摘要:

The methodology for the collection, extraction, separation and measurement of urinary angiotensin II [the octapeptide, ANG(1-8)] is described. To determine the origin of urinary ANG(1-8), mean arterial pressure, renal hemodynamics and the arterial, renal venous and urinary concentrations of ANG(1-8) were examined prior to and following the constant intra-arterial infusion of tritiated angiotensin II [3H-ANG(1-8)] in graded doses of 0.5,2.0 and 2.5 ng/kg/min in 5 uninephrectomized, anesthetized female dogs. The infusion of 3H-ANG-(1-8) had no significant effect on mean arterial pressure, glomerular filtration rate, renal blood flow or urine flow rate. The mean concentration of ANG(1-8) in the urine was 3.7 fmol/ml. None or only trace amounts of 3H-ANG(1-8) were detected in the urine in spite of marked increases in renal arterial 3H-ANG(1-8) concentrations. These observations suggest that urinary ANG(1-8) was derived de novo from the intrarenal generation of angiotensin II. In addition, plasma and urinary concentrations of ANG(l-8) were assessed in patients with essential hypertension undergoing treatment with either a diuretic (n = 14) or an angiotensin-converting enzyme inhibitor (n = 14). Although the concentrations of plasma ANG(1-8) responded appropriately to the respective therapies, the urinary excretion of ANG(1-8) was not different following either therapy. These data suggest that ANG(1-8) collected from the urinary bladder may not occur in adequate concentrations to accurately assess the activity of the intrarenal reninangiotensin system.

ISSN:1660-8151    

DOI:10.1159/000188215

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

To investigate the potential roles of oxidized lipoproteins and glomerular macrophages in the pathogenesis of lipid-induced glomerular injury, we examined the effects of administration of probucol on the development of renal injury in ExHC rats. ExHC rats are derived from the Sprague-Dawley strain and are highly susceptible to dietary hypercholesterolemic stimuli. We reported previously that ExHC rats fed a cholesterol-supplemented diet (HCD) develop proteinuria and characteristic glomerular lesions. These lesions include marked accumulation of numerous lipid-filled foam cells, which have a surface marker that identifies them as macrophages, within mesangial regions, as well as segmental clusters of foam cells that are associated with capsular adhesions, the destruction of glomerular tufts and glomerular sclerosis. ExHC rats were maintained on an HCD or on an HCD supplemented with 5% (wt/wt) probucol for 8 weeks. Probucol reduced the extent of renal injury, as evidenced by proteinuria and segmental glomerular lesions, in ExHC rats fed an HCD, in the absence of any significant reduction in plasma cholesterol levels. Both low-density lipoprotein and β-very-low density lipoprotein isolated from the plasma of probucol-treated rats were found to be resistant to oxidative modification by cupric ions. Both the size and the number of foam cells within glomeruli in the probucol-treated rats were significantly reduced as compared to those of foam cells in the untreated rats. Probucol might reduce renal injury in ExHC rats by limiting the oxidative modification of lipoproteins and, subsequently, by restricting the foam cell transformation of macrophages within glomeruli and by inhibiting the recruitment of macrophages into glomeruli. The results of the present study may be interpreted to indicate that local glomerular oxidative modification of lipoproteins might occur in vivo, and both oxidized lipoproteins and glomerular macrophages may play important roles in the pathogenesis of lipid-induced glomerular injury

ISSN:1660-8151    

DOI:10.1159/000188021

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Hypercholesterolemic Imai rats, especially males, spontaneously develop proteinuria and glomerulosclerosis. We have shown that castration attenuated the progression of glomerular injury in male Imai rats. The present study was designed to investigate whether the attenuating effect of castration on glomerulosclerosis is eliminated by administration of testosterone. Testosterone propionate (TP) eliminated the attenuating effect of castration on the progression of glomerular injury by significantly and dose dependently increasing proteinuria and enhancing glomerular sclerosis. TP at 1 mg failed to reverse glomerulosclerosis to the control levels, despite a dose of TP sufficient to restore urinary protein excretion, serom testosterone level and glomerular growth. The results indicated that besides testosterone other sex-related hormones may be involved in the development of glomerulosclerosis in male Imai rats.

ISSN:1660-8151    

DOI:10.1159/000188022

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Sarcoid reactions have been described in association with lymphomas and rarely with other solid tumors. We describe a patient with renal papillary adenocarcinoma and prominent sarcoid-like granulomatous infiltration of the ipsilateral and most likely the contralateral kidney. There was no evidence of extrarenal granulomas. This is the first description of impairment in renal function in a patient with renal carcinoma and with sarcoid reaction to this tumor isolated in the kidney.

ISSN:1660-8151    

DOI:10.1159/000188023

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

A patient with severe Crohn’s disease was treated with 5-aminosalicylic acid (5-ASA). Following initiation of treatment, serum creatinine increased slowly from 105 to 530 μmol/l (creatinine clearance 16 ml/min). The diagnosis of an interstitial nephritis was made based on normal urinary findings and the renal biopsy histology of intestitial mononuclear infiltrates and normal glomeruli, 5-ASA was discontinued and serum creatinine decreased to 245 μmol/l (creatinine clearance 40 ml/min) during the following 3 months. Partial reversibility of renal failure following discontinuation of 5-ASA and the absence of other drugs possibly causing interstitial nephritis suggest a causal relationship between 5-ASA and interstitial nephri

ISSN:1660-8151    

DOI:10.1159/000188024

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188025

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188026

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188027

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188028

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188029

出版商:S. Karger AG    

年代:1994

数据来源: Karger