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Ann Rheum Dis. 2007 July; 66(7): 981–982.
Published online 2007 March 2. doi:  10.1136/ard.2006.069211
PMCID: PMC1955094

Anti‐tumour necrosis factor α therapy in patients with impaired renal function

Renal insufficiency is a common comorbidity in patients with inflammatory rheumatic diseases such as rheumatoid arthritis and psoriatic arthritis. Decreased renal function is a limiting factor for the use of non‐steroidal anti‐inflammatory drugs and disease‐modifying antirheumatic drugs. Therefore, the availability of therapeutic alternatives would improve our treatment options for these patients. For tumour necrosis factor α (TNFα) inhibitors, no data about their use in patients with impaired renal function are available, because it has been an exclusion criterion in all major clinical trials.

We therefore retrospectively analysed all patients from our institution who had increased serum creatinine levels before or during treatment with TNFα antagonists. All patients with a serum creatinine [gt-or-equal, slanted]1.1 mg/dl and treatment with infliximab, etanercept or adalimumab were included. We were able to identify nine patients with rheumatoid arthritis, one patient with psoriatic arthritis and one patient with juvenile rheumatoid arthritis who had end‐stage renal disease (ESRD) and was receiving haemodialysis (excluded from the analysis because of ESRD). Table 11 shows demographic data, reasons for decreased renal function and comorbidities.

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Table 1 Characteristics of patients with renal insufficiency and anti‐tumour necrosis factor α therapy

The mean age of patients was 62.3 years (range 30–76 years) and the mean creatinine level at the start of the study was 1.6 mg/dl. Risk factors for kidney disease were hypertension (n = 10), diabetes (n = 4) and non‐steroidal anti‐inflammatory drug induced nephropathy (n = 2).

Figure 1A1A shows the course of serum creatinine concentrations during anti‐TNFα therapy. The follow‐up period was up to 24 months. In a statistical analysis of creatinine levels after 3 and 6 months using Friedman's test, no significant increases from baseline could be detected (p>0.05, fig 1B1B).). Additionally, no differences among the TNFα antagonists could be observed. Adalimumab, however, was given to only two of the 10 outpatients for a relatively short period. The mean change in creatinine was 0.07 mg/dl after 3 months and 0.09 mg/dl after 6 months. However, in some patients, there was a trend towards an increase in creatinine at later time points, presumably because of a progression of the underlying kidney disease. No severe infections or other serious adverse events were observed in our patients during anti‐TNFα therapy. According to the European League Against Rheumatism response criteria, we observed four patients with good response, one with moderate response and five with no response in the first 3 months.

figure ar69211.f1
Figure 1 Course of creatinine in renal insufficiency with concomitant anti‐tumour necrosis factor alpha (TNFα) therapy. (A) Time course of change (Δ) in serum creatinine concentrations in 10 patients during anti‐TNFα ...

Reports on the occurrence of renal side effects during anti‐TNFα therapy are scarce. These have included immune complex vasculitis, lupus nephritis and nephritic syndrome.1,2,3 In these cases, renal symptoms were reversible after withdrawal of TNFα antagonists. One case report demonstrated safe application in a patient with ESRD receiving haemodialysis, which is confirmed by one case reported here.4 In addition, anti‐TNFα treatment was well tolerated and safe in the 15 patients with renal involvement of amyloid A amyloidosis.5 No side effects on renal function have been reported so far from randomised clinical trials; however, patients with impaired renal function have been excluded from these trials.6,7,8 In conclusion, our data indicate that the use of TNFα inhibitors has no negative effect on renal function in patients with kidney disease.


We thank the Committee “Pharmakotherapie” of the German Society of Rheumatology for support, and Dr Uppenkamp (Klinikum Ludwigshafen, Germany) and Dr Schmitter (Munich, Germany) for providing patient data; we also thank Dr F. Schiller for the statistical analysis.


ESRD - end‐stage renal disease

TNFα - tumour necrosis factor α


Funding: AJH received funding for lectures from Abbott. AT has nothing to disclose. BM received honoraria for lectures and participation in advisory boards from Abbott, Wyeth and Schering‐Plough, and GS received honoraria for lectures and participation in advisory boards from Abbott, Amgen, Essex, Bristol‐Myers Squibb and Schering‐Plough.

Competing interests: None.


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