Wang Ruiqiang, Wu Yunqi, An Dongyue, Ma Pupu, Guo Yuanyuan, Tang Lin
Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Front Med (Lausanne). 2021 Jan 15;7:563020. doi: 10.3389/fmed.2020.563020. eCollection 2020.
Acromegaly is a chronic disease caused by excessive secretion of growth hormone (GH), which circulates and stimulates the liver and body tissues to produce insulin-like growth factor type 1 (IGF-1). Experimental studies have shown that excessive secretion of GH is related to glomerular sclerosis, and elevated IGF-1 levels may be involved in the occurrence of glomerular hypertrophy. But relevant clinical cases are rare. Here, we reported a case of acromegaly complicated with focal segmental glomerulosclerosis (FSGS). A 49-year-old man was admitted to our hospital because of acromegaly for more than 10 years and proteinuria for more than 3 years. Acromegaly was confirmed by contrast-enhanced magnetic resonance imaging, minimally invasive surgery and pathology. The results of renal biopsy showed FSGS-NOS (not otherwise specified) with ischemic renal injury and mesangial IgA deposition. One month after transnasal transsphenoidal space occupying resection, GH and urinary protein decreased significantly, and nephropathy was partially relieved. In the next 4 months, GH stabilized at the normal level, while urinary protein gradually increased. When the urinary protein increased to 4.2 g/d, the dosage of glucocorticoids increased to 20 mg/d, and tacrolimus 1 mg/d were added, and the urinary protein decreased again. However, when the urinary protein decreased to 0.43 g/d, the patient stopped taking glucocorticoids and tacrolimus, and the urinary protein increased to 2.85 g/d after 8 months, but the GH was still in the normal range. In this case, GH is partially involved in the formation of FSGS. Not only does surgery reduce the effects of GH, but low doses of glucocorticoids and immunosuppressant are effective in slowing the progression of kidney disease, at least in reducing urinary protein.
肢端肥大症是一种由生长激素（GH）分泌过多引起的慢性疾病，GH在体内循环并刺激肝脏和身体组织产生1型胰岛素样生长因子（IGF-1）。实验研究表明，GH分泌过多与肾小球硬化有关，而IGF-1水平升高可能参与肾小球肥大的发生。但相关临床病例罕见。在此，我们报告一例肢端肥大症合并局灶节段性肾小球硬化（FSGS）的病例。一名49岁男性因肢端肥大症10余年、蛋白尿3年余入院。经增强磁共振成像、微创手术及病理检查确诊为肢端肥大症。肾活检结果显示为未分类的FSGS（NOS），伴有缺血性肾损伤和系膜IgA沉积。经鼻蝶窦占位切除术后1个月，GH和尿蛋白显著下降，肾病部分缓解。在接下来的4个月里，GH稳定在正常水平，而尿蛋白逐渐增加。当尿蛋白增加至4.2 g/d时，糖皮质激素剂量增加至20 mg/d，并加用他克莫司1 mg/d，尿蛋白再次下降。然而，当尿蛋白降至0.43 g/d时，患者停用糖皮质激素和他克莫司，8个月后尿蛋白增至2.85 g/d，但GH仍在正常范围内。在该病例中，GH部分参与了FSGS的形成。手术不仅能降低GH的影响，低剂量的糖皮质激素和免疫抑制剂对减缓肾病进展有效，至少在降低尿蛋白方面有效。
