Academic literature on the topic 'Hypoproteinemia'

Abstract ZEN MACROBIOTIC DIETS Developed by George Ohsawa in the early 1960s. Based on the misconception that human diseases were unnecessary and could be prevented by diets consisting of unpolished brown rice. Some of the diets included some kinds of vegetables. Nutritionists claim that strict adherence to the Zen diets will result in severe malnutrition in the form of scurvy, anemia, hypoproteinemia, and emaciation qq.v.

Patients with glomerular diseases develop a wide variety of biochemical disturbances and pathophysiologic alterations leading to overt clinical manifestations (Remuzzi, 1993; Glassock et al., 1995, Remuzzi and Bertani, 1998; Schrier and Fassett, 1998; Vaziri, 2003; Floege and Feehally, 2007; Kim et al., 2007; Haraldsson et al., 2008). These occur as a direct result of injury to the capillary wall and disturbances in normal glomerular function, including loss of filtration capacity and excessive transfer of erythrocytes and/or plasma proteins from blood to tubular lumina eventuating in hematuria and/or proteinuria. Proteinuria—which is believed to be the consequence of disturbed glomerular capillary wall permselectivity (Haraldsson et al., 2008) —when substantial, can lead to hypoproteinemia and thereby to a reduction in plasma oncotic pressure. Changes in the synthesis, turnover, and plasma concentration of various proteins and lipids develop and can lead to an imbalance of pro-thrombotic and anti-thrombotic factors promoting a ‘thrombophilic’ state (Vaziri, 2003; Crew et al., 2004; Glassock, 2007) Disturbances in the renal handling of sodium chloride (NaCl) and water are often associated with edema formation and/or hypertension (Perico and Remuzzi, 1993; Schrier and Fassett, 1998). Finally, the rapid or slow loss of the glomerular filtration capacity (glomerular filtration rate, GFR) due to damage of single nephrons (perhaps mediated by filtered proteins and their reabsorption) as well as by the ‘drop out’ of functioning nephrons from the overall population of nephrons in the two kidneys is responsible for ultimate progression to end-stage renal disease (ESRD) in many, but not all, of the primary glomerular disorders (Drummond et al., 1994; Remuzzi and Bertani, 1998; Squarer, et al., 1998; Floege and Feehally, 2007). Collectively these abnormalities give rise to ‘syndromes’ of glomerular disease. These ‘syndromes’ can be arbitrarily, but usefully, grouped into five categories which may overlap to some degree; namely, the acute nephritic syndrome, rapidly progressive glomerulonephritis, the nephrotic syndrome, ‘symptomless’, haematuria and/or proteinuria, and slowly progressive ‘chronic’ nephritis (Glassock et al., 1995). The cardinal features of these syndromes and the diseases to which they are most closely associated are discussed in this monograph. This monograph will deal largely with those glomerular diseases which primarily affect the kidneys and in which the extra-renal manifestations are the consequence of the impairment or disturbance of kidney function itself (the so-called primary glomerular diseases).