Impaired adaptation to renal mass reduction in the polycystic rat.
Impaired adaptation to renal mass reduction in the polycystic rat.
复制标题
多囊大鼠对肾质量减少的适应受损。
DOI：
10.1016/s0272-6386(00)70264-2
复制
发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Anderson,S
中科院分区：
文献类型：
--
作者：
Kang,SH;Oyama,TT;Kennefick,TM;Thompson,MM;Anderson,S
常染色体显性多囊肾病（ADPKD）是肾衰竭的一种严重原因。在许多肾脏疾病模型中，手术减少肾脏质量加速疾病进展。我们探讨了手术肾脏质量减少和肾脏质量减少的方法是否加速ADPKD的进程。在雄性杂合子囊性Han：SPRD大鼠和未受影响的同窝对照组中进行了研究。对照组和囊性大鼠通过单侧肾切除术进行50%的肾质量减少，通过每个肾的一半梗死或假手术进行50%的肾质量减少。大多数组都随访至20周，并连续测量血压和蛋白尿。20周时，测量肾小球滤过率（GFR）和肾血浆流量（RPF）。在另外的对照组和假手术或50%肾梗死的囊性大鼠组中进行了12周龄的类似研究。在非囊性大鼠中，单侧肾切除术对血压和蛋白尿的影响最小，并导致实质性代偿性肾脏肥大、过度滤过和过度灌注。类似的节段性梗死导致的肾质量减少导致血压和蛋白尿的值更大，并有显著的代偿性超滤。相比之下，囊性大鼠显示基线肾血流量显著减少，血压和蛋白尿更显著增加，肾脏质量减少后GFR和RPF无代偿性增加。这些研究表明，囊性肾对获得性肾单位丢失的反应能力受损，当额外的肾损伤叠加时，这些肾脏的风险更大。
Autosomal dominant polycystic kidney disease (ADPKD) is a serious cause of renal failure. In many renal-disease models, surgical renal mass reduction accelerates disease progression. We explored whether surgical renal mass reduction and the method of renal mass reduction accelerate the course of ADPKD. Studies were conducted in male heterozygous cystic Han:SPRD rats and unaffected littermate controls. Control and cystic rats were subjected to 50% renal mass reduction by uninephrectomy, 50% renal mass reduction by infarction of half of each kidney, or sham operation. Most groups were followed up to the age of 20 weeks, with serial measurements of blood pressure and proteinuria. At 20 weeks, glomerular filtration rate (GFR) and renal plasma flow (RPF) rate were measured. Similar studies to 12 weeks of age were performed in additional groups of control and cystic rats with either sham operation or 50% renal infarction. In noncystic rats, uninephrectomy led to minimal effects on blood pressure and proteinuria and to substantial compensatory renal hypertrophy, hyperfiltration, and hyperperfusion. Similar renal mass reduction by segmental infarction led to greater values for blood pressure and proteinuria and significant compensatory hyperfiltration. In contrast, the cystic rats showed a significant reduction in baseline renal blood flow, more profound increases in blood pressure and proteinuria, and no compensatory increases in GFR and RPF after reduction of renal mass. These studies suggest that the ability of cystic kidneys to respond to acquired loss of nephrons is impaired and that these kidneys are at greater risk when additional renal injury is superimposed.