{'fraction_non_alphanumeric': 0.024617431803060547, 'fraction_numerical': 0.004657351962741184, 'mean_word_length': 5.240663900414938, '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}}
Stenosis of the Glomerulotubular Neck

The problem of progressive loss of renal function in chronic renal failure remains important in the laboratory as well as the clinic. The recognition of hypertension and proteinuria as ‘bad actors’ is logical support for use of antihypertensive drugs and for lowering the urine protein in progressive renal diseases [1]. Yet our therapies remain incomplete. In fact, while the rate of renal function decline may be slowed by current drug treatments, often enough, it is not stopped, and end-stage renal disease may occur. New insights are thus needed. The correlation of interstitial disease to kidney function is an idea that is over 30 years old [2]. Its meaning has been obscure, however. Specifically, how could injury and fibrosis in the interstitial compartment affect glomerular function? It has been proposed that interstitial fibrosis impairs pressure natriuresis, which leads to progressive renal injury via hypertension [3, 4]. Others have stated that tubulointerstitial injury is a single nephron phenomenon, being dependent on glomerular injury, which would then neatly explain the correlation of the two [5]. Both of these ideas are plausible, but they lack confirmation. The first seems to depend on hypertensive injury, whereas mere control of hypertension does not stop most progressive chronic renal failure. The second appears to relegate the tubulointerstitium to an accessory role, which may be an oversimplification. The Glomerulotubular Neck