Pathology of progressive nephropathies

Current Opinion in Nephrology and Hypertension

Volumn 9, Issue 3, 2000, Pages 241-246

  Fogo, Agnes B ^a  

^a VANDERBILT UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALDOSTERONE; ANGIOTENSIN; BROMELAIN; CONNECTIVE TISSUE GROWTH FACTOR; DIPEPTIDYL CARBOXYPEPTIDASE INHIBITOR; MEVINOLIN; MYCOPHENOLIC ACID 2 MORPHOLINOETHYL ESTER; RETINOIC ACID; RUTOSIDE; TACROLIMUS; TRANSFORMING GROWTH FACTOR BETA; TRYPSIN; VASCULOTROPIN;

EXTRACELLULAR MATRIX; GENETIC ASSOCIATION; GLOMERULUS EPITHELIUM; HISTOPATHOLOGY; HUMAN; KIDNEY BIOPSY; KIDNEY DISEASE; MESANGIUM CELL; PRIORITY JOURNAL; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; REVIEW; TREATMENT OUTCOME;

CELL CYCLE; CELL DIVISION; HUMANS; KIDNEY DISEASES; RENIN-ANGIOTENSIN SYSTEM;

EID: 0034071847     PISSN: 10624821     EISSN: None     Source Type: Journal    
DOI: 10.1097/00041552-200005000-00006     Document Type: Review

References (59)

