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Transforming Growth Factor-β: A Cytokine Paradigm
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Michelle R. Frazier-Jessen, Nancy McCartney-Francis, Sharon M. Wahl
The excessive accumulation of extracellular matrix in renal glomeruli (glomerulo–sclerosis) is the main pathological change in human kidney disease that leads to end-stage renal failure, and the only treatment options for such patients are dialysis and/or kidney transplantation. Regardless of the origin of the glomerulosclerosis, TGF-β has been implicated as a major causative agent of fibrosis [111,115]. In diseased glomeruli, TGF-β aids in matrix accumulation by increased ECM synthesis, increased integrin synthesis, and increased synthesis and deposition of protease inhibitors within the matrix. Production of all three isoforms of TGF-β (at the level of gene expression as well as localization of protein via immunostaining) has been observed to be up-regulated in animal models of kidney fibrosis as well as in human biopsy results from patients with fibrotic kidney disease [116].
Animal Models of Osteonecrosis
Published in Yuehuei H. An, Richard J. Friedman, Animal Models in Orthopaedic Research, 2020
Kensaku Masuhara, Minoru Matui, Katsuya Nakata, Keiro Ono
Immune complexes were demonstrated immunohistochemically in bone marrow (Figure 8) as well as in renal glomeruli (53%). Immune complex deposition both in the sinusoidal space of femoral bone marrow (p=0.0385) and in the renal glomeruli (p=0.0209) associated with extravasation of erythrocytes correlated well with the presence of arteriolar microthrombi in the early stage of this model. Early microcirculatory injury associated with immune complex deposition was present surrounding osteonecrotic regions.
The Renin-Angiotensin System
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
Angiotensin-II binding sites in renal glomeruli increase in number and affinity after sodium loading, and the opposite changes occur with dietary sodium deficiency. These changes are the reverse of those occurring in the adrenal cortex.
Therapeutic role of Azadirachta indica leaves ethanolic extract against diabetic nephropathy in rats neonatally induced by streptozotocin
Published in Ultrastructural Pathology, 2021
Abd El-Fattah B. M. El-Beltagy, Amira M.B. Saleh, Amany Attaallah , Reham A. Gahnem
Urea and creatinine are metabolic waste products that are normally filtered through the renal glomeruli.45 Their changes in serum are considered as an indicator for the progression of DN.46,47 In the current work, creatinine and urea levels were shown to be higher in diabetic rats if compared with control. Such result is in agreement with the previous reports applied on experimental model of DN.48–50 On the other side, the levels of serum creatinine and urea appeared significantly lowered in the diabetic group supplemented with neem. This result indicatied the ameliorative effect of neem leaves extract against STZ-induced renal dysfunction. Similar observation was recorded by Kpela et al.51 who found that neem leaves extract can decrease the elevated levels of serum urea and creatinine in cisplatin-induced nephrotoxicity in rats.
The role of Garcinol in abrogating cyclophosphamide/radiation nephrotoxicity via suppressing Mincle/Syk/NF-κB signaling pathway
Published in Toxin Reviews, 2021
Enas Mahmoud Moustafa, Asmaa A. Hassan, Iman Hesham EL-Khashab, Somaya Zakaria Mansour
Normal histological structure of the renal glomeruli and renal tubules are shown in Figure 4(A) in the control group. Nevertheless, rats injected with cyclophosphamide or exposed to γ-irradiation manifested histological abnormalities illustrated by shrinkage of the glomeruli with detectable vacuolation and degeneration in the epithelial lining cells of the renal tubules. Also, loss of brush border in convoluted tubules was also seen (Figure 4(B,D)). However, treatment with Garcinol in rats injected with cyclophosphamide or exposed to γ-irradiation showed amelioration in glomeruli with few inflammatory cells and mild necrosis (Figure 4(C,E)). Furthermore, kidney sections of γ-irradiated rats injected with cyclophosphamide illustrated congestion in Bowman’s capsule and hemorrhage of glomeruli and interstitial tissue. Also degeneration, cloudy swelling of convoluted tubules and inflammatory cells were also seen (Figure 4(F)). On the other hand, treatment with Garcinol in rats injected with cyclophosphamide and exposed to γ-irradiation revealed slight recovery in Bowman’s capsules and convoluted tubules with persistence of some necrotic changes in the convoluted tubules (Figure 4(G)).
Cystatin C as a biomarker of chronic kidney disease: latest developments
Published in Expert Review of Molecular Diagnostics, 2020
Stefanie W. Benoit, Eileen A. Ciccia, Prasad Devarajan
The most commonly used method of estimating glomerular filtration rate (GFR) is measurement of serum creatinine. Creatinine is a breakdown product of creatine phosphate in skeletal muscle and is derived from a patient’s native muscle metabolism as well as consumption of dietary creatine (e.g. meat and creatine supplements). While it is freely filtered by the renal glomeruli, with no reabsorption or renal metabolism, it is actively secreted by the proximal tubule. Due to the substantial amount of urinary creatinine derived from tubular secretion, GFR calculated by 24-creatinine clearance can exceed the measured GFR by the gold standard inulin clearance by 10% to 40% [4]. In addition, given the endogenous source of creatinine is skeletal muscle, there are a variety of demographic factors that affect serum creatinine, including age, gender, and race/ethnicity [5]. Multiple GFR estimating equations have been developed in an attempt to account for these variations. The equations recommended in 2012 by Kidney Disease Outcomes Quality Initiative are the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation for adults and the Updated ‘Bedside’ Schwartz equation for children [5]. However, only approximately 85% and 79% of estimated GFRs using these two equations, respectively, are within 30% of simultaneously accurately measured GFR values [5].