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Kidney Disease
Published in Amy J. Litterini, Christopher M. Wilson, Physical Activity and Rehabilitation in Life-threatening Illness, 2021
Amy J. Litterini, Christopher M. Wilson
Chronic kidney disease (CKD) results from conditions which either damage or reduce the function of one or both kidneys. Nephritis refers to inflammation of the kidneys, while nephrosis refers to non-inflammatory kidney disease associated with damage or degeneration. Nephrotic syndrome refers to small vessel damage within the kidneys causing excess protein to be released into the urine.
Mechanisms of Chemically Induced Glomerular Injury
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
While allopurinol was effective in reducing proteinuria and glomerular injury caused by PAN treatment of rats171, it caused no important changes in ADR nephrosis.105 However, platelet activating factor (PAF) receptor antagonists and 5-lipoxygenase inhibitor significantly reduced proteinuria and glomerular injury in ADR nephrosis.105
Ethylmalonic encephalopathy
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
Dilated tortuous retinal vessels (Figures 102.11 and 102.12) may be seen as early as three to four months of life. Hematuria may be observed and erythrocytes were reported in the cerebrospinal fluid (CSF) [5, 7, 11]. An association with nephrotic syndrome has been previously reported [12], and we have encountered a case with an episode of nephrosis which was responsive to conventional steroid treatment. One patient had a terminal hemoperitoneum [7]. Biopsies of the skin lesions showed nothing but hemorrhage [7]. There was no evidence for an immunologic abnormality, nor were there abnormalities of bleeding, clotting, or platelets. A markedly elevated level of plasminogen activator inhibitor-1 has been encountered [9]. Terminal events in two patients appeared to be pulmonary edema and one had cerebral edema.
Non-diabetic urine glucose in idiopathic membranous nephropathy
Published in Renal Failure, 2022
Lingling Liu, Ke Zuo, Weibo Le, Manman Lu, Zhihong Liu, Weiwei Xu
Another interesting phenomenon in our research was that urine glucose usually occurred when the patient had massive proteinuria, and if proteinuria was controlled, the urine glucose and scr would gradually become normal. Previous research has shown that there was a strong relationship between tubulointerstitial nephritis and the severity of proteinuria in experimental nephrosis [23]. Albumin overload could indeed induce renal tubular injury [24]. A recent research with single cell sequence also showed that proximal tubular cells had higher TNF signaling pathway, IL-17 signaling pathway, NOD like receptor, and apoptosis expression in massive proteinuria patients than nonmassive proteinuria patients [19]. Thus, it would be of importance to discriminate the tubular injury when patients had massive proteinuria. Some previous researches tried to find out the relationship between the time average proteinuria and the long-term renal outcome [25]. This procedure was complicate. However, our research showed that the occurring of urine glucose was corelated to proteinuria and was a risk factor of renal function deterioration. Moreover, urine glucose was easily to detect in clinical practice.
Fumonisin-containing diets decrease the metabolic activity of myenteric neurons in rats
Published in Nutritional Neuroscience, 2022
Fernando Carlos Sousa, Christiano Rodrigues Schamber, Eneri Vieira de Souza Leite Mello, Fernanda Andrade Martins, Miguel Machinski Junior, Cleverson Busso, Mario Henrique de Barros, Maria Raquel Marçal Natali
The blood parameters also did not indicate intense liver or kidney injury or signs of blood glucose disturbances. These data are consistent with Voss et al. [24], in which Fischer 344 rats were fed FB1-containing diets at doses of 1, 3, 9, 27, and 81 mg/kg, and blood parameters were assessed for 4 and 13 weeks. Only blood creatinine levels were significantly higher after 13 weeks of consuming the FB1-containing diet at doses greater than 27 mg/kg. However, the histopathological analysis revealed signs of nephrosis at doses above 9 mg/kg. Similarly, Gelderblom et al. [25] fed rats diets that contained FB1 at doses of 1, 10, and 25 mg/kg for 24 months and observed hepatic lesions at all doses tested and renal injury at the highest dose. However, a significant increase in plasma ALT levels was not detected, and significant increases in AST and creatinine levels were observed at doses of 10 and 25 mg/kg. Even at low doses, fumonisins can cause renal and hepatic injuries, but these mycotoxins tend to cause plasma alterations only at higher doses or with more prolonged periods of consumption compared with those in the present study. Therefore, the chronic ingestion of low doses of fumonisins, although it does not lead to the appearance of clinical signs of intoxication, can cause cellular alterations that can impair normal development of the organism.
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).