Masoumi Amirali, Elhassan Elwaleed, Schrier Robert W
Department of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Iran J Kidney Dis. 2011 Jan;5(1):1-8.
Autosomal dominant polycystic kidney disease (ADPKD) is the most common life-threatening hereditary disease of the kidney. It presents with progressive enlargement of the kidneys with numerous cysts that distort the parenchyma and result in progressive decline in kidney function. Autosomal dominant polycystic kidney disease is genetically modified with the responsible genes localized to separate loci on chromosome 16 (PKD1 gene), accounting for the majority of ADPKD cases, and chromosome 4 (PKD2 gene), accounting for the remainder. This review discusses the current understanding of the pathogenesis of ADPKD, focusing on renal volume and its pivotal role on the manifestations of the disease. Specifically, activation of the renin-angiotensin-aldosterone system, hypertension, left ventricular hypertrophy, kidney function deterioration, pain, and hematuria are examined as consequences of renal volume increase. Recent developments on diagnostic modalities and criteria of the ADPKD are also discussed.
常染色体显性多囊肾病(ADPKD)是最常见的危及生命的遗传性肾病。其表现为肾脏逐渐增大,伴有大量囊肿,这些囊肿使肾实质变形,导致肾功能逐渐下降。常染色体显性多囊肾病是由基因改变引起的,相关基因定位于16号染色体上的不同位点(PKD1基因),占大多数ADPKD病例,以及4号染色体上的(PKD2基因),占其余病例。本综述讨论了目前对ADPKD发病机制的理解,重点关注肾脏体积及其在疾病表现中的关键作用。具体而言,探讨了肾素 - 血管紧张素 - 醛固酮系统激活、高血压、左心室肥厚、肾功能恶化、疼痛和血尿等作为肾脏体积增加的后果。还讨论了ADPKD诊断方式和标准的最新进展。