{'fraction_non_alphanumeric': 0.025234318673395817, 'fraction_numerical': 0.021629416005767843, 'mean_word_length': 5.1415929203539825, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Abnormal renal prostaglandin production during the evolution of chronic nephropathy.

To investigate the role of renal prostaglandins (PGs) in the evolution of kidney parenchymal disease, PGE2 and PGF2a excretion rates were measured in 62 subjects (22 control subjects, 24 patients with different forms of nephropathy and varying degrees of renal failure, and 16 patients with end-stage kidney disease on chronic hemodialysis). Patients with kidney disease and severe renal failure (inulin clearance less than 25 ml/min) showed significant decreases in urinary PGE2 and PGF2a (p less than 0.05 for both PGs), and the values were markedly diminished in patients with end-stage renal failure on chronic hemodialysis. Conversely, in patients with nephropathy and normal renal function, urinary PGE2 was slightly elevated compared to age- and sex-matched control subjects. A significant correlation (r = 0.74, p less than 0.01) was found between inulin clearance and PGF2a in the group of 24 patients with chronic renal failure, both not between PGE2 and inulin clearance. These results indicate that except for patients at the early stage of kidney disease the renal excretion of PGE2 and PGF2a appears greatly diminished in parenchymal renal lesion with severe renal failure and in end-stage kidney disease. The latter phenomenon may be the consequence of diminished functional renal mass.