1. 1 Iyer VR, Eisen MB, Ross DT, Schuler G, Moore T, Lee JCF, et al. The transcriptional program in the response of human fibroblasts to serum. Science 1999; 283:83-87. Sophisticated microchip gene array analysis demonstrates a linkage of responses of growth, angiogenesis and wound healing.
2. 2 Savill J. Regulation of glomerular cell number by apoptosis. Kidney Int 1999; 56:1216-1222. Excellent review of pathophysiological significance of apoptosis.
3. Kip1. Kidney Int 1999;56:1262-1265. Excellent review of cell cycle regulatory proteins in growth responses.
4. 4 Schöcklmann HO, Lang S, Sterzel RB. Regulation of mesangial cell proliferation. Kidney Int 1999; 56:1199-1207. Excellent review of complex growth responses influencing mesangial cell response to injury, and effects on ultimate phenotype.
5. 5 Shankland SJ. Cell cycle regulatory proteins in glomerular disease. Kidney Int 1999;56:1208-1215. Excellent review of role of in-vivo manipulations of cell cycle regulatory proteins and consequences for glomerular injury.
6. 6 Lee GS, Nast CC, Peng SC, Artishevsky A, Ihm CG, Guillermo R, et al. Differential response of glomerular epithelial and mesangial cells after subtotal nephrectomy. Kidney Int 1998; 53:1389-1398.
7. WAF1/CIP1 resulted in a shift from hypertrophic, more profibrotic responses to a less injurious hyperplastic response.
8. kip1 in the immature GVEC.
9. 9 Kriz W, Hosser H, Hähnel B, Gretz N, Provoost AP. From segmental glomerulosclerosis to total nephron degeneration and interstitial fibrosis: a histopathological study in rat models and human glomerulopathies. Nephrol Dial Transplant 1998; 13:2781-2798.
10. 10 Sharif K, Goyal M, Kershaw D, Kunkel R, Wiggins R. Podocyte phenotypes as defined by expression and distribution of GLEPP1 in the developing glomerulus and in nephrotic glomeruli from MCD, CNF, and FSGS. A dedifferentiation hypothesis for the nephrotic syndrome. Exp Nephrol 1998; 6:234-244. Loss of a GVEC-specific differentiation marker is found in FSGS, even in nonsclerotic glomeruli, supporting dedifferentiation injury in the pathogenesis of FSGS.
11. 11 Bariéty J, Nochy D, Mandet C, Jacquot C, Glotz D, Meyrier A. Podocytes undergo phenotypic changes and express macrophagic-associated markers in idiopathic collapsing glomerulopathy. Kidney Int 1998; 53:918-925. Loss of several GVEC differentiation markers is observed in collapsing glomerulopathy.
12. 12 Barisoni L, Kriz W, Mundel P, d'Agati V. The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy. J Am Soc Nephrol 1999; 10:51-61. Loss of several GVEC differentiation markers is demonstrated in both HIV-associated and collapsing glomerulopathy, and is linked with segmental GVEC proliferation, supporting dysregulated differentiation and growth of the GVEC in the pathogenesis of these diseases.
13. 13 Denamur E, Bocquet N, Mougenot B, Da Silva F, Martinat L, Loirat C, et al. Mother-to-child transmitted WT1 splice-site mutation is responsible for distinct glomerular diseases. J Am Soc Nephrol 1999; 10:2219-2223. WT1 mutation is associated with FSGS, suggesting loss of normal WT1 may not just be a marker of dedifferentiation, but could also play a causal role in development of FSGS.
14. CIP1/WAF1 may be protective or injurious, depending on the type of injury.
15. 15 Meyer TW, Bennett PH, Nelson RG. Podocyte number predicts long-term urinary albumin excretion in Pima Indians with Type II diabetes and microalbuminuria. Diabetologia 1999; 42:1341-1344.
16. 16 Lenkkeri U, Männikkö M, McCready P, Lamerdin J, Gribouval O, Niaudet P, et al. Structure of the gene for congenital nephrotic syndrome of the Finnish type (NPHS1) and characterization of mutations. Am J Hum Genet 1999; 64:51-61. Identification of the gene responsible for congenital nephrotic syndrome sets the stage for advances in understanding of GVEC function and development of sclerosis.
17. 17 Ruotsalainen V, Ljungberg P, Wartiovaara J, Lenkkeri U, Kestilä M, Jalanko H, et al. Nephrin is specifically located at the slit diaphragm of glomerular podocytes. Proc Natl Acad Sci USA 1999; 96:7962-7967. The specific localization of nephrin provides added insight into its possible function.
