{'fraction_non_alphanumeric': 0.02006335797254488, 'fraction_numerical': 0.012671594508975714, 'mean_word_length': 5.405405405405405, '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}}
Elevated Level of Hypoxia Inducible Factor 1α Can Alter Renal Epithelial Function

In the United States, about 600,000 people have Polycystic Kidney Disease (PKD) characterized by fluid filled structures (cysts) formed inside the kidney. Cysts interfere with normal renal function and lead to kidney failure. In the cystic epithelia, hypoxia inducible factor 1α (HIF1α) and HIF2α were found to be elevated. It is hypothesized that kidney cystic epithelia transform from normal absorption to secretion leading to accumulation of fluid within the cyst lumen. The fluid accumulation and insufficient vascular supply result in localized chronic hypoxia i.e., elevated HIF1α levels which may further promote cyst growth. We hypothesize that increased level of HIF1α can promote switching of renal epithelial function from absorptive to a secretory phenotype, possibly due to loss of epithelial tight junction integrity and altered active ion transport.