu Keung, Tang, Colin S.O., Wong, Raymond W.S., Fang, Guo Xiang, Ji, Yu Lian, Lau, Chak Sing, Wong, Andrew K.M., Tong, Matthew K.L., Chan, Kwok Wah, Lai, Kar Neng, . (2000) Efficacy of Mycophenolate Mofetil in Patients with Diffuse Proliferative Lupus Nephritis. New England Journal of Medicine 343:16, 1156-1162
Full Text77
O Bautista. (2000) A Flexible Stochastic Curtailing Procedure for the Log-Rank Test. Controlled Clinical Trials 21:5, 428-439
CrossRef78
Kimihiro Suzuki. (2000) The Role of Immunoadsorption Using Dextran-Sulfate Cellulose Columns in the Treatment of Systemic Lupus Erythematosus. Therapeutic Apheresis and Dialysis 4:3, 239-243
CrossRef79
James E. Balow, Howard A. Austin. (2000) Progress in the treatment of proliferative lupus nephritis. Current Opinion in Nephrology and Hypertension 9:2, 107-115
CrossRef80
Gabor G. Illei, John H. Klippel. (2000) APHERESIS. Rheumatic Disease Clinics of North America 26:1, 63-73
CrossRef81
Bruce C. McLeod. (2000) Introduction to the Third Special Issue: Clinical Applications of Therapeutic Apheresis. Journal of Clinical Apheresis 15:1-2, 1-5
CrossRef82
Anna P. Koo. (2000) Therapeutic apheresis in autoimmune and rheumatic diseases. Journal of Clinical Apheresis 15:1-2, 18-27
CrossRef83
H. Michael Belmont. (1999) Initial management of proliferative lupus nephritis: To cytotoxic or not to cytotoxic?. Current Rheumatology Reports 1:2, 87-88
CrossRef84
R. Bambauer, A. Arnold. (1999) Plasmapheresis with a Substitution Solution of Human Serum Protein (5%) Versus Plasmapheresis with a Substitution Solution of Human Albumin (5%) in Patients Suffering from Autoimmune Diseases. Artificial Organs 23:12, 1079-1087
CrossRef85
(1999) Guidelines for referral and management of systemic lupus erythematosus in adults. Arthritis & Rheumatism 42:9, 1785-1796
CrossRef86
Elizabeth B. Brooks, Matthew H. Liang. (1999) Evaluation of recent clinical trials in lupus. Current Opinion in Rheumatology 11:5, 341-347
CrossRef87
Ralf Schiel, Rolf Bambauer. (1999) Therapeutic Plasma Exchange and Cyclosporine in the Treatment of Systemic Lupus Erythematosus. Therapeutic Apheresis and Dialysis 3:3, 234-239
CrossRef88
Edmund J. Lewis. (1999) Plasmapheresis in Collagen Vascular Diseases. Therapeutic Apheresis and Dialysis 3:2, 172-177
CrossRef89
Du Le Thi Huong, Thomas Papo, Helene Beaufils, Bertrand Wechsler, Olivier Bletry, Alain Baumelou, Pierre Godeau, Jean-Charles Piette. (1999) Renal Involvement in Systemic Lupus Erythematosus. Medicine 78:3, 148-166
CrossRef90
Andre A. Kaplan. (1999) Therapeutic Apheresis for Renal Disorders. Therapeutic Apheresis and Dialysis 3:1, 25-30
CrossRef91
Michael Klein, MD, Jai Radhakrishnan, MD, Gerald Appel, MD. (1999) CYCLOSPORINE TREATMENT OF GLOMERULAR DISEASES. Annual Review of Medicine 50:1, 1-15
CrossRef92
Hricik, Donald E., Chung-Park, Moonja, Sedor, John R., . (1998) Glomerulonephritis. New England Journal of Medicine 339:13, 888-899
Full Text93
Takashi Harada, Masanobu Miyazaki, Yoshiyuki Ozono, Osamu Sasaki, Kei Shioshita, Shigeru Kohno, Masaharu Nishikido, Yutaka Saito, Takashi Taguchi. (1998) Therapeutic Apheresis for Renal Diseases. Therapeutic Apheresis and Dialysis 2:3, 193-198
CrossRef94
