Nutcracker phenomenon (NCP) is caused by a compression of left renal vein between aorta and superior mesenteric artery. The traditional clinical manifestations of nutcracker syndrome is usually accompanied with abdomi...Nutcracker phenomenon (NCP) is caused by a compression of left renal vein between aorta and superior mesenteric artery. The traditional clinical manifestations of nutcracker syndrome is usually accompanied with abdominal pain, hematuria, orthostatic proteinuria, and varicocele formation, however, hypertension is rarely reported as main clinical feature. We describe a male adolescent with manifestation of hypertension who was identified as NCP. Renal ultrasound and computed tomography angiography have provided evidences of left renal vein dilatation, probably due to the compression through the decreased angle between aorta and superior mesenteric artery. There were no other signs for secondary hypertension for the blood levels of renin and aldosterone being between normal limits and urinalysis being negative of hematuria and proteinuria. This patient was conservatively observed without any anti-hypertensive drugs and was asked for appropriately putting on weight. Three months later, the hypertension symptom was alleviated. In conclusion, although there were no established direct pathogenetic links between hypertension and NCP, no other definite etiology was shown to be the cause of this main manifestation. Thus we speculate that the NCP might be the main cause of hypertension in this patient.展开更多
文摘Nutcracker phenomenon (NCP) is caused by a compression of left renal vein between aorta and superior mesenteric artery. The traditional clinical manifestations of nutcracker syndrome is usually accompanied with abdominal pain, hematuria, orthostatic proteinuria, and varicocele formation, however, hypertension is rarely reported as main clinical feature. We describe a male adolescent with manifestation of hypertension who was identified as NCP. Renal ultrasound and computed tomography angiography have provided evidences of left renal vein dilatation, probably due to the compression through the decreased angle between aorta and superior mesenteric artery. There were no other signs for secondary hypertension for the blood levels of renin and aldosterone being between normal limits and urinalysis being negative of hematuria and proteinuria. This patient was conservatively observed without any anti-hypertensive drugs and was asked for appropriately putting on weight. Three months later, the hypertension symptom was alleviated. In conclusion, although there were no established direct pathogenetic links between hypertension and NCP, no other definite etiology was shown to be the cause of this main manifestation. Thus we speculate that the NCP might be the main cause of hypertension in this patient.
