scholarly journals Structural and ultrastructural renal lesions in rats fed high-fat and high-phosphorus diets

2020 ◽  
Author(s):  
Paula Esquinas ◽  
Rafael Rios ◽  
Ana I Raya ◽  
Carmen Pineda ◽  
Mariano Rodriguez ◽  
...  
Keyword(s):  
Basal Membrane ◽  
Endothelial Damage ◽  
Mesangial Matrix ◽  
Interstitial Edema ◽  
Tubular Atrophy ◽  
Capillary Membrane ◽  
Two Factors ◽  
Glomerular Lesions ◽  
Histopathological Studies ◽  
Bowman's Capsule

Abstract Background Foods prone to deteriorate renal function are rich in fat and in phosphorus (P), but the interaction between these two factors is not well studied. Method Detailed structural and ultrastructural histopathological studies were performed on the kidneys of rats fed different amounts of fat and P: low (4%) fat (LF) and normal (0.6%) P (NP), LF and high (1.2%) P (HP), high (35%) fat (HF) and NP, HF and HP, and HF with low (0.2%) P (LP) for 28 weeks. Results Glomeruli of the HF groups showed segmental areas of retraction, sclerosis and thickening of the Bowman’s capsule and basal membranes, which were more accentuated in the HF–HP group. Ultrastructural lesions in the glomeruli also were prominent in rats fed HF, particularly in the HF–HP group, and included thickening of the capillary membrane, endothelial damage, mesangial matrix hypercellularity and podocyte effacement. P restriction reduced the severity of endothelial damage, mesangial matrix hypercellularity, thickening of capillary basement membrane and podocyte effacement. The kidneys of rats fed HP showed significant tubular atrophy and dilatation, focal tubular hyperplasia, thickening of the tubular basal membrane, interstitial edema, inflammation and calcification. All groups fed HF also showed tubular lesions that were more prominent in the HF–HP group. P restriction had a beneficial effect on inflammation and calcification. Conclusions Intake of both HF and HP damages the kidneys and their noxious effects are additive. HF intake was preferentially associated with glomerular lesions, while lesions related to HP intake were located mainly in the tubuli and in the interstitium.

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

MO070NEW ASPECTS OF THE PATHOMORPHOLOGIC SEQUENCE OF NEPHRON LOSS IN DIABETIC NEPHROPATHY

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Hermann Gröne ◽  
Wilhelm Kriz ◽  
Jana Loewen ◽  
Elisabeth Groene
Keyword(s):  
Diabetic Nephropathy ◽  
Basement Membrane ◽  
Mesangial Cells ◽  
Capillary Endothelium ◽  
Tubular Damage ◽  
Mesangial Matrix ◽  
Nephron Loss ◽  
Bowman's Capsule ◽  
Glomerular Damage ◽  
Glomerular Capillaries

Abstract Background and Aims Diabetic nephropathy (DN) is the leading cause of end-stage-renal disease in western countries. Despite of innumerable studies undertaken to elucidate the pathogenesis of DN the underlying morphologic alterations have been insufficiently analyzed. Method Re-evaluation of more than 800 biopsies was done showing several unknown features. Results: 1. Matrix accumulation in the mesangium: Thickening of the glomerular basement membrane (GBM) and expansion of the mesangial matrix are hallmarks of DN, generally considered to emerge from different sites of overproduction: GBM components from podocytes and mesangial matrix from mesangial cells. We show, that the accumulation of matrix in the mesangium emerges from an overproduction of GBM material by podocytes and endothelial cells and an impaired degradation by mesangial cells. The progressing deposition of worn-out GBM material into the mesangium accounts for the advancement from diffuse mesangial sclerosis (DMS) to nodular sclerosis (NS) and to the herniation of the tuft through the glomerular vascular pole to the outside; the latter is associated with the outgrowth of glomerular capillaries into the peri-glomerular space leading to the destruction of the juxtaglomerular apparatus. 2.The role of podocytes Podocytes have frequently been accused to play a central role in DN. This is correct, but in another way than generally assumed. Damage to podocytes cannot be seen in DMS. The albuminuria regularly seen during this stage derives, as previously suggested by others, from an increased leakiness of the glomerular capillary endothelium based on a deranged glycocalyx. Podocyte detachments start at the transition from DMS to NS, based on the loss of cross talk signals with the capillary endothelium: the increasing deposition of matrix leads to the collapse of many capillaries. These podocytes contribute little to the further progression of the damage: they are lost into primary urine or they undergo cell lysis.In addition to their role in increased matrix production, podocytes take an active role in the formation of tuft adhesions to Bowman’s capsule (BC), starting the progression to NS. Expansion of the matrix within the mesangium has led to expansion of the tuft (frequently associated with nodules) towards Bowman’s capsule (BC) or towards the urinary orifice. Podocytes on the surface of these expansions are in their majority structurally intact, exhibiting an intact pattern of foot processes. These podocytes come into contact with parietal epithelial cells and initiate DN-specific tuft adhesions to BC allowing the proliferation of glomerular capillaries into BC. There they deliver an exudate into BC that spreads around the entire circumference of the glomerulus presenting as giant insudative spaces. Moreover, this process encroaches via the glomerulo-tubular junction onto the tubule constituting the major pathway of glomerular damage extending to the tubulointerstitium. 3. Tubulointerstitial fibrosisIt is current opinion that the tubulointerstitial fibrosis may start from tubular damage resulting in an own, glomerular-independent pathway to nephron loss. However, there is scant evidence for such a mechanism. Studying 162 glomerulo-tubular transitions, we did not see a tubular epithelial or interstitial damage in those biopsies without any evidence of a glomerulo-tubular damage transfer. The only exception consists of the well-known prominent thickening of the tubular basement membrane, which may result in functional loss but does not lead to structural epithelial damage. Conclusion We consistently found that tubulo-interstitial damage develops after encroachment of the glomerular damage onto the tubule, leading first to a gradual degeneration of tubules which subsequently initiate the process of interstitial fibrosis.

