Changes in medullary glycosaminoglycan histochemistry and microvascular filling during the development of 2-bromoethanamine hydrobromide-induced renal papillary necrosis

Bach, Peter H.; Grasso, P.; Molland, E. A.; Bridges, James W.

doi:10.1016/0041-008x(83)90257-0

Cited by 33 publications

(23 citation statements)

References 27 publications

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“…Hyperplastic bladder cells also show changes in histochemical profiles which include an increased loss of Alk Phos and an increased staining for GGT (16,29). The absence of these 2 features from the hyperplastic urothelia reported in these investigations suggests that the proliferative changes that follow the BEA-induced lesion probably represents a repair of injured tissue (1,28), rather than a premalignant change per se. This difference could also be due to differences in methodology used to determine histochemical staining.…”

Section: Discussionmentioning

confidence: 84%

“…There is no extra-renal pathology (1,2). The loss of proximal tubular brush border marker enzymes at 12 hr shows that these changes occur relatively late in the development ofthe lesion, considering that the matrix changes occurred as early as 2-4 hr after BEA (1,13) and the interstitial cells showed frank degeneration at 8 hr (13).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, it is unlikely that proximal tubular changes play any role in the primary de-velopment ofRPN. More importantly, routine morphology (e.g., hematoxylin and eosin staining) ofthe proximal tubule, using 5~m wax embedded sections, only shows mild and transient hydropic changes (1). The data from the investigations we have described above do not make it possible to be certain if the loss of proximal tubular marker enzymes represents subtle BEA-associated cellular injury to this part of the nephron, damage to the glomeruli leading to a protein overloading of the proximal tubular cells, or ifthe brush border changes resulted from the diuresis that follows early papillary injury (11,24,27,30).…”

Section: Discussionmentioning

confidence: 99%

“…BEA is a highly target selective chemical probe that damages the renal papilla and causes a dose related necrosis within 24-48 hr (1,15). There is no extra-renal pathology (1,2).…”

Section: Discussionmentioning

confidence: 99%

“…2-Bromoethanamine (BEA)hydrobromide causes a reproducible model renal papillary necrosis (RPN) within [24][25][26][27][28] hr that has been characterized in terms offunctional changes and some morphology (1,13,15,24). This BEA-induced lesion has allowed the progression of RPN to be studied and shows the marked similarities between this acute model and the changes that have been reported in the clinical condition in human analgesic abusers and also in animals dosed chronically with analgesics and nonsteroidal anti-inflammatory drugs (2,3).…”

Section: Introductionmentioning

confidence: 99%

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Enzyme Histochemical Changes in an Acutely Induced Renal Papillary Necrosis

1990

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Enzyme histochemistry was assessed in semi-thin glycolmethacrylate sections after 100 mg/kg 2-bromoethanamine (BEA) hydrobromide had been given ip to male Wistar rats to induce renal papillary necrosis. Changes in the proximal tubular marker enzymes alkaline phosphatase (A1k Phos), gamma-glutamyltranspeptidase (GGT) and adenosine triphosphatase (ATPase) were not apparent before 8 hr, but there was a progressive loss up to 144 hr. The proteinaceous PAS-positive casts in the loops of Henle and the collecting ducts stained for A1k Phos and GGT (from 12 hr) and for ATPase (from 18 hr). Acid phosphatase (Acid Phos) staining was increased in the proximal tubule lysosomes from 18 hr. There was a marked increase in Alk Phos in all hyperplastic upper urothelial cells from 8 to 24 hr, and a mosaic of staining remained in the pelvis adjacent to the necrosed papilla at 144 hr. At 12 hr, there was an increase in the staining of the pelvic, ureter and bladder vascular endothelial ATPase, the intensity and area of which increased progressively from 18 hr and almost occluded the capillary lumens in the worst affected areas by 144 hr. These data show several distinct series of pathological changes after the administration of BEA. The subtle degenerative changes in the proximal tubule followed the papillary lesion, but exfoliated brush border and proximal tubular cells were important components of the protein casts in the distal nephron. Similarly, the intense Alk Phos staining in the hyperplastic regions of the upper urothelium and the increased pelvic, ureteric and bladder endothelial ATPase staining suggested they develop as a consequence of the papillary lesion.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…BEA is a highly target selective chemical probe that damages the renal papilla and causes a dose related necrosis within 24-48 hr (1,15). There is no extra-renal pathology (1,2).…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Enzyme Histochemical Changes in an Acutely Induced Renal Papillary Necrosis

1990

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Chemically induced analgesic nephropathy in the rat monitored by proton‐electron double‐resonance imaging (PEDRI)

Seimenis

Foster

Lurie

et al. 1998

Magnetic Resonance in Med

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Proton-electron double-resonance imaging (PEDRI) was used to assess renal function by monitoring the flow of the exogenous nitroxide free radical proxyl carboxylic acid (PCA) through normal and injured kidneys in the living rat. Kidney damage was induced by treatment with 2-bromoethylamine (BEA), which provides a well established model for human analgesic nephropathy. PCA clearance rates for liver, abdominal blood vessels, and renal tissues were determined from serial PEDRI images of normal rats (n = 6) and rats treated with BEA (n = 21). Different groups of BEA-treated animals were imaged on day 4 (n = 6), day 6 (n = 6), and day 9 (n = 9) after treatment. In BEA-treated rats, there was an increase in PCA half-life in all tissues studied. This increase was greatest in the kidney tissues and the effect progressed with time after treatment. The effect is probably due to BEA-induced damage to the tubules in the renal cortex and may not be related to the primary lesions in the renal medulla.

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