INCREASING INCIDENCE OF FOCAL-SEGMENTAL GLOMERULOSCLEROSIS AMONG ADULT NEPHROPATHIES - A 20-YEAR RENAL BIOPSY STUDY

INCREASING INCIDENCE OF FOCAL-SEGMENTAL GLOMERULOSCLEROSIS AMONG ADULT NEPHROPATHIES - A 20-YEAR RENAL BIOPSY STUDY
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DOI:
10.1016/0272-6386(95)90437-9
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发表时间:
1995-11-01
影响因子:
13.2
通讯作者:
COVENTRY, S
COVENTRY, S
中科院分区:
医学1区
文献类型:
--
作者:
HAAS, M;SPARGO, BH;COVENTRY, S

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20世纪70年代和80年代早期的研究和教科书列出局灶节段性肾小球硬化(FSGS)占成人特发性肾病综合征病例的10%至15%,尽管最近D 'Agati的综述(Kidney Int 46:1223-1241,1994)报道了从1974年至1993年在主动肾活检实践中FSGS的发病率增加了约7倍。为了研究我们肾活检实践中FSGS发生率的可能变化,我们回顾了1974年至1993年我们实验室收到的所有非移植成人(大于或等于18岁)肾活检报告,其中包括7,420例病例。对每年膜性肾病(MN)、微小病变肾病(MCN)和FSGS的所有诊断进行汇编;排除明确或怀疑继发于基础系统性疾病、肾小球肾炎或药物反应的病例。计算研究期间每年MM、MCN和FSGS在这三种疾病和所有活检中的相对频率。回归分析显示,在研究期间,FSGS的诊断几率显著增加(P < 0.001):所有活检中每年增加7.6%,仅FAN、MCN和FSGS病例中每年增加6.8%。在所有活检中,FSGS的年发病率从1974年至1979年期间的4.0% +/- 0.6%(平均值+/- SD)增加到1987年至1993年期间的12.2% +/- 20%。在研究期间,MN诊断的几率(平均年发病率,9.5% +/- 1.9%)没有显著变化,而MCN诊断的几率(平均年发病率,4.0% +/- 1.2%)以每年2.2%的速度下降(P < 0.03)。两名病理学家对MN、MCN和FSGS的诊断频率几乎相同。对FSGS病例的可用切片进行审查,发现21例(1980年以前无)具有FSGS塌陷性肾小球病(CG)变体的特征性组织学特征。在研究的任何一年中,观察到的CG病例不超过4例,结束CG占可获得诊断载玻片的FSGS病例总数的4.7%。与42名非CG FSGS患者相比,CG队列显示黑人患者的比例更高(86%对38%),血清肌酐平均水平显著升高(3.8 +/- 2.7 mg/dL v 1.9 +/- 1.5 mg/dL)和尿蛋白(14.3 +/- 9.6 g/24 hr vs 7.7 +/- 5.8 g/24 hr),并且更可能和更快地进展为终末期肾衰竭。我们的研究结果证实,在1974年至1993年的20年间,FSGS的发病率增加,无论是总体还是原发性肾病导致肾病综合征。与其他人一致,我们发现CG似乎代表了FSGS的一种特别“恶性”的变体,尽管在我们的经验中这种变体相对不常见。(C)1995年由国家肾脏基金会,公司。
Studies and textbooks from the 1970s and early 1980s list focal-segmental glomerulosclerosis (FSGS) as accounting for 10% to 15% of cases of idiopathic nephrotic syndrome in adults, although a recent review by D'Agati (Kidney Int 46:1223-1241, 1994) reported an approximately sevenfold increase in the incidence of FSGS from 1974 to 1993 in an active renal biopsy practice. To investigate possible changes in the incidence of FSGS in our renal biopsy practice, we reviewed reports from all nontransplant, adult (greater than or equal to 18 years) renal biopsies received in our laboratory from 1974 to 1993, which comprised 7,420 cases. All diagnoses of membranous nephropathy (MN), minimal change nephropathy (MCN), and FSGS made in each year were compiled; cases clearly or suspicious of being secondary to an underlying systemic disease, glomerulonephritis, or drug reaction were excluded. Relative frequencies of MM, MCN, and FSGS among these three diseases and among all biopsies were calculated for each year of the study. Regression analysis showed a significant (P < 0.001) increase in the odds of a diagnosis of FSGS over the study period: 7.6% per year among all biopsies and 6.8% per year among cases of FAN, MCN, and FSGS only. Among all biopsies, the yearly incidence of FSGS increased from 4.0% +/- 0.6% (mean +/- SD) during the period between 1974 and 1979 to 12.2% +/- 20% during the period from 1987 to 1993. The odds of a diagnosis of MN (mean yearly incidence, 9.5% +/- 1.9%) did not vary significantly over the study period while the odds of a diagnosis of MCN (mean yearly incidence, 4.0% +/- 1.2%) declined at a rate of 2.2% per year (P < 0.03). Frequencies of diagnosis of MN, MCN, and FSGS by two pathologists were almost identical. Review of available slides from cases of FSGS revealed 21 (none before 1980) with characteristic histologic features of the collapsing glomerulopathy (CG) variant of FSGS. No more than four cases of CG were observed in any year of the study, end CG accounted for 4.7% of total FSGS cases for which diagnostic slides were available. Compared with 42 patients with non-CG FSGS, the CG cohort showed a greater percentage of black patients (86% v 38%), significantly higher mean levels of serum creatinine (3.8 +/- 2.7 mg/dL v 1.9 +/- 1.5 mg/dL) and urinary protein (14.3 +/- 9.6 g/24 hr v 7.7 +/- 5.8 g/24 hr) at the time of renal biopsy, and a greater likelihood of and more rapid progression to end-stage renal failure. Our findings confirm an increase in the incidence of FSGS over the 20 years between 1974 and 1993, both overall and among primary nephropathies leading to the nephrotic syndrome. In agreement with others, we find that CG appears to represent a particularly ''malignant'' variant of FSGS, although in our experience this variant is observed relatively infrequently. (C) 1995 by the National Kidney Foundation, Inc.