scholarly journals Effect of a Single Apolipoprotein L1 Gene Nephropathy Variant on the Risk of Advanced Lupus Nephritis in Brazilians

2019 ◽  
Vol 47 (8) ◽  
pp. 1209-1217 ◽  
Author(s):  
Gisele Vajgel ◽  
Suelen Cristina Lima ◽  
Diego Jeronimo S. Santana ◽  
Camila B.L. Oliveira ◽  
Denise Maria N. Costa ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Interstitial Fibrosis ◽  
Nucleotide Polymorphisms ◽  
Endstage Renal Disease ◽  
Tubular Atrophy ◽  
Risk Alleles ◽  
Increased Risk ◽  
Tubulointerstitial Damage ◽  
Glomerular Lesions ◽  
Apolipoprotein L1

Objective.Apolipoprotein L1 gene (APOL1) G1 and G2 renal risk alleles (RRA) are associated with endstage renal disease in blacks with lupus nephritis (LN). The present study determined frequencies of APOL1 RRA in nonwhite Brazilian patients with LN and controls to assess association with renal outcomes.Methods.APOL1 RRA were genotyped in 222 healthy blood donors (controls) and 201 cases with LN from 3 outpatient clinics. Two single-nucleotide polymorphisms in the G1 (rs73885319 and rs60910145) and an indel for the G2 (rs71785313) variant were genotyped.Results.The frequency of APOL1 RRA in nonwhite Brazilian LN cases did not differ significantly from healthy controls, and few participants had 2 RRA. In the sample, 84.6% of LN cases and 84.2% of controls had 0 RRA, 13.4% and 15.3% had 1 RRA, and 2.0% and 0.4% had 2 RRA, respectively. LN cases with ≥ 1 APOL1 RRA had similar baseline characteristics and renal responses to treatment, yet faced higher risk for progressive chronic kidney disease (CKD) to an estimated glomerular filtration rate < 30 ml/min/1.73 m2 compared to those with 0 RRA (11.2% with 0, 29.6% with 1; 50% with 2 RRA, p = 0.005). Although glomerular lesions and activity scores on initial kidney biopsy did not differ significantly between individuals based on APOL1 genotype, chronicity scores, tubular atrophy, and interstitial fibrosis were more severe in those with ≥ 1 RRA (p = 0.011, p = 0.002, p = 0.018, respectively).Conclusion.Although initial kidney lesions and treatment responses were similar, a single APOL1 RRA in nonwhite Brazilians with LN was associated with increased risk of advanced CKD and possibly more tubulointerstitial damage.

scholarly journals Codistribution of collagen types IV and AB2 in basement membranes and mesangium of the kidney. an immunoferritin study of ultrathin frozen sections.

