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Diabetic Nephropathy
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Aside from diabetes causing glomerular sclerosis and other nephropathies, risk factors include persistent hyperglycemia (glucotoxicity), hyperlipidemia, hypertension, lack of physical activity, smoking, and a diet that is high in fat and protein. Genetics are also linked to the disease, and a family history of any diabetic glomerulopathy increases risks.
Mechanisms of Chronic Glomerular Injury
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Numerous clinical factors (e.g., hypertension) and pathogenetic abnormalities have been cited as potential mechanisms in the propagation of glomerular injury, regardless of etiology, to glomerulosclerosis, which is one of the major histologic features of renal failure. The uncertainty that exists as to the precise process that accounts for progressive glomerulopathy is a result of both the complex glomerular and tubulointerstitial pathobiology that ensues after initial glomerular injury occurs as well as the myriad experimental models that have been utilized for investigation. Although each model of progressive glomerular disease is valuable, the unique nuances of each adds to the complexity of understanding how chronic glomerular injury develops. Also, progressive glomerulopathy is a common result of a diverse set of immunologic, toxic, age-related, and genetic disorders that cause initial glomerular injury. Despite this lack of resolution, it should be noted that the pathologic processes of mesangial expansion and matrix overproduction, as well as mesangial cell proliferation, coupled with tubular dysfunction, atrophy, and eventually interstitial fibrosis, all comprise a final histologic common pathway by which chronic glomerular injury progresses.
Nutrition, Chronic Kidney Disease, and Kidney Failure
Published in David Heber, Zhaoping Li, Primary Care Nutrition, 2017
Obesity can affect the kidneys directly through so-called obesity-related glomerulopathy. It is characterized histologically by enlargement of glomeruli, which can be accompanied by focal and segmental glomerulosclerosis observed in association with hypertrophied glomeruli (D’Agati et al. 2011). There are also lipid deposits in mesangial and tubular cells, along with changes similar to those seen in type 2 diabetes, including focal mesangial sclerosis. Focal thickening of glomerular and tubular basement membranes, a feature of diabetic nephropathy, is also seen in obese patients without diabetes.
Polymorphisms in glucose homeostasis genes are associated with cardiovascular and renal parameters in patients with diabetic nephropathy
Published in Annals of Medicine, 2022
Sonia Mota-Zamorano, Luz M. González, Nicolás R. Robles, José M. Valdivielso, José C. Arévalo-Lorido, Juan López-Gómez, Guillermo Gervasini
Samples of the NEFRONA repository were analysed in this work if they corresponded to (i) patients over 18 years of age with T2DM (fasting glucose >126 mg/dL or non-fasting glucose >200 mg/dL) and deterioration of kidney function [eGFR <60 ml/min/1.73 m2 and >300 mg albumin (or >500 mg protein) in 24-hour urine]; or (ii) healthy subjects over 18 years of age with eGFR > 60 ml/min/1.73 m.2 The diagnosis of classical diabetic nephropathy was made using clinical criteria (proteinuria higher than 500 mg/day or microalbuminuria higher than 300 mg/day associated with documented diabetic retinopathy (confirmed by examining the back of the eye). A kidney biopsy was carried out to confirm the diagnosis in those cases where the patient did not present diabetic retinopathy and proteinuria was higher than 1 g/day, after patient consent was obtained. Other possible diagnoses were adequately ruled out using clinical protocols for glomerulopathy and immunological screening. NEFRONA exclusion criteria included previous history of any CV event, transplantation of any organ, carotid artery surgery, active infection, pregnancy, or life expectancy below one year.
Zataria multiflora and its main ingredient, carvacrol, affect on the renal function, histopathological, biochemical and antioxidant parameters in adriamycin-induced nephrotic rats
Published in Archives of Physiology and Biochemistry, 2021
Reza Mohebbati, Mohammad Jalili-Nik, Hossein Saghi, Hamed Sadatfaraji, Mohammad Soukhtanloo
Nephrotic syndrome (NS) is described as a renal disorder in which the level of urinary protein exceeds 3.5 g per 1.73 m2 body surface per day (Orth et al.1998). It usually results in glomerulopathy manifested by hypoalbuminemia, excessive proteinuria, and hyperlipidemia (Schachter 2004). Extensive investigations illustrate that the nephrosis might originate from both inflammatory and degenerative disorders. In other words, nephrosis may associate with systemic disorders caused by renal lesions (Souto et al.2007). Pathophysiologically, inflammation, oxidative damage by free radicals, and their following activities have been implicated in various disorders. Reactive oxygen species (ROS) promote cellular malfunction by lipid peroxidation, destroy the tubular endothelial barrier integrity and rise the glomerular permeability of protein that alters the glomerular hemodynamics leading to the peripheral edema and proteinuria in the inflammation context (Boueiz et al.2009, Lucas et al.2009).
The ratio of urinary TREM-1/TREM-2 mRNA expression in chronic kidney disease and renal fibrosis
Published in Annals of Medicine, 2021
Yuhan Cao, Yuwei Wang, Nana Peng, Jie Xiao, Sufen Wang, Cong Fu
A total of 77 biopsy-proven CKD patients were selected from the Department of Nephrology, Yi Ji Shan Hospital, Wannan Medical College from 2018–2019. The flow diagram for selecting patients was shown in Figure 1. The 77 patients containing IgA nephropathy (n = 38), membranous nephropathy (n = 8), minimal change disease (n = 6), focal segmental glomerulosclerosis (n = 7), diabetic nephropathy (n = 8), hypertensive nephropathy (n = 2) and non-IgA mesangioproliferative glomerulopathy (n = 8). The exclusion criteria were used: patients younger than 18 years old or older than 80 years old; patients with chronic liver disease, urinary tract infection, cancer, or organ transplantation; CKD patients with severe complications: cardiovascular disorder; or the use of steroids or immunosuppressive medications. The clinical data of all participants were collected. A total of age- and gender-matched healthy volunteers (n = 15) from the Yi Ji Shan Hospital Health Care Centre were also enrolled in the study as controls. Healthy controls were defined by the absence of abnormalities on a routine urinalysis and normal renal function [estimated glomerular filtration rate (eGFR)>90 ml−1·min−1·1.73 m−2].