18. 18 Holzman LB, St John PL, Kovari IA, Verma R, Holthofer H, Abrahamson DR. Nephrin localizes to the slit pore of the glomerular epithelial cell. Kidney Int 1999; 56:1481-1491. Further evidence on the specific localization of nephrin provides added insight into its possible function.
19. 19 Tryggvason K. Unraveling the mechanisms of glomerular ultrafiltration: nephrin, a key component of the slit diaphragm. J Am Soc Nephrol 1999; 10:2440-2445. Excellent review on nephrin and its potential roles in normal and pathological GVEC function.
20. 20 Ostendorf T, Kunter U, Eitner F, Loos A, Regele H, Kerjaschki D, et al. VEGF (165) mediates glomerular endothelial repair. J Clin Invest 1999; 104:913-923. Modulation of endothelial growth is shown to be crucial for remodeling after injury.
21. 21 Kitamura H, Shimizu A, Masuda Y, Ishizaki M, Sugisaki Y, Yamanaka N. Apoptosis in glomerular endothelial cells during the development of glomerulosclerosis in the remnant-kidney model. Exp Nephrol 1998; 6:328-336.
22. 22 Thomas SE, Anderson S, Gordon KL, Oyama TT, Shankland SJ, Johnson RJ. Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia. J Am Soc Nephrol 1998; 9:231-242.
23. 23 Ruiz-Torres MP, Bosch RJ, O'Valle F, Del Moral RG, Ram'rez C, Masseroli M, et al. Age-related increase in expression of TGF-β1 in the rat kidney: relationship to morphologic changes. J Am Soc Nephrol 1998; 9:782-791.
24. 24 Gilbert RE, Wu LL, Kelly DJ, Cox A, Wilkinson-Berka JL, Johnston CI, Cooper ME. Pathological expression of renin and angiotensin II in the renal tubule after subtotal nephrectomy. Implications for the pathogenesis of tubulointerstitial fibrosis. Am J Pathol 1999; 155:429-440.
25. 25 Fern RJ, Yesko CM, Thornhill BA, Kim HS, Smithies O, Chevalier RL. Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice. J Clin Invest 1999; 103:39-46. Elegant 'gene dosing' manipulations implicate angiotensin in the development of interstitial fibrosis, independent of blood pressure effects.
26. 26 Riser BL, Denichilo M, Cortes P, Baker C, Grondin JM, Yee J, Narins RG. Regulation of connective tissue growth factor activity in cultured rat mesangial cells and its expression in experimental diabetic glomerulosclerosis. J Am Soc Nephrol 2000; 11:25-38. A downstream effector of TGF-β actions is identified.
27. 27 Ito Y, Aten J, Bende RJ, Oemar BS, Rabelink TJ, Weening JJ, Goldschmeding R. Expression of connective tissue growth factor in human renal fibrosis. Kidney Int 1998; 53:853-861. Expression of this downstream effector of TGF-β is localized to areas of fibrosis in human tissues.
28. 28 Rocha R, Chander PN, Khanna K, Zuckerman A, Stier CTJ. Mineralocorticoid blockade reduces vascular injury in stroke-prone rats. Hypertension 1998; 31:451-458. Demonstration of protective effect of spironolactone on tissue injury provides evidence suggesting that aldosterone contributes to fibrosis.
29. 29 Brown NJ, Soo K-K, Chen Y-Q, Blevins LS, Nadeau JH, Meranze SG, Vaughan DE. Synergistic effect of adrenal steroids and angiotensin II on plasminogen activor inhibitor-1 production. J Clin Endocrinol Metab 2000; 85:336-344. A possible mechanism of aldosterone profibrotic effects is elucidated by demonstrating synergism of aldosterone on angiotensin induction of PAI-1.
30. 30 Fogo AB. The role of angiotensin II and plasminogen activator inhibitor-1 in progressive glomerulosclerosis. Am J Kidney Dis 2000; 35:179-188. In depth review of angiotensin mechanisms, including its link to the prothrombotic/ profibrotic actions of PAI-1.
31. 31 Brown NJ, Agirbasli M, Vaughan DE. Comparative effect of angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor antagonism on plasma fibrinolytic balance in humans. Hypertension 1999; 34:285-290. Linkage of aldosterone and PAI-1 levels is shown. The higher PAI-1 levels after ATRA versus ACEI are hypothesized to relate to higher aldosterone levels in the former, and possibly AT4 receptor-mediated induction of PAI-1 after the angiotensin type 1 receptor antagonist, a mechanism that is inhibited by ACEI.
32. 32 Ibrahim HN, Hostetter TH. The renin-aldosterone axis in two models of reduced renal mass in the rat. J Am Soc Nephrol 1998; 9:72-76. Increased aldosterone is linked to increased injury.
