Vaidyanathan Subramanian, Abraham Kottarathil Abraham, Singh Gurpreet, Soni Bakul, Hughes Peter
Regional Spinal Injuries Centre, Southport and Formby District General Hospital, Town Lane, Southport PR8 6PN, UK.
Department of Renal Medicine, Southport and Formby District General Hospital, Town Lane, Southport PR8 6PN, UK.
Patient Saf Surg. 2014 Jun 9;8:25. doi: 10.1186/1754-9493-8-25. eCollection 2014.
Spinal cord injury patients may develop proteinuria as a result of glomerulosclerosis due to urosepsis, hydronephrosis, vesicoureteric reflux, and renal calculi. Proteinuria in turn contributes to progression of kidney disease. We report one paraplegic and two tetraplegic patients, who developed recurrent urine infections, urinary calculi, and hydronephrosis. These patients required several urological procedures (nephrostomy, cystoscopy and ureteric stenting, ureteroscopy and lithotripsy, extracorporeal shock wave lithotripsy). These patients had not received antimuscarinic drugs nor had they undergone video-urodynamics. Proteinuria was detected only at a late stage, as testing for proteinuria was not performed during follow-up visits. Urine electrophoresis showed no monoclonal bands in any; Serum glomerular basement membrane antibody screen was negative. Serum neutrophil cytoplasmic antibodies screen by fluorescence was negative. All patients were prescribed Ramipril 2.5 mg daily and there was no further deterioration of renal function. Spinal cord injury patients, who did not receive antimuscarinic drugs to reduce intravesical pressure, are at high risk for developing reflux nephropathy. When such patients develop glomerulosclerosis due to recurrent urosepsis, renal calculi, or hydronephrosis, risk of proteinuria is increased further.
(1) Screening for proteinuria should be performed regularly in the 'at-risk' patients. (2) In the absence of other renal diseases causing proteinuria, spinal cord injury patients with significant proteinuria may be prescribed angiotensin-converting enzyme inhibitor or angiotensin-II receptor antagonist to slow progression of chronic renal disease and reduce the risk of cardiovascular mortality.
脊髓损伤患者可能因泌尿道感染、肾积水、膀胱输尿管反流和肾结石导致肾小球硬化而出现蛋白尿。蛋白尿反过来又会促使肾脏疾病进展。我们报告了1例截瘫患者和2例四肢瘫患者,他们出现了反复的尿液感染、尿路结石和肾积水。这些患者需要进行多次泌尿外科手术(肾造瘘术、膀胱镜检查和输尿管支架置入术、输尿管镜检查和碎石术、体外冲击波碎石术)。这些患者未接受抗胆碱能药物治疗,也未进行影像尿动力学检查。蛋白尿仅在晚期才被检测到,因为随访期间未进行蛋白尿检测。尿液电泳在任何患者中均未显示单克隆条带;血清肾小球基底膜抗体筛查为阴性。血清中性粒细胞胞浆抗体荧光筛查为阴性。所有患者均每日服用2.5毫克雷米普利,肾功能未进一步恶化。未接受抗胆碱能药物以降低膀胱内压的脊髓损伤患者发生反流性肾病的风险很高。当此类患者因反复泌尿道感染、肾结石或肾积水而发生肾小球硬化时,蛋白尿风险会进一步增加。
(1)应定期对“高危”患者进行蛋白尿筛查。(2)在没有其他导致蛋白尿的肾脏疾病的情况下,有明显蛋白尿的脊髓损伤患者可使用血管紧张素转换酶抑制剂或血管紧张素II受体拮抗剂,以减缓慢性肾病进展并降低心血管死亡风险。