University Hospital Aintree, Academic Rheumatology Unit, Liverpool and 1Department of Rheumatology, St Helens Hospital, Marshalls Cross Road, St Helens, UK
Correspondence to: S. Mpofu, Academic Rheumatology Unit, University Hospital Aintree, Lower Lane, Liverpool L9 7AL, UK. E-mail: smpofu{at}liv.ac.uk
SIR, We read with interest the article by Kitas and Erb [1], where an interesting parallel is drawn between rheumatoid arthritis (RA) and type-2 diabetes (T2D) with respect to ischaemic heart disease (IHD). The association between RA and IHD, as with T2D, is clearly important, yet in the case of RA too little is known about the underlying pathophysiology. Defining the underlying mechanism for such associations is important if prevention or therapy is to improve. However, whilst comparing T2D with RA is important to illustrate the risk of developing IHD, different mechanisms may underlie this association in RA. We have investigated the use of microalbuminuria as a potential predictor of the development of IHD in RA and found that, in contrast to T2D, it is not helpful in RA. This contributes to the concept that different mechanisms are at play in the development of IHD in RA, compared with, for example, T2D.
Microalbuminuria is a well-established marker for incipient nephropathy in patients with T2D [2], early subclinical renal dysfunction and drug-induced renal damage in RA [3]. It is well recognized as an index of vascular damage and excess cardiovascular mortality in both diabetic and non-diabetic subjects [4]. It may also have a prognostic value in IHD, stroke and peripheral arterial disease.
Microalbuminuria has been reported to occur in as many as 27.7% patients with RA compared with 7.8% of controls [3]. We therefore recently assessed 39 patients with RA attending rheumatology out-patient clinics for the presence of microalbuminuria. Patients with risk factors for renal disease (hypertension, diabetes mellitus) or evidence of previous renal disease were not included. Disease activity was assessed by the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). The urinary albumin concentration and the urinary albumin/creatinine ratio were determined in urine specimens using a turbidimetric immunoassay (Olympus, Middlesex, UK). Microalbuminuria was defined as a urinary albumin excretion rate between 20 and 200 µg/min. A spot urine sample was taken, as this has been shown to be an accurate estimate of true albumin excretion [5]. We found that only 3 out of 39 (7.7%) patients with RA had microalbuminuria, comparable to controls reported in other microalbuminuria studies [3] (Table 1).
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There is therefore considerable scope, and a pressing need, for further research to identify the mechanisms underlying the development of IHD in RA and also to identify useful predictive markers. The experience with T2D is a helpful model on which to base such research, but we believe that RA still has much more to reveal.
The authors have declared no conflicts of interest.
References