Phosphate is an integral part of human cellular structure and function. Though most recognised disorders of phosphaturia are genetic in origin, phosphate loss due to acquired conditions is commonly encountered in clinical practice. Acquired hypophosphatemia is most commonly due to renal phosphate wasting and can produce significant morbidity. It also heralds future kidney damage, and continued exposure can lead to progressive kidney injury and potentially renal failure. These conditions are a diverse group of disorders with common shared mechanisms causing loss of phosphate in the urine. Renal phosphate loss can occur as an isolated entity or as a part of generalised proximal tubular dysfunction, i.e., Fanconi's syndrome. An insight into the pathophysiological mechanisms of acquired phosphaturia can help clinicians monitor their patients better and avoid potential harms.

中文翻译：

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获得性磷酸盐尿症：肿瘤诱发的骨软化症之外的疾病

磷酸盐是人体细胞结构和功能的组成部分。尽管大多数公认的磷酸盐尿症是遗传性的，但在临床实践中，由于后天条件导致的磷酸盐丢失也很常见。获得性低磷血症最常见的原因是肾脏磷酸盐消耗，并可产生显着的发病率。它还预示着未来的肾脏损害，持续接触可能导致进行性肾损伤和潜在的肾功能衰竭。这些病症是一组不同的疾病，具有导致尿液中磷酸盐流失的共同机制。肾磷酸盐丢失可以作为孤立的实体发生，也可以作为广泛性近端肾小管功能障碍（即范科尼综合征）的一部分发生。了解获得性磷酸尿症的病理生理机制可以帮助临床医生更好地监测患者并避免潜在的危害。