Children born with a solitary functioning kidney (SFK) are predisposed to develop hypertension and kidney injury. Glomerular hyperfiltration and hypertrophy contribute to the pathophysiology of kidney injury. Angiotensin-converting enzyme inhibition (ACEi) can mitigate hyperfiltration and may be therapeutically beneficial in reducing progression of kidney injury in those with an SFK.

SFK was induced in male sheep fetuses at 100 days gestation (term=150 days). Between 4 and 8 weeks of age, SFK lambs received enalapril (SFK+ACEi; 0.5mg/kg per day, once daily, orally) or vehicle (SFK). At 8 months, we examined BP, basal kidney function, renal functional reserve (RFR; GFR response to combined amino acid and dopamine infusion), GFR response to nitric oxide synthase (NOS) inhibition, and basal nitric oxide (NO) bioavailability (basal urinary total nitrate and nitrite [NOx]).

SFK+ACEi prevented albuminuria and resulted in lower basal GFR (16%), higher renal blood flow (approximately 22%), and lower filtration fraction (approximately 35%), but similar BP, compared with vehicle-treated SFK sheep. Together with greater recruitment of RFR (approximately 14%) in SFK+ACEi than SFK animals, this indicates a reduction in glomerular hyperfiltration–mediated kidney dysfunction. During NOS inhibition, the decrease in GFR (approximately 14%) was greater among SFK+ACEi than among SFK animals. Increased (approximately 85%) basal urinary total NOx in SFK+ACEi compared with SFK animals indicates elevated NO bioavailability likely contributed to improvements in kidney function and prevention of albuminuria.

Brief and early ACEi in SFK is associated with reduced glomerular hyperfiltration–mediated kidney disease up to 8 months of age in a sheep model.

出生时患有孤立功能肾（SFK）的儿童容易患高血压和肾损伤。肾小球过度滤过和肥大导致肾损伤的病理生理学。血管紧张素转换酶抑制 (ACEi) 可以减轻过度滤过，并且可能有利于减少 SFK 患者肾损伤的进展。

SFK 在妊娠 100 天（足月 = 150 天）的雄性绵羊胎儿中诱导。4 至 8 周龄之间，SFK 羔羊接受依那普利（SFK+ACEi；每天 0.5mg/kg，每天一次，口服）或赋形剂（SFK）。8 个月时，我们检查了血压、基础肾功能、肾功能储备（RFR；GFR 对氨基酸和多巴胺联合输注的反应）、GFR 对一氧化氮合酶 (NOS) 抑制的反应以及基础一氧化氮 (NO) 生物利用度（基础尿总硝酸盐和亚硝酸盐 [NOx]）。

与媒介物处理的 SFK 羊相比，SFK+ACEi 可预防白蛋白尿，并导致基础 GFR 较低（16%）、肾血流量较高（约 22%）和滤过率较低（约 35%），但血压相似。与 SFK 动物相比，SFK+ACEi 中的 RFR 募集更多（约 14%），这表明肾小球高滤过介导的肾功能障碍有所减少。在 NOS 抑制期间，SFK+ACEi 动物的 GFR 下降幅度（约 14%）比 SFK 动物更大。与 SFK 动物相比，SFK+ACEi 的基础尿总 NOx 增加（约 85%），表明 NO 生物利用度升高可能有助于改善肾功能和预防白蛋白尿。

在绵羊模型中，SFK 中短暂且早期的 ACEi 与 8 个月龄以下肾小球高滤过介导的肾脏疾病的减少有关。