{'fraction_non_alphanumeric': 0.01866251944012442, 'fraction_numerical': 0.01866251944012442, 'mean_word_length': 5.217391304347826, '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}}
Hyperglycemic pseudorejection in the diabetic transplant patient.

Serum creatinine elevation in a stable transplant recipient most often suggests rejection of the transplant and requires further evaluation and management. In our series of juvenile diabetic patients who have received kidney transplants, we frequently have observed creatinine elevations in association with hyperglycemia. Correction of the hyperglycemia resulted in return of serum creatinine to normal levels and no rejection therapy was required. To better define this syndrome, 2,734 paired measurements of blood glucose and serum creatinine were obtained in 52 stable post-transplant diabetic patients. A mean increase in blood glucose of 100 mg. per 100 ml. was found to increase serum creatinine by 0.5 mg. per 100 ml. in these patients (r=0.93; p less than or equal to 0.001). Evidence strongly suggests that the pathogenesis of this phenomenon is not a result of a laboratory artifact due to the technique used to determine serum creatinine. The pathogenesis may be due to the increased serum osmolarity and resulting intracellular dehydration associated with hyperglycemia. Recognition of this syndrome is important to all centers participating in the care and management of the diabetic transplant recipient.