Pediatric transplantation · 2026
Incidental Finding of Secondary Focal Segmental Glomerulosclerosis in Renal Allograft due to Renal Artery Stenosis.
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Huang Zhixin, Guo Fangzhou, Wu Tong, Jiang Zeying, Huang Shuqi, Teng Yunfei, Wang Qihua, Wang Jue, Xu Zhenyu, Yang Shicong, Wang Yan, Liu Longshan, Chen Wenfang
Аннотация
BACKGROUND: Focal segmental glomerulosclerosis (FSGS), which can be caused by many etiologies, is one of the major causes of nephrotic syndrome and end-stage kidney disease. Multiple etiologies, including glomerular hyperperfusion, can cause secondary FSGS. Unilateral renal artery stenosis can lead to FSGS of the contralateral native kidney, but it is not well demonstrated whether transplant renal artery stenosis can cause a similar change in a single transplanted kidney.
CASE PRESENTATION: A female underwent kidney transplantation at the age of 17 on January 14, 2020. Her renal function remained stable until 25 months later, when the patient presented with hypertension and elevated serum creatinine (SCr), with an unremarkable urine test. Ultrasound and computed tomography angiography (CTA) revealed stenosis at the initial segment of the main transplant renal artery. After percutaneous transluminal angioplasty of the main transplant renal artery, her SCr and blood pressure recovered. 5 months later, hypertension recurred with moderate proteinuria (2.5 g/d). An allograft biopsy showed a remarkable cellular FSGS lesion. Due to the absence of glomeruli in the electronic microscope sample, a second biopsy was performed a month later. Unexpectedly, no FSGS, except for very mild glomerular hypoperfusion and remarkably enlarged juxtaglomerular apparatus, was found. Hemodynamic abnormality in the kidney was suspected as the two biopsy sites were from the lower pole and upper pole, respectively. The donor kidney had an accessory renal artery on a common aortic patch with the main renal artery. Doppler ultrasonography confirmed two different hemodynamic areas in the kidney. Transplant renal artery stenosis of the main artery induced an FSGS lesion in the region dominated by the accessory artery. Endovascular stenting was performed, and her proteinuria turned negative, with SCr recovering only 3 days later. The patient had long-term follow-up after discharge and had a favorable condition.
CONCLUSIONS: Transplant renal artery stenosis can cause regional hyperperfusion leading to adaptive FSGS, presenting with proteinuria and morphologically manifesting as a cellular variant of FSGS instead of the classic variant, which is usually closely related to hyperperfusion. The lesion must be differentiated from primary and other secondary FSGS. Removal of the hemodynamic abnormality can quickly relieve hypertension and proteinuria.
CASE PRESENTATION: A female underwent kidney transplantation at the age of 17 on January 14, 2020. Her renal function remained stable until 25 months later, when the patient presented with hypertension and elevated serum creatinine (SCr), with an unremarkable urine test. Ultrasound and computed tomography angiography (CTA) revealed stenosis at the initial segment of the main transplant renal artery. After percutaneous transluminal angioplasty of the main transplant renal artery, her SCr and blood pressure recovered. 5 months later, hypertension recurred with moderate proteinuria (2.5 g/d). An allograft biopsy showed a remarkable cellular FSGS lesion. Due to the absence of glomeruli in the electronic microscope sample, a second biopsy was performed a month later. Unexpectedly, no FSGS, except for very mild glomerular hypoperfusion and remarkably enlarged juxtaglomerular apparatus, was found. Hemodynamic abnormality in the kidney was suspected as the two biopsy sites were from the lower pole and upper pole, respectively. The donor kidney had an accessory renal artery on a common aortic patch with the main renal artery. Doppler ultrasonography confirmed two different hemodynamic areas in the kidney. Transplant renal artery stenosis of the main artery induced an FSGS lesion in the region dominated by the accessory artery. Endovascular stenting was performed, and her proteinuria turned negative, with SCr recovering only 3 days later. The patient had long-term follow-up after discharge and had a favorable condition.
CONCLUSIONS: Transplant renal artery stenosis can cause regional hyperperfusion leading to adaptive FSGS, presenting with proteinuria and morphologically manifesting as a cellular variant of FSGS instead of the classic variant, which is usually closely related to hyperperfusion. The lesion must be differentiated from primary and other secondary FSGS. Removal of the hemodynamic abnormality can quickly relieve hypertension and proteinuria.