33. 33 Nataraj C, Oliverio MI. Mannon RB, Mannon PJ, Audoly LP, Amuchastegui CS, et al. Angiotensin II regulates cellular immune responses through a calcineurin-dependent pathway. J Clin Invest 1999; 104:1693-1701. A novel mechanism of angiotensin actions is demonstrated, implicating that angiotensin inhibition is also immunosuppressive by inhibiting lymphocyte activation.
34. 34 Esposito C, He C-J, Striker GE, Zalups RK, Striker LJ. Nature and severity of the glomerular response to nephron reduction is strain-dependent in mice. Am J Pathol 1999; 154:891-897. Marked variations in strain response to injury is demonstrated. Resistance to sclerosis is linked to threshold of glomerular growth response.
35. 35 Zidek V, Musilova A, Vorlieek J, Simakova M, Pravenec M. Quantitative trait loci for compensatory renal hypertrophy in the mouse. Biochem Biophys Res Commun 1998; 248:473-475.
36. 36 Lenz O, Zheng F, Vilar J, Doublier S, Lupia E, Schwedler S, et al. The inheritance of glomerulosclerosis in mice is controlled by multiple quantitative trait loci. Nephrol Dial Transplant 1998; 13:3074-3078. Multiple loci are implicated in governing response to injury.
37. 37 Van Dokkum RPE, Jacob HJ, Provoost AP. Genetic differences define severity of renal damage after L-NAME-induced hypertension in rats. J Am Soc Nephrol 1998; 9:363-371. Two loci are identified modulating response to hypertensive injury in the rat.
38. 38 Winn MP, Conlon PJ, Lynn KL, Howell DN, Gross DA, Rogala AR, et al. Clinical and genetic heterogeneity in familial focal segmental glomerulosclerosis. International Collaborative Group for the Study of Familial Focal Segmental Glomerulosclerosis. Kidney Int 1999; 55:1241-1246.
39. 39 Sorof JM, Hawkins EP, Brewer ED, Boydstun II, Kale AS, Powell DR. Age and ethnicity affect the risk and outcome of focal segmental glomerulosclerosis. Pediatr Nephrol 1998; 12:764-768.
40. 40 Bonilla-Felix M, Parra C, Dajani T, Ferris M, Swinford RD, Portman RJ, Verani R. Changing patterns in the histopathology of idiopathic nephrotic syndrome in children. Kidney Int 1999; 55:1885-1890.
41. 41 Lee DY, Kim W, Kang SK, Koh GY, Park SK. Angiotensin-converting enzyme gene polymorphism in patients with minimal-change nephrotic syndrome and focal segmental glomerulosclerosis. Nephron 1997; 77:471-473.
42. 42 Frishberg Y, Becker-Cohen R, Halle D, Feigin E, Eisenstein B, Halevy R, et al. Genetic polymorphisms of the renin-angiotensin system and the outcome of focal segmental glomerulosclerosis in children. Kidney Int 1998; 54:1843-1849. The ACE I/I genotype is associated with better prognosis than I/D or D/D genotypes.
43. 43 Fernandez-Llama P, Poch E, Oriola J, Botey A, Coll E, Darnell A, et al. Angiotensin converting enzyme gene I/D polymorphism in essential hypertension and nephroangiosclerosis. Kidney Int 1998; 53:1743-1747. The ACE D allele is overrepresented in those hypertensive patients who showed decreased GFR in comparison to those with normal GFR.
44. 44 Teranishi M, Ono H, Ishimitsu T, Matsuoka H. Insertion/deletion angiotensin converting enzyme gene polymorphism affects the microvascular structure of the kidney in patients with nondiabetic renal disease. J Hypertens 1999; 17:351-356. Linkage of worse morphological lesions with ACE D genotype.
45. 45 Kimura H, Gejyo F, Suzuki Y, Suzuki S, Miyazaki R, Arakawa M. Polymorphisms of angiotensin converting enzyme and plasminogen activator inhibitor-1 genes in diabetes and macroangiopathy. Kidney Int 1998; 54:1659-1669. Compound risk for more severe disease in patients with both ACE D/D and PAI-1 4G/4G genotypes, both associated with increased risk for cardiovascular disease.
46. 46 Li B, Khanna A, Sharma V, Singh T, Suthanthiran M, August P. TGF-beta1 DNA polymorphisms, protein levels, and blood pressure. Hypertension 1999; 33:271-275. Intriguing evidence of a link of TGF-β blood levels and blood pressure, hypothesized to relate to a gene polymorphism for TGF-β.
47. 47 Gulmann C, Rudberg S, Østerby R. Renal arterioles in patients with type I diabetes and microalbuminuria before and after treatment with antihypertensive drugs. Virchows Arch 1999; 434:523-528. A small, but highly significant study with repeat renal biopsies demonstrating subtle effects of intervention on renal structure, with mild progressive arteriolar lesions with beta blocker treatment and no significant change with ACEI.
