{'fraction_non_alphanumeric': 0.028751123090745734, 'fraction_numerical': 0.011680143755615454, 'mean_word_length': 4.654822335025381, '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}}
Plasma C-peptide in uraemic patients.

The kidney has been suggested as the main organ for the degradation of C-peptide. This hypothesis was tested in subjects with normal fasting blood glucose concentration and varying degrees of renal failure. Forty-nine subjects with endogenous creatinine clearance ranging from 0--25 ml/min were studied. The basal steady state concentrations of C-peptide (CP) and the immunoreactivity of insulin (IRI) were determined in plasma from fasting patients. The average IRI was similar to that found in normal subjects while a higher CP was found in all patients but two. The average CP in the nephrectomized patients was six times higher than the mean CP in normal subjects (0.35 pmol/ml). There was a significant inverse correlation between clearance and CP (r = 0.51, P less than 0.001) with the highest CP in nephrectomized patients. It is concluded that the increased CP in renal failure, and especially the markedly increased CP in the nephrectomized group supports the hypothesis of the kidney being the organ mainly responsible for the degradation of C-peptide also in man.