Alberto Ortiz, Silvia González Cuadrado, Corina Lorz, Jesús Egido.

Division of Nephrology. Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain.

Received 12/01/95; Accepted 01/26/96; On-line 03/01/96

2. RENAL DISEASE AND CELL NUMBER

Homeostasis of cell number is the outcome of the coordination of cell birth (mitosis) and cell death. Physiological cell death usually takes place by apoptosis. Occasionally other processes, such as cell migration (chemotaxis) and differentiation, are also involved in the regulation of cell number.

Abnormalities of cell number are a frequent feature of renal disorders. Parenchymal cell depletion leading to renal atrophy is characteristic of any chronic, progressive, renal disease. Depletion of tubular cells is the hallmark of acute tubular necrosis. Other nephropathies are defined by an abnormal accumulation of renal cells. Examples may be mesangial hypercellularity in proliferative glomerulonephritis, and the increased number of fibroblasts observed in renal fibrosis. The possible role of altered mitotic rates in renal disease has been extensively studied. However, derangements in the regulation of cell death may also lead to diseases characterized by insufficient or excessive number of cells (1) and may contribute to renal damage (2-4). In the past 2 years, a flurry of papers have unraveled the intracellular regulation of apoptosis. We will first summarize the current knowledge on the regulation of cell death, with special emphasis on renal cells. Subsequently we will review evidence regarding changes in cell death regulation in renal disease.