Cellular Biology of Tubulointerstitial Growth

Abstract

The capacity of the kidney to grow has been known for more than 2000 years. Aristotle (384–322 B.C.) was probably the first to describe that animals born with one kidney can develop normally, and that the single kidney is enlarged compared with the kidneys of normal two-kidney control animals (WOLF 1993). In the early nineteenth century, the French physician Pierre-Francois-Olivier Rayer (1793–1867) reported enlargement of the renal cortex in diabetes mellitus and observed that the size of the remnant kidney in patients in whom one kidney is missing approaches that of the two kidneys of healthy individuals (RAYER 1837). Rayer also undertook microscopic studies and found that “if the kidney is partially disorganized, the healthy parts become hypertrophied, resulting in a curious mixture of atrophic and hypertrophic parts” (RItz et al. 1989). Gustav Simon (1824–1876), a professor of surgery at the University of Heidelberg in Germany, performed the first unilateral nephrectomy in human subjects. The question of whether compensatory renal growth is solely an increase in protein and size (hypertrophy) or rather is caused by proliferation has puzzled students of renal growth for a long time. The famous Viennese pathologist Carl Rokitansky (1804–1878) believed that the increase in renal size after nephrectomy is true hypertrophy of all tissue constituents, whereas Simon thought that an increase in cell number was responsible for compensatory renal growth (WOlf 1993). However, most of these confusing early opinions can be attributed to the different ages of the animals used and the degree of renal ablation.