scholarly journals Tubular basement membrane changes in 2-amino-4,5-diphenylthiazole-induced polycystic disease

1985 ◽  
Vol 28 (5) ◽  
pp. 744-751 ◽  
Author(s):  
Ralph J. Butkowski ◽  
Frank A. Carone ◽  
Jared J. Grantham ◽  
Billy G. Hudson
Keyword(s):  
Basement Membrane ◽  
Tubular Basement Membrane ◽  
Polycystic Disease ◽  
Membrane Changes

scholarly journals Tubular basement membrane changes during induction and regression of drug-induced polycystic kidney disease

1994 ◽  
Vol 46 (5) ◽  
pp. 1368-1374 ◽  
Author(s):  
Frank A. Carone ◽  
Ralph J. Butkowski ◽  
Sakie Nakamura ◽  
Momir Polenakovič ◽  
Yashpal S. Kanwar
Keyword(s):  
Kidney Disease ◽  
Basement Membrane ◽  
Polycystic Kidney Disease ◽  
Polycystic Kidney ◽  
Tubular Basement Membrane ◽  
Drug Induced ◽  
Membrane Changes

scholarly journals BIOMARKERS OF KIDNEY DAMAGE IN PATIENTS WITH ARTERIAL HYPERTENSION

2014 ◽  
pp. 48-51 ◽  
Author(s):  
O.V. Kraydaschenko ◽  
M.A. Dolinnaya
Keyword(s):  
Renal Function ◽  
Basement Membrane ◽  
Interstitial Fibrosis ◽  
Chronic Glomerulonephritis ◽  
Tubular Epithelium ◽  
Urine Ngal ◽  
Tubular Basement Membrane ◽  
Hypertensive Patients ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Membrane Changes

Involving of renal tubulointerstitial tissue (TIT) with fibrosis development plays an important role in the persistent renal dysfunction. This circumstance gave rise to the attempts of neutrophil gelatinase–associated lipocalin (NGAL), interleukin–18 (IL–18) use to estimate kidney TIT lesion in chronic glomerulonephritis (CGN) and essential hypertension (EH). Aim. To study the relationship between the biomarkers and clinical, morphological parameters reflecting renal TIT damage in CGN and EH patients. Materials and methods. We examined 44 hypertensive patients and 49 patients with CGN and hypertension. We used data of the kidney morphological study for the analysis of renal TIT lesion in CGN patients. Levels of blood and urine NGAL and IL–18 were determined using immunoassay kits. Results. All patients had preserved renal function. In hypertensive patients microalbuminuria (MAU) was detected in 32%. Patients with CGN had average daily proteinuria 0,5 (0,1:1,2) g/day. Morphologically tubular epithelium dystrophy was observed in 98% ofpatients with CGN. Interstitial fibrosis (IF) was seen in all patients with CGN, and 45% had focal character, while 55% – diffuse. Necrotic changes in the tubular epithelium were observed in 69% of cases, thickening of tubular basement membrane – 61% of patients. Correlation analysis found an association between the level of serum NGAL and IF(r=0,35, p=0,05), tubular basement membrane thickening (r=0,42, p=0,05); urinary NGAL levels and tubular epithelium dystrophy (r=0,29, p=0,05). Serum IL–18 was correlated with tubular epithelium dystrophy (r=0,69, p=0,05); tubular epithelium necrosis (r=0,37, p=0,05), IF (r=0,31, p=0,05). Despite normal renal function and absence of MAU (in 64% of cases), the indicators of renal TIT damage in hypertensive patients are increased. Conclusions. Serum, urine NGAL and serum IL–18 can be used as markers of renal TIT lesion in CGN and EH patients. Serum NGAL reflects most accurately IF and tubular basement membrane changes; urine NGAL – tubular epithelium dystrophy. Serum IL–18 is an indicator of tubular epithelium necrosis, IF.

scholarly journals Renal calcitonin receptors and adenylate cyclase in rats immunized against tubular basement membrane

1977 ◽  
Vol 12 (3) ◽  
pp. 184-192 ◽  
Author(s):  
Nadine Loreau ◽  
Jean-Pierre Cosyns ◽  
Chantal Lepreux ◽  
Pierre Verroust ◽  
Raymond Ardaillou
Keyword(s):  
Basement Membrane ◽  
Adenylate Cyclase ◽  
Tubular Basement Membrane ◽  
Calcitonin Receptors

An electron microscope study of kidney basement membrane changes in the mouse by lipoteichoic acid from Streptococcus pyogenes

1987 ◽  
Vol 33 (8) ◽  
pp. 709-717 ◽  
Author(s):  
Ofra Leon ◽  
Charles Panos
Keyword(s):  
Basement Membrane ◽  
Streptococcus Pyogenes ◽  
Membrane Damage ◽  
Lipoteichoic Acid ◽  
Poststreptococcal Glomerulonephritis ◽  
Membrane Morphology ◽  
Proximal Tubular ◽  
Weight Analysis ◽  
Membrane Changes ◽  
Almost All

