Urinary excretion of viable podocytes in health and renal disease

被引:272
作者
Vogelmann, SU
Nelson, WJ
Myers, BD
Lemley, KV
机构
[1] Stanford Univ, Dept Med, Sch Med, Div Nephrol, Stanford, CA 94305 USA
[2] Stanford Univ, Dept Pediat, Sch Med, Stanford, CA 94305 USA
[3] Stanford Univ, Dept Cellular & Mol Physiol, Sch Med, Stanford, CA 94305 USA
关键词
glomerulus; cell culture; podocalyxin; cytospin;
D O I
10.1152/ajprenal.00404.2002
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The loss of glomerular visceral epithelial cells (podocytes) has been associated with the development of glomerular sclerosis and loss of renal function. Viability of podocytes recovered from urine of subjects with glomerular disease and of healthy controls was investigated by propidium iodide exclusion and TUNEL staining. Podocyte loss was quantified by cytospin. The growth behavior in culture of urinary cells and their expression of specific markers were examined. The majority of urinary podocytes are viable, although apoptosis occurs in about one-half of the cells. Patients with active glomerular disease excreted up to 388 podocytes/mg creatinine, whereas healthy controls and patients with quiescent disease generally excreted <0.5 podocytes/mg creatinine. The identity of cultured cells was confirmed by their morphology, growth behavior, and expression of podocyte- specific markers. The difference in growth behavior between healthy controls and subjects with active glomerular disease suggests that in active disease viable podocytes detach from the glomerular tuft due to local environmental factors rather than defects in the podocytes per se, whereas in healthy individuals mostly senescent podocytes are shed.
引用
收藏
页码:F40 / F48
页数:9
相关论文
共 24 条
[1]   INVITRO CULTURE OF CELLS EXFOLIATED IN THE URINE BY PATIENTS WITH DIABETES-MELLITUS [J].
DETRISAC, CJ ;
MAYFIELD, RK ;
COLWELL, JA ;
GARVIN, AJ ;
SENS, DA .
JOURNAL OF CLINICAL INVESTIGATION, 1983, 71 (01) :170-173
[2]   STRUCTURAL DETERMINANTS OF GLOMERULAR HYDRAULIC PERMEABILITY [J].
DRUMOND, MC ;
DEEN, WM .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (01) :F1-+
[3]   Update in podocyte biology [J].
Endlich, K ;
Kriz, W ;
Witzgall, R .
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, 2001, 10 (03) :331-340
[4]  
FRIES JWU, 1989, LAB INVEST, V60, P205
[5]   Immunohistochemical and urinary markers of podocyte injury [J].
Hara, M ;
Yanagihara, T ;
Itoh, M ;
Matsuno, M ;
Kihara, I .
PEDIATRIC NEPHROLOGY, 1998, 12 (01) :43-48
[6]   URINARY-EXCRETION OF PODOCALYXIN INDICATES GLOMERULAR EPITHELIAL-CELL INJURIES IN GLOMERULONEPHRITIS [J].
HARA, M ;
YAMAMOTO, T ;
YANAGIHARA, T ;
TAKADA, T ;
ITOH, M ;
ADACHI, Y ;
YOSHIZUMI, A ;
KAWASAKI, K ;
KIHARA, I .
NEPHRON, 1995, 69 (04) :397-403
[7]  
KEMENY E, 1995, CLIN NEPHROL, V43, P71
[8]   Caught flat-footed: podocyte damage and the molecular bases of focal glomerulosclerosis [J].
Kerjaschki, D .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 108 (11) :1583-1587
[9]   Podocyte depletion and glomerulosclerosis have a direct relationship in the PAN-treated rat [J].
Kim, YH ;
Goyal, M ;
Kurnit, D ;
Wharram, B ;
Wiggins, J ;
Holzman, L ;
Kershaw, D ;
Wiggins, R .
KIDNEY INTERNATIONAL, 2001, 60 (03) :957-968
[10]   Progression of glomerular diseases: Is the podocyte the culprit? [J].
Kriz, W ;
Gretz, N ;
Lemley, KV .
KIDNEY INTERNATIONAL, 1998, 54 (03) :687-697