PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 8253544

Kidney dysfunction in the arthritic rat.

J F Dijoseph·T L Walter·D A Hartman·R P Carlson
View original source ↗Export metadata ↓

Abstract

Kidney function and histopathology were investigated in the adjuvant-induced arthritic rat. Rats injected with Mycobacterium butyricum exhibited symptoms of arthritis (i.e. paw edema and loss of body weight) by day 9 which worsened and included systemic manifestations of the disease on days 16 and 30. Definite signs of kidney dysfunction were observed by day 16 which included elevated urine output and plasma creatinine values and decreased creatinine clearance. By day 30, these parameters were similar to the values obtained from normal rats; however, kidney weights from arthritic rats than those from normal rats. Histopathologic abnormalities observed in the kidneys of arthritic rats on day 30 included tubular lesions consisting of focal basophilia, edema, granular deposits and basement membrane thickening. Changes in the glomerulus included granular deposits with focal glomerulopathy. These findings are the first to clearly demonstrate kidney dysfunction and histopathologic alterations associated with the early expression of the adjuvant-induced disease process in the rat. Our observations in the rat suggest that renal dysfunction in man can be mediated by the inflammatory disease process and is not solely a drug treatment-induced side effect.

Explore related subjects

AlbuminsAnimalsArthritis, ExperimentalCreatinineFibrinogenHaptoglobinsKidneyMaleRatsRats, Inbred LewJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J F Dijoseph, T L Walter, D A Hartman, R P Carlson. 1993. Kidney dysfunction in the arthritic rat.. https://doi.org/10.1016/0192-0561(93)90011-m

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2008

Contrast-enhanced tissue Doppler imaging of the left atrial appendage is a new quantitative measure of spontaneous echocardiographic contrast in atrial fibrillation.

AIMS: Although left atrial appendage spontaneous echo contrast (LAASEC) is a marker of increased thromboembolic risk in atrial fibrillation, it has previously only been evaluated qualitatively. We sought to determine if an intravenous contrast echocardiographic agent combined with tissue Doppler imaging (TDI) of the LAA could accurately quantify LAA-SEC in patients with atrial fibrillation. METHODS AND RESULTS: We prospectively identified 55 patients with persistent atrial arrhythmias (mean age 63+/-13 years) undergoing a transesophageal echocardiography (TEE), with LAA-SEC prior to direct current cardioversion. In addition to off-line calculation of backscatter index and shear rate, quantification of the velocity in a color TDI region of interest was performed in the LAA cavity following a 0.5-mL intravenous bolus of Optison. LAA-SEC was qualitatively graded by a blindedreader as mild (n = 29) or severe (n = 26), and was compared off-line to TEE-derived quantitative variables. Compared to patients with mild LAA-SEC, those with severe LAA-SEC had significantly decreased LAA emptying velocity, LAA TDI mean velocities and shear rate. Over the whole group, the mean maximal velocity of the LAA using TDI correlated with LAA emptying velocity (r = 0.59; P < 0.0001), shear rate (r = 0.55; P < 0.0001) and LAA area (r = 0.34; P = 0.014). Severe LAA-SEC was found with 72% sensitivity and 82% specificity if TDI mean velocity was <6.13 cm/s. On logistic regression analysis, LAA-TDI was the only predictor of qualitative LAA-SEC grade. CONCLUSION: Contrast-enhanced TDI is an original new tool that provides a quantification of the mean velocity of LAA-SEC that might improve our decision making in patients with atrial fibrillation.

Albumins↗
PubMed2007

Preparation and preliminary characterization of concentric multi-walled chitosan microspheres.

Chitosan was first converted into micro-droplets by using a high voltage electrostatic field system. The droplets were then dropped into a series of Na(5)P(3)O(10)/NaOH solution mixtures with volume ratio of 17:3, 19:1, 1:0 (pure aqueous Na(5)P(3)O(10)) or 0:1 (pure aqueous NaOH) in order to fabricate chitosan microspheres with different membrane structures. The microspheres exhibit distinct chemical and physical properties, including release behaviors of encapsulated drugs. These chitosan microspheres prepared by this method exhibited good sphericity within the range of (286.6 +/- 15.9) to (356 +/- 9.5) microm in diameters. SEM observations have indicated that the chitosan microspheres exhibited distinct surface structures depending on the post-treatment solutions. The mechanical strength of the chitosan microspheres significantly improved upon treatment with Na(5)P(3)O(10)/NaOH solution at ratio of 17:3 (v/v), as compared with the same but at ratio of 19:1, 1:0 (pure Na(5)P(3)O(10)) and 0:1 (pure NaOH) solutions. In addition, chitosan microspheres with unique multi-walled concentric shell membrane structures were prepared by treating with Na(5)P(3)O(10)/NaOH solution at ratio of 19:1. Release studies were carried out to evaluate the kinetic profiles of two model drugs (5-fluorouracil and cytochrome C) from these prepared chitosan microspheres. When chitosan microspheres treated with Na(5)P(3)O(10)/NaOH ratio at 17:3, the release of cytochrome C was found to be the slowest as compared to those treated by the same Na(5)P(3)O(10)/NaOH solution of other mixing ratios, after a period of 35-day "endurance" test. However, in one case, 5-fluorouracil released quite quickly in a period of 30 min (about 80% completion). The wide range of drug release results might be attributed to the unique and wide range of surface characteristics, porosities, and various structures of chitosan microspheres upon treatment with Na(5)P(3)O(10)/NaOH solutions. These results indicate that, by adjusting the Na(5)P(3)O(10)/NaOH ratios, without extra manipulation on polymer material formulation, one could obtain an additional degree of freedom in drug release profile that permits the simultaneous regulation of morphologies of surface texture and internal structure, mechanical properties, and molecular permeability of the microspheres.

Albumins↗
PubMed2007

CD36 is a novel and potential anti-fibrogenic target in albumin-induced renal proximal tubule fibrosis.

Albumin is not only a risk factor for diabetic nephropathy (DN), but also a therapeutic target. Hence, scientists have long sought ways to elucidate the interactions between albumin and diabetic renal tubule fibrosis. CD36, a surface receptor for thrombospondin-1, has been reported to interact with latent transforming growth factor-beta1 (TGF-beta1) and activate its fibrogenic bioactivity. This study elucidates the interactions between CD36 and renal tubule fibrosis. LLC-PK1 cells were applied to represent renal proximal tubule cells. The expression of CD36 was evaluated by flow cytometry. Fibronectin was assayed by Western blot and enzyme-linked immunosorbent assay (ELISA). Bioactive TGF-beta1 was assayed by ELISA. We demonstrated that albumin was shown significantly to inhibit cell growth without affecting hypertrophy status since protein content and cell size remained unaffected under albumin treatment. Moreover, albumin dose-dependently (0, 1, or 10 mg/ml) enhanced the secretion of bioactive TGF-beta1 and fibronectin with the upregulation of CD36. Intriguingly, CD36 siRNA, a potent silencer for CD36 effectively suppressed the albumin-induced increase in CD36, TGF-beta1, and even fibronectin level. Accordingly, albumin is a pro-fibrogenic factor for proximal tubule cells since albumin per se markedly upregulated the expression of TGF-beta1 and fibronectin. Most importantly, CD36 may mediate albumin-induced cellular fibrosis since CD36 siRNA appeared to have anti-fibrosis effects. This work suggests that CD36 is a novel and potential therapeutic target for diabetic renal tubule fibrosis.

Albumins↗