D.K Seidel, H.-C Geiss, M.G Donner, M.M Ritter, P Schwandt, R.A Koll, E Standl, A.-G Ziegler. (1998) Course of Islet Autoantibody Titers During Ig-immunoadsorption in a Patient with Newly Diagnosed Type 1 Diabetes. Journal of Autoimmunity 11:3, 273-277
CrossRef95
B. A. PUSSELL. (1998) Plasma exchange therapy. Australian and New Zealand Journal of Medicine 28:3, 289-290
CrossRef96
Martin Aringer, Josef S. Smolen, Winfried B. Graninger. (1998) Severe infections in plasmapheresis-treated systemic lupus erythematosus. Arthritis & Rheumatism 41:3, 414-420
CrossRef97
Jing CHEN, Dwomoa ADU, Robert ATKINS, John DOWLING. (1998) The glomerulus in disease: Renal lupus. Nephrology 4:1-2, 119-122
CrossRef98
Daniel J. Wallace, Dennis Goldfinger, Samuel H. Pepkowitz, Marshal Fichman, Allan L. Metzger, Johann O. Schroeder, Hans H. Euler. (1998) Randomized controlled trial of pulse/synchronization cyclophosphamide/apheresis for proliferative lupus nephritis. Journal of Clinical Apheresis 13:4, 163-166
CrossRef99
Gerald B. Appel. (1997) Cyclophosphamide therapy of severe lupus nephritis. American Journal of Kidney Diseases 30:6, 872-876
CrossRef100
Takashi Harada, Yoshikuki Ozono, Masanobu Miyazaki, Osamu Sasaki, Kenichi Miyazaki, Katushige Abe, Junko Nagashima, Shoko Tukazaki, Takashi Shioshita, Hiroshi Ichinose, Ryosuke Shimamine, Yasuhiko Nishikawa, Masaharu Nishikido, Koichi Yamaguchi, Shigeru Kohno, Takashi Taguchi. (1997) Plasmapheresis in the Treatment of Rapidly Progressive Glomerulonephritis. Therapeutic Apheresis and Dialysis 1:4, 366-369
CrossRef101
Uli Weber, Werner Riegel, Hans Köhler. (1997) Therapeutischer Plasmaaustausch 1996. Medizinische Klinik 92:10, 615-620
CrossRef102
Jo H M Berden. (1997) Lupus nephritis. Kidney International 52:2, 538-558
CrossRef103
Hiroyuki Hirasawa, Takao Sugai, Shigeto Oda, Hidetoshi Shiga, Kenichi Matsuda, Hirokazu Ueno, Tomohito Sadahiro. (1997) Efficacy and Limitation of Apheresis Therapy in Critical Care. Therapeutic Apheresis and Dialysis 1:3, 228-232
CrossRef104
Andre A. Kaplan. (1997) Therapeutic Plasma Exchange for the Treatment of Rapidly Progressive Glomerulonephritis. Therapeutic Apheresis and Dialysis 1:3, 255-259
CrossRef105
MARTIN R. ZAMORA, MARY LAIRD WARNER, RUBIN TUDER, MARVIN I. SCHWARZ. (1997) Diffuse Alveolar Hemorrhage and Systemic Lupus Erythematosus. Medicine 76:3, 192-202
CrossRef106
Vinod K. Bansal, Judith A. Beto. (1997) Treatment of lupus nephritis: A meta-analysis of clinical trials. American Journal of Kidney Diseases 29:2, 193-199
CrossRef107
David S. Pisetsky, Gary Gilkeson, E. William St. Clair. (1997) SYSTEMIC LUPUS ERYTHEMATOSUS. Medical Clinics of North America 81:1, 113-128
CrossRef108
V KHER, P ARORA, N KRISHNANI, RK PANDEY, Amit GUPTA. (1996) Role of intravenous cyclophosphamide in lupus nephritis patients with renal impairment. Nephrology 2:5, 345-349
CrossRef109
J STEWART CAMERON. (1996) The treatment of severe lupus nephritis. Nephrology 2:s1, s35-s41
CrossRef110
Thomas Bosch. (1996) Current Status in Extracorporeal Immunomodulation: Immune Disorders. Artificial Organs 20:8, 902-905
CrossRef111
Peter C. Gøtzsche, Alessandro Liberati, Valter Torri, Luca Rossetti. (1996) Beware of Surrogate Outcome Measures. International Journal of Technology Assessment in Health Care 12:02, 238
