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Clinical features and long-term outcome of obesity-associated focal segmental glomerulosclerosis.

机译:肥胖相关性局灶节段性肾小球硬化症的临床特征和长期预后。

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BACKGROUND: Several cases of obesity-associated focal segmental glomerulosclerosis (OB-FSG) have been reported but little is known about the clinico-pathological features of this entity and its long-term outcomes. METHODS: We studied 15 obese patients (BMI 35+/-5.2 kg/m(2)) with biopsy-proven FSG. They were compared with a control group of 15 non-obese patients with idiopathic FSG (I-FSG). RESULTS: Mean proteinuria at the time of renal biopsy was 3.1+/-2 g/24 h in OB-FSG; it reached the nephrotic range (> or =3.5 g/24 h) during follow-up in 12 patients (80%), but none of them had oedema, hypoproteinaemia, or hypoalbuminaemia. Proteinuria was more marked amongst I-FSG (6.5+/-4.2 g/24 h) and most of them developed oedema and biochemical nephrotic syndrome. Glomerulomegaly was observed in all renal biopsies from OB-FSG patients (mean glomerular diameter 256+/-24 microm in OB-FSG vs 199+/-26 microm in I-FSG, P<0.001). Twelve OB-FSG patients (80%) were treated with ACE inhibitors (ACEI) and proteinuria significantly decreased within the first 6 months of treatment but showed a later increase. None of the obese patients achieved a sustained weight loss. Seven (46%) patients with OB-FSG experienced a progressive renal insufficiency and five of them started intermittent dialysis. Kaplan-Meier estimated probabilities of renal survival after 5 and 10 years were 77 and 51%, respectively, in OB-FSG patients, and 52 and 30% in I-FSG (P<0.05). The risk of developing progressive renal failure among OB-FSG patients was statistically correlated with serum creatinine and creatinine clearance at presentation. CONCLUSIONS: OB-FSG indicates a poor prognosis with almost one-half of patients developing advanced renal failure. Knowledge of the clinico-pathological features of this entity (obesity, FSG lesions with glomerulomegaly, absence of nephrotic syndrome despite nephrotic-range proteinuria) should be helpful in establishing an accurate and early diagnosis.
机译:背景:已经报道了肥胖相关的局灶节段性肾小球硬化症(OB-FSG)的几例,但对该实体的临床病理特征及其长期预后知之甚少。方法:我们研究了15名经活检证实的FSG的肥胖患者(BMI 35 +/- 5.2 kg / m(2))。将他们与15名非肥胖性特发性FSG(I-FSG)患者的对照组进行比较。结果:OB-FSG肾活检时的平均蛋白尿为3.1 +/- 2 g / 24 h。在随访期间,有12位患者(80%)达到肾病范围(>或= 3.5 g / 24 h),但没有人出现水肿,低蛋白血症或低白蛋白血症。在I-FSG(6.5 +/- 4.2 g / 24 h)中,蛋白尿更为明显,并且大多数人发展为水肿和生化性肾病综合征。在OB-FSG患者的所有肾脏活检中均观察到肾小球肥大(OB-FSG中的平均肾小球直径为256 +/- 24微米,I-FSG中的平均肾小球直径为199 +/- 26微米,P <0.001)。 12例OB-FSG患者(80%)用ACE抑制剂(ACEI)治疗,在治疗的前6个月内蛋白尿明显减少,但后来有所增加。没有肥胖患者实现持续的体重减轻。七名(46%)OB-FSG患者经历了进行性肾功能不全,其中五名开始间歇性透析。 Kaplan-Meier估计的OB-FSG患者5年和10年肾存活率分别为77%和51%,I-FSG患者为52%和30%(P <0.05)。 OB-FSG患者发生进展性肾衰竭的风险与就诊时的血清肌酐和肌酐清除率有统计学相关性。结论:OB-FSG预后差,几乎一半的患者发展为晚期肾衰竭。了解该实体的临床病理特征(肥胖,FSG伴肾小球肿大病变,尽管存在肾病范围蛋白尿而无肾病综合征)应有助于建立准确的早期诊断。

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