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Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Inhibition of ferrochelatase activity localized only in mitochondria is connected with chronic lead toxicity.161 Inhibition of this enzyme causes accumulation of iron pigments in mitochondria of the bone marrow. Lead poisoning also results in chronic mitochondrial lesion in kidney tubules, associated with the Fanconi syndrome due to intoxication.3 Cardiac myopathy brought about by cobalt ingestion results in chronic defects of heart mitochondria involving pyruvate decarboxylase activity.
Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Glucagon is ketogenic as well as hyperglycemic. It also activates adipose tissue lipase. It inhibits sodium resorption by the kidney tubules. It activates adenylate cyclase in the cardiocytes and increases both cardiac contractility and rate.
Renal Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
To summarize, pathological findings in severely cadmium-poisoned workers include damage to the proximal renal tubules, sometimes associated with glomerular damage. In several cases proteinuria was found without morphological changes, but there were no cases with the opposite picture. Apparently the functional changes in the kidney can occur before the microscopic structure of the kidney cells is severely damaged. On the other hand, the human data on pathological changes are limited and animal data (Section IV.A.4) show that in some studies morphological changes in the kidney tubules emerge before measurable proteinuria. When a person suffers severe renal damage through the toxic action of cadmium, his kidney concentration of cadmium will decrease considerably. Thus, he may have lower levels in the kidneys than a person with only slight or no renal dysfunction.
A new role for an old drug: acetazolamide in decompensated heart failure
Published in Expert Opinion on Pharmacotherapy, 2023
Like acetazolamide, the thiazide diuretics have an alternative mechanism of action to the loop diuretics. The thiazide diuretics inhibit the Na+/Cl− cotransporter in the distal convoluted kidney tubule, to induce a natriuresis. However, the extra sodium in the kidney tubule can trigger K+ loss, and to prevent this, the dose of the thiazide diuretic must be limited. The thiazide metolazone has been added to furosemide in a retrospective trial of 132 subjects with acute heart failure and shown to produce a better diuretic response and improve congestion score than furosemide alone, without causing hypokalaemia [11]. Thus, the thiazides should be considered as an alternative to acetazolamide as an add-on to loop diuretics in the treatment of acute decompensated heart failure.
The anti-hypertensive effects of sodium-glucose cotransporter-2 inhibitors
Published in Expert Review of Cardiovascular Therapy, 2023
Luxcia Kugathasan, Lisa Dubrofsky, Andrew Advani, David Z.I. Cherney
Low-affinity, high-volume SGLT2 is postulated to account for 80–90% of the filtered glucose reabsorbed in the kidney proximal tubule of healthy individuals [64,65]. Under physiological conditions, it is estimated that 5% of total reabsorbed sodium in the kidney tubule corresponds to SGLT2 activity [65,66]. An increase in SGLT2 mRNA expression of up to 36% in the proximal tubule epithelium has been observed in hyperglycemic states. Consequently, in the setting of hyperglycemia in individuals with diabetes mellitus, SGLT2 can account for up to 14% of the total renal sodium reabsorption [67,68]. SGLT2 inhibitor use leads to glucosuria-linked reductions in glycated hemoglobin (HbA1c) by 0.6–0.8% in patients with T2D, and reductions in body weight by 2–3 kg [69]. The mechanisms responsible for the antihypertensive effects of SGLT2 inhibitors are unclear. The interplay of natriuresis, loop diuresis, and vascular function changes with SGLT2 inhibitors has been proposed to be responsible for BP lowering [70].
Effects of contralateral nephrectomy timing and ischemic conditions on kidney fibrosis after unilateral kidney ischemia-reperfusion injury
Published in Renal Failure, 2022
Junhua Zhang, Ruihua Shen, Hui Lin, Juan Pan, Xinyuan Feng, Ling Lin, Dan Niu, Yanjuan Hou, Xiaole Su, Chen Wang, Lihua Wang, Xi Qiao
Neutral formalin-fixed kidney tissues were routinely dehydrated, embedded in paraffin, sectioned (3 μm) and stained with HE to observe the damage of kidney tissues. Ten randomly selected fields of the kidney cortex of each section were captured with light microscopy at 400× magnification. Two pathologists scored the injury to the glomerulus and kidney tubules separately. The tubular injury was scored on a scale of 0–4 using the following criteria [17]: 0, no injury; 1, affecting 1–25% of the kidney area; 2, affecting 26–50% of the kidney area; 3, affecting 51–75% of the kidney area; and 4, affecting 75–100% of the kidney area. The degree of tubular injury was evaluated semi-quantitatively by calculating the area of kidney tubular injury. The glomerular injury was evaluated and scored on a scale of 0–4 according to the percentage area of mesangial expansion or sclerosis using the following criteria [17]: 0, normal glomeruli; 1, 1–25% of area injured; 2, 26–50% of area injured; 3, 51–75% of area injured; and 4, 76–100% of area injured. The final glomerular damage score = 0 × (% grade 0 glomeruli) + 1 × (% grade 1 glomeruli) + 2 × (% grade 2 glomeruli) + 3 × (% grade 3 glomeruli) + 4 × (% grade 4 glomeruli). More than 50 glomeruli were scored per mouse.