48. 48 Cordonnier DJ, Pinel N, Barro C, Maynard C, Zaoui P, Halimi S, et al. Expansion of cortical interstitium is limited by converting enzyme inhibition in type 2 diabetic patients with glomerulosclerosis. J Am Soc Nephrol 1999; 10:1253-1263. Structural evidence of beneficial effect of intervention on progression of lesions in diabetic patients.
49. 49 Fioretto P, Steffes MW, Sutherland DE, Goetz FC, Mauer M. Reversal of lesions of diabetic nephropathy after pancreas transplantation. N Engl J Med 1998; 339:69-75. Groundbreaking study demonstrating the potential for regression of diabetic lesions in patients whose diabetes was cured by pancreas transplantation. Comparison of repeat biopsies in the same patients show regression of existing lesions over a 10-year follow-up period.
50. 50 Ots M, MacKenzie HS, Troy JL, Rennke HG, Brenner BM. Effects of combination therapy with enalapril and losartan on the rate of progression of renal injury in rats with 5/6 renal mass ablation. J Am Soc Nephrol 1998; 9:224-230. There was no additional benefit of combination therapy over single drug therapy with the same antihypertensive effect.
51. 51 Richer C, Bruneval P, Menard J, Guidicelli JF. Additive effects of enalapril and losartan in (mREN-2)27 transgenic rats. Hypertension 1998; 31:692-698. Additional benefit of combination therapy was associated with additional antihypertensive effect.
52. 52 Ma J, Nishimura H, Fogo A, Kon V, Inagami T, Ichikawa I. Accelerated fibrosis and collagen deposition develop in the renal interstitium of angiotensin type 2 receptor null mutant mice during ureteral obstruction. Kidney Int 1998; 53:937-944. Increased interstitial fibrosis in the AT2 knockout mouse after injury was linked to defective apoptosis.
53. 53 Hisada Y, Sugaya T, Yamanouchi M, Uchida H, Fukimura H, Sakurai H, et al. Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice. J Clin Invest 1999; 103:627-635. The angiotensin type 1a receptor was implicated in an immune injury model.
54. 54 Hamar P, Peti-Peterdi J, Rázga Z, Kovács G, Heemann U, Rosivall L. Coinhibition of immune and renin-angiotensin systems reduces the pace of glomerulosclerosis in the rat remnant kidney. J Am Soc Nephrol 1999; 10:5234-5238. Inhibition of angiotensin and immune mechanisms showed additional benefit over angiotensin inhibition alone.
55. 55 Fujihara CK, Malheiros DMAC, Zatz R, de Lourdes Noronha I. Myoophenolate mofetil attenuates renal injury in the rat remnant kidney. Kidney Int 1998; 54:1510-1519. Immunosuppression ameliorates injury in a model where immune mechanisms are not the primary mode of injury, demonstrating complex interactions of secondary mechanisms of progression.
56. 56 Romero F, Rodriguez-Iturbe B, Parra G, Gonzalez L, Herrera-Acosta J, Tapia E. Mycophenolate mofetil prevents the progressive renal failure induced by 5/6 renal ablation in rats. Kidney Int 1999; 55:945-955. Additional evidence of a beneficial effect of immunosuppression in the remnant kidney model.
57. 57 Remuzzi G, Zoja C, Gagliardini E, Corna D, Abbate M, Benigni A. Combining an antiproteinuric approach with mycophenolate mofetil fully suppresses progressive nephropathy of experimental animals. J Am Soc Nephrol 1999; 10:1542-1549. Inhibition of angiotensin and immune mechanisms showed additional benefit over angiotensin inhibition alone, attributed to antiproteinuric effects of angiotensin inhibition.
58. 58 Essig M, Vrtovsnik F, Nguyen G, Sraer J-D, Friedlander G. Lovastatin modulates in vivo and in vitro the plasminogen activator/plasmin system of rat proximal tubular cells: role of geranylgeranylation and rho protein. J Am Soc Nephrol 1998; 9:1377-1388.
59. 59 Sebekova K, Dämmrich J, Fierlbeck W, Krivosiková Z, Paczek L, Heidland A. Effect of chronic therapy with proteolytic enzymes on hypertension-induced renal injury in the rat model of Goldblatt hypertension. Am J Nephrol 1998; 18:570-576. Enhancing ECM degradation with this novel approach resulted in amelioration of progressive injury.