作者: Bryan T. Emmerson , Roy Axelsen , Michael Cross
DOI: 10.1007/978-1-4684-5673-8_33
关键词: Urinary system 、 Acute uric acid nephropathy 、 Chemistry 、 Vascular disease 、 Chemotherapy 、 Nephropathy 、 Kidney 、 Endocrinology 、 Uric acid 、 Biochemistry 、 Internal medicine 、 Gout
摘要: It is generally accepted that many factors, such as hypertension, vascular disease, renal calculi and infection, may contribute to disease in patients with gout. However, these are usually regarded secondary phenomena which often superimposed on a primary nephropathy. Most studies of the gouty kidney, however, have found evidence nephropathy deposits urate uric acid crystals (1, 2, 3); Talbott Terplan (4), study almost two hundred kidneys, concluded “the only distinct pathological feature kidney presence crystals”. Crystallographic indicated were either acicular monosodium monohydrate (urate or MSUM) (UA) (5). Subsequent urinary over-excretion, following chemotherapy malignancy (6) due HPRT deficiency (7, 8), established importance intratubular deposition development an acute Interstitial micro-tophi containing also been demonstrated kidneys there suggestive might develop not local formation, but by passage through lining epithelium distal nephron into interstitial tissues. This has other animals (9). Indeed, electron microscopy within tubular cells leukemia (10). Thus, support for hypothesis that, at least some cases, damage from begins reaction between intraluminal nephron. For this reason, was planned cultured acid.