1980 ◽  
Vol 85 (3) ◽  
pp. 597-616 ◽  
Author(s):  
F J Roll ◽  
J A Madri ◽  
J Albert ◽  
H Furthmayr
Keyword(s):  
Ultrastructural Level ◽  
Basement Membranes ◽  
Frozen Sections ◽  
Mesangial Matrix ◽  
Collagen Types ◽  
Type Iv ◽  
Collagen Antibodies ◽  
Ultrathin Frozen Sections ◽  
Bowman's Capsule ◽  
Large Vessels

Affinity-purified rabbit antibodies specific for collagen types I, III, AB2 and for a partially characterized type IV collagen derived from a murine tumor were used to study the distribution of collagens in the normal mouse kidney. Immunofluorescence staining of conventional frozen sections demonstrated that types I and III were present in bundles around large vessels and in fibers surrounding glomeruli and tubules, whereas types IV and AB2 were distributed in a linear fashion along basement membranes of tubules, glomeruli, and Bowman's capsule and in the mesangial stalk. The distribution of types IV nd AB2 was examined at the ultrastructural level by staining of 600- to 800-A thick frozen sections with a three-stage procedure employing specific collagen antibodies, biotinyl sheep antirabbit IgG, and avidin-ferritin conjugates. Labeling by this procedure demonstrated codistribution of types AB2 and the putative type IV in all three basement membranes. In addition, mesangial matrix was shown to contain both of these collagen types. These results support recent biochemical evidence of collagen heterogeneity in basement membranes, and also support the concept of a structural relationship between mesangial matrix and glomerular basement membranes.

scholarly journals Acute toxicity of Leaf extracts of Enydra fluctuans Lour in Zebrafish (Danio rerio Hamilton)

2020 ◽  
Author(s):  
Jobi Xavier ◽  
Kshetrimayum Kripasana
Keyword(s):  
Acute Toxicity ◽  
Basal Membrane ◽  
Brain Parenchyma ◽  
Herbaceous Plant ◽  
Histopathological Changes ◽  
Oral Toxicity ◽  
Leaf Extracts ◽  
Toxicity Studies ◽  
Histopathological Studies ◽  
Oral Acute Toxicity

AbstractThe present study was focused on the concentration dependent changes in oral acute toxicity of leaf extracts of E. fluctuans in zebrafish. The study was also aimed at the details of histopathological changes in gill, liver, brain and intestine of zebrafish exposed to the leaf extracts of the plant E. fluctuans. Enydra fluctuans Lour is an edible semi-aquatic herbaceous plant used widely for the alleviation of the different diseases. Since there were no toxicity studies conducted on this plant the present study was an attempt to look into the elements of toxicity of the plants. Two types of experiments are conducted in the present study. First, the acute oral toxicity study was conducted as per the OECD guidelines 203. Second, histopathological changes were observed in the fishes exposed to the lethal concentrations of plant extract. The oral acute toxicity studies conducted on Zebrafish have revealed that the leave extracts of E. fluctuans were toxic to the tested fish at the concentration of 200 mg/kg body weight. The histopathological studies conducted on intestine of treated fishes showed that treatment has induced rupturing of villi structure and fusion of villi membrane and detachment of villi structure from basal membrane of intestine. The histology of the liver also showed severe vacuolization in the cells while it is not affected in control. The studies on gills showed the detachment of basal epithelial membrane in gills compared to control which might have led to death of the fish. The histopathological observations of brain tissues treated with test samples also revealed the marked impingement in brain parenchyma while the control is normal without impingement of brain.

scholarly journals Ultrastructural localization of fibronectin and laminin in the basement membranes of the murine kidney.

1980 ◽  
Vol 86 (2) ◽  
pp. 682-687 ◽  
Author(s):  
J A Madri ◽  
F J Roll ◽  
H Furthmayr ◽  
J M Foidart
Keyword(s):  
Mesangial Cell ◽  
Ultrastructural Localization ◽  
Ultrastructural Level ◽  
Basement Membranes ◽  
Frozen Sections ◽  
Mesangial Matrix ◽  
Lamina Densa ◽  
Rabbit Igg ◽  
Cell Processes ◽  
Bowman's Capsule

Affinity-purified rabbit antibodies specific for two large noncollagenous gycoproteins--laminin and fibronectin--were used to study the distribution of these proteins in normal murine kidneys. Immunofluorescence staining of conventional frozen sections demonstrates fibronectin within mesangial areas of the glomerulus. Laminin is also found in mesangial areas. However, it also appears to be distributed in typical basement membranelike patterns on glomerular and tubular basement membranes and Bowman's capsule. At the ultrastructural level, by labeling 600-800-A thick frozen sections with a three-stage procedure consisting of specific antibodies, biotinyl sheep anti-rabbit IgG, and avidin-ferritin conjugates, fibronectin is present ony in the mesangial matrix and is specifically localized to areas immediately surrounding mesangial cell processes. Laminin, on the other hand, is found uniformly distributed throughout tubular basement membranes, the mesangial matrix, and Bowman's capsule. In glomerular basement membranes, laminin labeling is restricted to the lamina rara interna and adjacent regions of the lamina densa.

