The Modern Conception of Bright's Disease

THE FIRST publication by Richard Bright on renal disease appeared in 1827 as part of a large and beautifully illustrated folio volume of Reports on Medical Cases. The relevant chapter described some " diseases terminating in dropsical effusions" and showed that in some of them there were changes in the kidneys. This work soon received universal acceptance but even the earliest of the subsequent writers on the subject applied the eponym " Bright's disease" to several clinical states other than anasarca if they were associated with renal changes. Subsequently Bright himself, in his most important renal publication The tabular tneu: of the morbid appearances in 100 cases connected with the secretion of albuminous urine (1836), discussed a much more diverse group of patients. The pathological changes tabulated also show considerable variation. The scope of Bright's disease cannot therefore be very rigidly defined and the development of histological technique and laboratory investigation soon made it clear that within this wide framework there were certain clear cut entities that could usefully be diagnosed separately in vivo. Thus, the characteristics of renal amyloidosis occupy a large section of Grainger Stewart's Practical treatise on Bright's diseases ofthekidneys (187 I) and the proof of its existence is the main piece of evidence he offers for his belief that there are several diseases included under the heading Bright's dis': ease. Complex morbid anatomical classifications were also soon developed, for example, the three forms of Bright becoming six in the writings of'Rayer (1840). These early classifications, however, covered the whole field of medical renal dysfunction and towards the end of the century it became recognized that they included the effects of such transient general states as cardiac failure and acute infections, the changes associated with hypertension and with abnormalities of the lower urinary tract, as well as amyloidosis and the changes ansmg primarily in the kidneys. While the picture 50 years ago was considerably clearer than it had been roo years earlier, physicians were still only able to frame more precisely some of the questions that Bright himself had asked without being able to do much more than offer intuitive answers. We may well set out these questions and consider whether in the last 50 years we have made any sensible progress towards answering them. (I) Are the several clinical variants and pathological states expressions of a single disease entity, Bright's disease? (2) If so, is it a continuous process all stages of which are invariably present in each patient, even if not clinically manifest, or may the several forms or stages occur in isolation? (3) What is the aetiology? (4) Alternatively, are the clinical syndromes and pathological appearances so non-specific that even the group of cases of apparently primary renal involvement is in fact made up of several different diseases requiring more refined pathological techniques and more exhaustive clinical investigations for their recognition? (5) What is the relationship of hypertension to the syndrome-is it all renal in origin or is there an essential hypertension; if there is can it cause secondary changes in the kidneys? (6) Can renal ischaemia, as in occlusive atheroma of the renal artery, cause Bright's disease? (7) What is the relationship of diabetes, pregnancy and some metallic intoxications to Bright's disease?