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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
Adjunctive testing can be done to determine the severity and complications of nephrotic syndrome. Blood urea nitrogen (BUN) and creatinine levels can vary based on the amount of kidney dysfunction. The serum albumin is often below 2.5 g/dL (which is 25 g/L). There are usually increases in total cholesterol and triglycerides. Though not regularly required to be measured, there can also be low levels of alpha-globulins, gamma-globulins, hormone-binding proteins, immunoglobulins, ceruloplasmin, complement components, and transferrin.
Habitual Abortion
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Dwight D. Pridham, Christine L. Cook
Alpha globulin is very important in hemoglobin formation, as it is common to all normal hemoglobins except for several early embryonic types. Normal genomes contain four loci for this gene, two each on two homologous chromosomes. In mice, homozygosity for deletion of both loci is lethal during embryonic development. In humans, homozygosity for alpha thalassemia 1 (both alpha globulin loci inactive on the same chromosome) leads to fetal hydrops and death.48
The Basal Cell Nevus Syndrome
Published in Roger M. Browne, Investigative Pathology of the Odontogenic Cysts, 2019
Julia A. Woolgar, J. W. Rippin
In 1976, Rayner et al.17 reported low levels of alpha-globulins in syndrome patients, the main constituents of which are alpha 1-antitrypsin (alpha 1-globulin), and haptoglobin and alpha2-macroglobulin (alpha2-globulin). However, Gundlach and Kiehn39 reported normal levels of alpha-globulin, and Lindeberg et al.7 normal levels of the various constituents. Lindeberg et al.7 also found a number of immunological measures to be normal in syndrome patients.
Investigational plasma kallikrein inhibitors for the treatment of diabetic macular edema: an expert assessment
Published in Expert Opinion on Investigational Drugs, 2020
Ashay D. Bhatwadekar, Viral S. Kansara, Thomas A. Ciulla
Plasma kallikrein is a serine protease synthesized mainly in the liver as a proenzyme prekallikrein (PK). The mRNA for plasma kallikrein or PK is expressed in a variety of tissues such as the brain, heart, lung, kidneys, adrenal glands, pancreas, spleen, prostate glands, and ovaries. PK is also known as the Fletcher factor due to its involvement in the fletcher trait, a condition with markedly prolonged activated partial thromboplastin time (aPTT). PK is encoded by a single gene localized on a q34-q35 region of the long arm of chromosome 4 [32]. PK is a single chain gamma-globulin zymogen with a molecular weight of 85–88 kDa, and a plasma concentration of ~490 nM. The N terminal region of PK consists of four contagious repeats composed of 4 groups of 90–91 amino acids arranged in ‘apple domains’ (A1-A4), Figure 1. The N-terminal of the PK lacks intrinsic activity and mainly involved in the recruitment of certain proteins [33]. The majority of PK circulates in plasma as a complex with alpha globulin, high molecular weight kininogen (HK). The apple domains, A1 and A4, serve as binding sites for HK. The proteolytic processing of PK leads to activated plasma kallikrein via activated factor XII (αFXIIa) on the negatively charged surface, factor XII fragment (βFXIIa) in the fluid phase and prolycarboxypeptidase on endothelial cells. Plasma kallikrein then cleaves HK to liberate bradykinin. While bradykinin directly activates the B2 receptor, the cleavage of bradykinin by carboxypeptidase generates des-arg9 bradykinin (DABK) leads to activation of B1 receptors (Figure 2).
Beta-blockers in asthma: myth and reality
Published in Expert Review of Respiratory Medicine, 2019
Angelica Tiotiu, Plamena Novakova, Krzysztof Kowal, Alexander Emelyanov, Herberto Chong-Neto, Silviya Novakova, Marina Labor
Absorption of β-blockers depends on the route of administration with topical application leading to minimal systemic bioavailability [5,20,28–31]. As regular therapy of CVD, β-blockers are administered orally once daily, but in emergency situations, some β-blockers could be used intravenously with a rapid increase in their plasma concentration [32]. The absorption from the gastrointestinal tract occurs by passive diffusion [20,30,31]. In the blood, they circulate and bind to plasma albumins and alpha-globulins but the ratio of bound to free fraction is variable for different β-blockers (i.e. 90% for sotalol, 20% for propranolol) [30,31]. Lipid-soluble β-blockers (labetalol, metoprolol, pindolol, propranolol) depend upon hepatic metabolism for clearance, whereas water-soluble β-blockers (atenolol) are cleared by the kidney, usually as an unchanged form [30].
Amyloid cardiomyopathy: a hidden heart failure cause that is often misdiagnosed
Published in Acta Clinica Belgica, 2018
Yale Tung-Chen, Miguel-Ángel Arnau
During the following days, laboratory results came up, showing ESR 9 mm/h [normal: 1–7], CRP 4 mg/dL [0–5], TSH 1.346 mU/L [0.4–4.0], D-dimer 242 ng/mL [<500], NT pro-BNP 2617 pg/mL [<400]. Serum protein electrophoresis (albumin 3.70 g/dL [3.3–5.7], alpha-1 globulin 0.23 [0.1–0.4], alpha-2 globulin 0.49 g/dL [0.3–0.9], beta globulin 1.4 g/dL [0.7–1.5], gamma globulin 1.5 g/dL [0.5–1.4]), serum immunofixation, Immunoglobulins (IgA 214 mg/dL [70–400], IgM 79 mg/dL [40–230], IgG 1,200 mg/dL [700–1,600]), and free light chain assay (Kappa 20.8 mg/L [3.3–19.4], Lambda 23.1 mg/L [5.7–26.3], ratio 0.90 [0.26–1.65]) were unremarkable. No proteinuria, urinary free light chain excretion, and immunofixation were detected. The rest of laboratory tests were normal.