Correlation Between Renal Cortical Stiffness and Histological Determinants by Point Shear-Wave Elastography in Patients With Kidney Transplantation

2017 ◽  
Vol 27 (4) ◽  
pp. 346-353 ◽  
Author(s):  
A. L. Croci Chiocchini ◽  
C. Sportoletti ◽  
G. Comai ◽  
S. Brocchi ◽  
I. Capelli ◽  
...  
Keyword(s):  
Shear Wave ◽  
Gold Standard ◽  
Interstitial Fibrosis ◽  
Research Question ◽  
Intraclass Correlation ◽  
Shear Wave Elastography ◽  
Mesangial Matrix ◽  
Tubular Atrophy ◽  
Chronic Allograft Dysfunction ◽  
Allograft Dysfunction

Introduction: Renal allograft biopsy is the gold standard for the detection of histological lesions of chronic allograft dysfunction. The identification of a noninvasive routine test would be desirable. Elastosonography is used to assess tissue stiffness according to viscosity, and no data are available on the use of point quantification shear-wave elastography (ElastPQ) for the evaluation of renal chronic lesions. Research Question: To evaluate the feasibility of ElastPQ to assess cortical allograft stiffness and to determine the correlation of clinical, biological, and pathological factors with the diagnostic accuracy of kidney stiffness values in patients with histological lesions. Design: Forty-two patients underwent kidney transplant biopsy and 10 valid measurements of ElastPQ, blindly performed by 2 operators. The interobserver reproducibility was assessed according to intraclass correlation coefficient. The ElastPQ measurements and the clinical data were compared using the Spearman correlation analysis. Results: 97.6% reliable measurements were obtained using ElastPQ, with an excellent interobserver agreement. The kidney stiffness was significantly higher in the patients with a time since transplantation >12 months and was correlated with chronic lesions (interstitial fibrosis, tubular atrophy transplant glomerulopathy, and mesangial matrix), with the interstitial fibrosis/tubular atrophy, score and with the sum of the scores of the chronic lesions. Mesangial matrix increase is the only independent determinant of kidney stiffness. Discussion: ElastPQ is a noninvasive, reproducible, and sensitive diagnostic tool able to detect moderate/severe chronic lesions. Its routine use during follow-up can identify patients eligible for biopsy, which remains the gold standard exam for detecting chronic allograft dysfunction.

P0448CHARACTERISTICS OF PRIMARY GLOMERULAR DISEASE PATIENTS WITH HEMATURIA IN TURKEY: THE DATA FROM TSN-GOLD WORKING GROUP

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Abdullah Sumnu ◽  
Kultigin Turkmen ◽  
Egemen Cebeci ◽  
Aydin Turkmen ◽  
Necmi Eren ◽  
...  
Keyword(s):  
Interstitial Fibrosis ◽  
Basal Membrane ◽  
National Database ◽  
Tubular Atrophy ◽  
Laboratory Findings ◽  
Glomerular Diseases ◽  
Nephritic Syndrome ◽  
Serum Blood Urea Nitrogen ◽  
Primary Glomerular Diseases ◽  
Primary Glomerular Disease

Abstract Background and Aims Hematuria is one of the most common laboratory findings in nephrology practice. In different regions of the world, the etiologic causes differ. To date, there is no enough data regarding the clinical and histopathologic characteristics of primary glomerular diseases (PGD) patients with hematuria in our country. Method Data were obtained from national multicenter (47 centers) data entered into the Turkish Society of Nephrology Glomerular Diseases (TSN-GOLD) database between May 2009 and June 2019. The data of all PGD patients over the age of 16 years who were diagnosed with renal biopsy and had hematuria data were included in the study. The biopsy samples were processed using a light microscopy and immunofluorescence examination. Demographic characteristics such as age, sex, indications for biopsy, primary glomerular diseases, comorbidities, laboratory and biopsy findings of all patients were also recorded. Hematuria was defined as the presence of at least 5 red blood cells/hpf. Results Data of 3394 patients were included to the study after the exclusion of patients with secondary glomerulonephritis and patients with missing biopsy findings. While 1699 (50.1%) patients had hematuria, 1695 (49.9%) patients did not have hematuria. Demographic, laboratory, and histopathological characteristics of patients with and without hematuria are given in Table. Patients with hematuria had statistically higher systolic blood pressure (SBP), serum blood urea nitrogen, creatinine, albumin, levels and urine pyuria, however, these patients had statistically lower age, body mass index, presence of hypertension and diabetes, eGFR, 24-hour proteinuria, serum total, HDL and LDL-cholesterol and C3 levels when compared with patients without hematuria. Figure depicted the etiologic causes of patients with and without hematuria. According to histopathological findings, number of global sclerotic glomeruli, cellular and fibrocellular crescents, the levels of mesangial proliferation, endocapillary proliferation, exudative changes in glomeruli, severe tubular atrophy, interstitial inflammation, subendothelial deposition, moderate and severe IgA and C3 deposition were found to be significantly higher and the levels of basal membrane thickening, interstitial fibrosis, subepithelial deposition, severe IgG staining were found to be significantly lower in patients with hematuria. Conclusion This is the first multicenter national report regarding the demographic and histopathologic data of PGD patients with or without hematuria. Hematuria, a feature of nephritic syndrome, was found at a higher than expected in the PGDs presenting with nephrotic syndrome in our national database.

