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      Impaired proteolytic activity as a potential cause of progressive renal disease.

      Mineral and electrolyte metabolism
      Acidosis, Ammonia, pharmacology, Angiotensin II, physiology, Animals, Diabetes Mellitus, Experimental, physiopathology, Dietary Proteins, Endopeptidases, metabolism, Glomerulonephritis, Humans, Hypertrophy, Inflammation, Insulin-Like Growth Factor I, Kidney, drug effects, pathology, Kidney Diseases, enzymology, Proteins, Transforming Growth Factor beta

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          Abstract

          Renal hypertrophy (an increase in cellular protein content and cellularity as well as an accumulation of extracellular matrix) is due to the imbalance between protein synthesis and degradation. Proteolytic activity in the kidney plays an important role in maintaining this balance. Impaired renal proteolytic activity caused by such factors as high protein intake, metabolic acidosis, angiotensin II and transforming growth factor-beta 1 in vivo and in vitro may result in decreased protein degradation and subsequent induction of cellular hypertrophy, even in the absence of increased protein synthesis.

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