Angiotensin-converting enzyme inhibition prevents glomerular-tubule disconnection and atrophy in passive heymann nephritis, an effect not observed with a calcium antagonist

American Journal of Pathology

Volumn 159, Issue 5, 2001, Pages 1743-1750

  Benigni, Ariela ^a   Gagliardini, Elena ^a   Remuzzi, Andrea ^a   Corna, Daniela ^a   Remuzzi, Giuseppe ^a,b  

^a MARIO NEGRI INSTITUTE FOR PHARMACOLOGICAL RESEARCH   (Italy)

^b OSPEDALI RIUNITI   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM ANTAGONIST; DIPEPTIDYL CARBOXYPEPTIDASE INHIBITOR; LACIDIPINE; LISINOPRIL;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; DRUG EFFICACY; DRUG MECHANISM; ENZYME INHIBITION; HEYMANN NEPHRITIS; HYPERTENSION; KIDNEY INTERSTITIUM; MALE; NEPHRON; NICK END LABELING; NONHUMAN; PRIORITY JOURNAL; PROTEINURIA; RAT;

EID: 0035156004     PISSN: 00029440     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0002-9440(10)63021-0     Document Type: Article

References (33)

1. Hyperfiltration in remnant nephrons: A potentially adverse response to renal ablation
2. Control of glomerular hypertension limits glomerular injury in rats with reduced renal mass
3. Dietary protein intake and the progressive nature of kidney disease: The role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease
4. Contribution of tubular injury to loss of remnant kidney function
5. In progressive nephropathies, overload of tubular cells with filtered proteins translates glomerular permeability dysfunction into cellular signals of interstitial inflammation
6. Understanding the nature of renal disease progression
7. Albumin overload induces apoptosis in LLC-PK1 cells
8. Proteinuria induces tubular cell turnover: A potential mechanism for tubular atrophy
9. Pathophysiology of progressive nephropathies
10. Renoprotective effect of contemporary blocking of angiotensin II and endothelin-1 in rats with membranous nephropathy
11. Angiotensin-converting enzyme inhibition and calcium channel blockade both normalize early hyperfiltration in experimental diabetes, but only the former prevents late renal structural damage
12. Validity of an indirect tail-cuff method for determining systolic arterial pressure in unanesthetized normotensive and spontaneously hypertensive rats
13. Minimization of variation in the response to different proteins of the Coomassie blue G dye-binding assay for protein
14. The colorimetric determination of creatinine of the Jaffé reaction
15. Stenosis of tubular neck: A possible mechanism for progressive renal failure
16. Expression of apoptosis-related genes and proteins in experimental chronic renal scarring
17. Stenotic glomerulotubular necks in radiation nephropathy
18. Atubular glomeruli in lithium-induced chronic nephropathy in rats
19. Atubular glomeruli in cisplatin induced chronic interstitial nephropathy: An experimental stereologic investigation
20. Atubular glomeruli in patients with chronic allograft rejection
21. The remnant kidney model
22. Method of renal mass reduction is a critical modulator of subsequent hypertension and glomerular injury
23. Experimental insights into the tubulointerstitial disease accompanying primary glomerular lesions
24. Protein overload stimulates RANTES production by proximal tubular cells depending on NF-kB activation
25. Correlations between renal cortical interstitial fibrosis, atrophy of proximal tubules and impairment of glomerular filtration rate
26. The obliteration of the postglomerular capillaries and its influence upon the function of both glomeruli and tubuli
27. Atubular glomeruli in patients with chronic pyelonephritis
28. Angiotensin converting enzyme inhibition ameliorates glomerular filtration of macromolecules and water and lessens glomerular injury in the rat
29. Contribution of angiotensin II to late renal injury after acute ischemia
30. Nifedipine versus fosinopril in uninephrectomized diabetic rat
31. Renal hemodynamic effects of calcium antagonists in rats with reduced renal mass
32. “Intact nephrons” as the primary origin of proteinuria in chronic renal disease. Study in the rat model of subtotal nephrectomy