scholarly journals Subclinical pulmonary edema in endurance athletes

2015 ◽  
Vol 77 (2) ◽  
Author(s):  
M. Bussotti ◽  
S. Di Marco ◽  
G. Marchese ◽  
P.G. Agostoni
Keyword(s):  
Pulmonary Edema ◽  
Endurance Athletes ◽  
Strenuous Exercise ◽  
Intense Exercise ◽  
Interstitial Edema ◽  
Interstitial Oedema ◽  
Capillary Membrane ◽  
High Incidence ◽  
Consequent Increase ◽  
Alveolar Capillary

Strenuous exercise may cause progressive and proportional haemodynamic overload damage to the alveolar membrane, even in athletes. Despite the high incidence of arterial desaturation reported in endurance athletes has been attributed, into other factors, also to the damage of the alveolar-capillary membrane this evidence is equivocal. Some studies demonstrated flood of the interstitial space and consequent increase in pulmonary water content, but most of them were able to show this through indirect signs of interstitial oedema. The present review illustrates the literature’s data in favour or against pulmonary interstitial edema due to intense exercise in athletes.

Spontaneous Glomerular and Tubulointerstitial Lesions in Common Marmosets (Callithrix jacchus)

2011 ◽  
Vol 49 (5) ◽  
pp. 839-845 ◽  
Author(s):  
K. Isobe ◽  
K. Adachi ◽  
S. Hayashi ◽  
T. Ito ◽  
A. Miyoshi ◽  
...  
Keyword(s):  
Periodic Acid ◽  
Mesangial Matrix ◽  
Periodic Acid Schiff ◽  
Cytoplasmic Staining ◽  
Common Marmosets ◽  
Renal Lesions ◽  
Interstitial Inflammation ◽  
Mesangial Area ◽  
Tubulointerstitial Lesions ◽  
Glomerular Lesions

Spontaneous progressive nephropathy dominated by glomerular lesions in common marmosets has been reported. However, the histopathologic characteristics, including the relationship between glomerular and tubulointerstitial lesions, have not been described in detail. In the present study, the authors examined the histopathologic characteristics of the background renal lesions in common marmosets (3 males and 9 females, 3 to 8 years old). The severity of glomerular lesions was graded into 3 classes: grade I, no alteration; grade II, hilar/focal increase of mesangial matrix; grade III, global/diffuse increase of mesangial matrix. Tubulointerstitial lesions (tubular regeneration and hyperplasia and interstitial inflammation and fibrosis) were scored according to the area of each lesion. The renal lesions were characterized by enlargement of glomeruli, expanded mesangial area with increase of periodic acid–Schiff reaction-positive matrix, tubular regeneration and hyperplasia, and interstitial inflammation and fibrosis. Glomerular lesions progressed with increasing mesangial matrix and aging. Additionally, the tubulointerstitial lesions became exacerbated with progressing glomerular lesions. Tubular hyperplasia was divided into 4 types according to the structure of the cell layer (simple or stratified-like), the area of increased lining cells (partial or entire), cytoplasmic staining (eosinophilic or basophilic), brush border and thickness of basement membrane, and the activity of cell proliferation. In conclusion, the background renal lesions in common marmosets were characterized by glomerular lesions with increase of mesangial matrix, which progressed with aging, and secondary tubulointerstitial lesions, including tubular hyperplasia. Those lesions were thus diagnosed as progressive glomerulonephropathy in common marmosets.

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