Abstract

Diabetes mellitus has a long history during which it was considered to be a disease of the kidneys well into the middle of the 19th century. Recognized in antiquity from its excessive urine output and described as a disease of the urinary tract, its clinical features and fatal outcome were quite accurately recorded by the 1st century ad . Galen (129-200) described it as a disease specific to the kidneys because of a weakness in their retentive faculties. The sweet taste of diabetic urine, which is described in ancient Indian texts and noted by Avicenna (980-1037) and Morgagni (1635-1683), was attributed to the passage of absorbed water and nutrients unchanged into the urine. In 1674, Thomas Willis (1621-1675) first differentiated diabetes from other causes of polyuria by the sweet taste (quasi melle) of diabetic urine and suggested that the sweetness first appears in the blood. A century later, Matthew Dobson (1732-1784) showed that the urine sweetness was because of sugar and was preceded and accompanied by sugar in the blood. Although diabetes then came to be ascribed to increased sugar in the blood, the presence of sugar in the urine continued to be attributed to the decreased retentive properties of the kidneys. The experimental production of diabetes in pancreatectomized dogs that could be reversed by subcutaneous pancreatic transplantation in 1889, and ultimate isolation of insulin in 1922 clearly established diabetes as an endocrine disease. The stage of diabetes as a disease of the kidneys was now over but that of diabetes as a cause of kidney disease was yet to come. Diabetes as a cause of end stage kidney disease was first described in 1936 and extensively documented shortly thereafter, whereas the evidence of its increasing prevalence as a cause of chronic kidney disease continues to accrue.

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