CrossRef112
William D. Ratnoff. (1996) INHERITED DEFICIENCIES OF COMPLEMENT IN RHEUMATIC DISEASES. Rheumatic Disease Clinics of North America 22:1, 75-94
CrossRef113
Andre A. Kaplan. (1996) Plasma Exchange in Renal Disease. Seminars in Dialysis 9:1, 61-70
CrossRef114
Andre A. Kaplan. (1995) General Principles of Therapeutic Plasma Exchange. Seminars in Dialysis 8:5, 294-298
CrossRef115
Lee A. Hebert, John J. Dillon, Donald F. Middendorf, Edmund J. Lewis, James B. Peter. (1995) Relationship between appearance of urinary red blood cell/white blood cell casts and the onset of renal relapse in systemic lupus erythematosus. American Journal of Kidney Diseases 26:3, 432-438
CrossRef116
W KLINE BOLTON. (1995) Treatment of crescentic glomerulonephritis. Nephrology 1:4, 257-268
CrossRef117
S Caillard, T Martin, M Ginsbourger, JC Weber, JL Pasquali. (1995) Traitement des glomérulonéphrites lupiques par le cyclophosphamide en emboles intraveineux. La Revue de Médecine Interne 16:6, 413-420
CrossRef118
Hans H. Euler, Johann O. Schroeder, Pontus Harten, Rainald A. Zeuner, Hans J. Gutschmidt. (1994) Treatment-free remission in severe systemic lupus erythematosus following synchronization of plasmapheresis with subsequent pulse cyclophosphamide. Arthritis & Rheumatism 37:12, 1784-1794
CrossRef119
R.W. Erickson, W.A. Franklin, W. Emlen. (1994) Treatment of hemorrhagic lupus pneumonitis with plasmapheresis. Seminars in Arthritis and Rheumatism 24:2, 114-123
CrossRef120
Mills, John A.. (1994) Systemic Lupus Erythematosus. New England Journal of Medicine 330:26, 1871-1879
Full Text121
J. Stewart Cameron. (1994) Lupus nephritis in childhood and adolescence. Pediatric Nephrology 8:2, 230-249
CrossRef122
Michael Kashgarian. (1994) Lupus nephritis: Lessons from the path lab. Kidney International 45:3, 928-938
CrossRef123
M. Fukuda, Y. Kamiyama, K. Kawahara, K. Kawamura, T. Mori, M. Honda. (1994) The favourable effect of cyclophosphamide pulse therapy in the treatment of massive pulmonary haemorrhage in systemic lupus erythematosus. European Journal of Pediatrics 153:3, 167-170
CrossRef124
Gerald B. Appel, M.D, Anthony Valeri, M.D. (1994) THE COURSE AND TREATMENT OF LUPUS NEPHRITIS. Annual Review of Medicine 45:1, 525-537
CrossRef125
Neil L. Kao, G. Wendell Richmond, James N. Moy. (1993) Resoultion od serve lupus nephritis associated with Tripterygium wilfordii Hook F ingestion. Arthritis & Rheumatism 36:12, 1751-1752
CrossRef126
Jane G. Schaller. (1993) Therapy for childhood rheumatic diseases. have we been doing enough?. Arthritis & Rheumatism 36:1, 65-70
CrossRef127
Dobri D. Kiprov, Ronald G. Strauss, David Ciavareiia, Ronald O. Gilcher, Duke O. Kasprisin, Harvey G. Klein, Bruce C. McLeod. (1993) Management of autoimmune disorders. Journal of Clinical Apheresis 8:4, 195-210
CrossRef128
(1992) Plasma Exchange in Polymyositis and Dermatomyositis. New England Journal of Medicine 327:14, 1030-1031
Full Text129
(1992) Plasmapheresis for Lupus Nephritis. New England Journal of Medicine 327:14, 1028-1030
Full Text130
Campion, Edward W., . (1992) Desperate Diseases and Plasmapheresis. New England Journal of Medicine 326:21, 1425-1427
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