disease into nephrosis, nephritis (inflammatory renal disease), and arteriosclerosis, a classification that provided the basic framework for pathological diagnosis until the proliferation of histopathological entities that followed the widespread introduction of renal biopsy in the 1950s.

Since functional dynamic tests were introduced in the early 1900s, the understanding of Bright's disease began to follow a path that led away from morphology. Addis was concerned with determining the nature and extent of Bright's disease during life (i.e., making a clinical rather than a pathological diagnosis) while retaining the traditional anatomical basis for classifying the disease. He therefore tried to salvage clinical methods that others had rejected as unreliable or uninformative by learning how to reduce the considerable variability inherent in them. Addis, however, considered a functional approach alone to be inadequate. Owing to "the reserve power of the renal tissue," purely functional tests might fail to detect even the 50 percent loss of renal mass after uninephrectomy. At the same time, many of the physicians who favored functional tests rejected examination of urine sediment. Addis felt that this was also due primarily to methodological problems: "A superficial and casual examination of urinary sediments will make anyone feel inclined to agree with the modern view that little is to be gained from such studies." He also felt, however, that the troublesome day-to-day variability in the appearance of the sediment was due to variations in the conditions of the examination and not necessarily to changes in the disease process.

His approach to the clinical classification of Bright's disease was therefore twofold: quantitative examination of the urinary sediment (the Addis count)15 indicated the nature of the lesion, and the urinary urea clearance (the Addis urea ratio) indicated the extent of the lesion. From



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