Mice injected repeatedly, intraperitoneally or intravenously, for approximately 1 month with a total of 1.04 mg lipoteichoic acid from a nephritogenic strain of Streptococcus pyogenes lost weight. Analysis by electron microscopy revealed that they also exhibited extensive kidney changes in basement membrane morphology which resembled, in part, those observed in human poststreptococcal glomerulonephritis. For example, the glomerular basement membrane became electron dense and exhibited at least a twofold increase in width sporadically within the same preparation after exposure to lipoteichoic acid. Also, whereas appreciable loss or reduction in epithelial foot processes as a result of fusion was clearly evident, epithelial slits and slit membranes or diaphragms between normal foot processes were not selectively affected. In addition, another mostly thickened, highly coiled or serpentinelike basement membrane with amorphous nodules appeared in these preparations. This type membrane was not observed surrounding the capillary lumina and was the most pronounced abnormality apparent in almost all preparations from mice exposed to lipoteichoic acid. Likewise, the proximal tubular basement membrane became variable in width and increased in electron density in mice given lipoteichoic acid as compared with controls. In addition, this membrane was often punctuated with various morphological protrusions originating from only its thickened areas and which extended away from, and not into, the capillary space. This change was only associated with the basement membrane of the proximal tubular capillaries. All membrane changes persisted but gradually subsided, with normal kidney membrane morphology reappearing on the 4th day following the last injection of lipoteichoic acid. The use of mice and minute amounts of lipoteichoic acid to study membrane damage or change in the fine structure of the glomerular or proximal tubular areas at the immediate presymptomatic, and very early symptomatic, phase of streptococcal glomerulonephritis is noted.

scholarly journals Die Kaliumhydrogenphosphat-induzierte Nephropathie des Hundes. I. Pathogenese der Tubulusatrophiee [Potassium Hydrogen Phosphate Induced Nephropathy in the Dog. I. Pathogenesis of Tubular Atrophy—author's trans.]

1980 ◽  
Vol 17 (6) ◽  
pp. 699-719 ◽  
Author(s):  
P. Schneider ◽  
G. Pappritz ◽  
R. Müller-Peddinghaus ◽  
M. Bauer ◽  
H. Lehmann ◽  
...  
Keyword(s):  
Acid Phosphatase ◽  
Epithelial Cells ◽  
Basement Membrane ◽  
Basement Membranes ◽  
Tubular Epithelial Cells ◽  
Beagle Dogs ◽  
Lysosomal Degradation ◽  
Tubular Basement Membrane ◽  
Tubular Atrophy ◽  
Study Results

A nephropathy with severe tubular atrophy was observed in Beagle dogs after oral administration of K2HPO4 for 14 or 38 weeks. We describe the complete lysosomal degradation of atrophying tubular epithelial cells. During two experiments of 14 and 38 weeks duration, respectively, a total of 15 Beagle dogs received 0.8 g K2HPO4/kg body weight daily with their food. All dogs were examined clinically at regular intervals. Renal biopsies were taken in the fourth week from beagles of the 14-week study. Results were compared with those of control dogs. At the end of the experiments the animals were killed and necropsies done. Different stains and histochemical reactions were applied to paraffin sections of the kidneys. Acid phosphatase and β-glucuronidase were found on cryostat sections. Kidneys fixed by perfusion of five Beagles from the 38-week study and three Beagles of the 14-week study, and from five control dogs, were examined electron microscopically. Ultrahistochemically, acid phosphatase was demonstrated. Clinically, the dogs in both experiments vomited, were cachectic, and had elevated creatinine and blood urea nitrogen. Morphologically, qualitatively identical changes were seen, but the renal damage was most marked at 38 weeks. There were disseminated tubular atrophy (usually of the proximal tubules), focal scar tissue and nephrocalcinosis. The following pathogenesis was established for the lesions of the proximal tubule: Tubular atrophy begins with loss of differentiation of epithelial cells. Enzyme histochemistry, ultrahistochemistry and electron microscopy show an increase in autophagic vacuoles and autophagolysosomes. The lysosomal bodies showing fusion enclose large parts of the cytoplasm as the process continues. Complete lysosomal degradation of epithelial cells and extrusion of large lysosomes into the tubular lumen follow. After complete enzymatic digestion of the intratubular detritus, the residue is empty, convoluted and collapsed tubular basement membrane. Atrophic tubular epithelial cells have many organelle-free zones at their base, which contain fine filamentous material resembling that of the basement membrane. The degradation processes described here may explain why clinically the urinary sediment contains few cylinders and epithelial cells and why proteinuria decreases significantly toward the end of the experiment. So far, it is not clear whether the tubular basement membrane is synthesized by the tubular cells, by fibroblasts or by both cell types. The presence of basement membrane-like material in tubular epithelial cells and in parietal epithelial cells of the glomerulus favors the view that epithelial cells produce the basement membranes and that increased production of basement membrane-like material is a sign of loss of differentiation.

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