FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W159999462> ?p ?o ?g. }

• W159999462 endingPage "41" @default.
• W159999462 startingPage "228" @default.
• W159999462 abstract "At present the pathogenesis of diabetic nephropathy remains unresolved. Clearly lack of insulin, with its associated disorders of carbohydrate, protein, and/or lipid metabolism, initiates the process which eventually leads to the characteristic histologic picture of diabetic nephropathy. The disturbance in cellular metabolism per se could directly injure the kidney by altering the energy needs of the cell or by leading to the accumulation of cellular toxins (ie, polyols) or by causing the deficiency of key cellular metabolites (ie, myoinositol). Elevation of the plasma glucose concentration enhances the glycosylation of proteins, which in turn can lead to glomerular basement membrane thickening, loss of charge selectivity, and direct cellular damage. The multiple disturbances in intermediary metabolism are associated with increased levels of and/or enhanced sensitivity to a variety of growth factors, including IGF-I and angiotensin, and this could lead to glomerular hypertrophy. An increase in the filtered load and subsequent reabsorption of electrolytes and metabolites also could contribute to renal hypertrophy. In all animal models of nephropathy, including diabetes, glomerular hypertrophy has been shown to be the best correlate of glomerular sclerosis, proteinuria, and progressive renal deterioration. The potential mechanisms by which glomerular hypertrophy can lead to renal histologic damage were discussed previously. By increasing the luminal diameter, glomerular hypertrophy also would be expected to augment wall tension and thereby increase intraglomerular pressure. Derangements in cellular metabolism or altered sensitivity to angiotensin also can directly elevate the intraglomerular pressure and lead to structural renal damage. In this schema, elevated intraglomerular pressure is but one of many pathogenic factors that contribute to the development of diabetic glomerulopathy and albuminuria. The precise role of increased glomerular pressure in the evolution of diabetic nephropathy remains uncertain at present. In rats, severe diabetic nephropathy can occur without an increase in Pgc, while in humans, hyperfiltration does not appear to be a predictor of proteinuria and renal dysfunction. Lastly, it is likely that a variety of other factors, including the coagulation system, plasma/cell lipid levels, prostaglandins, etc, also play a role in the pathogenesis of diabetic nephropathy. According to the outline presented in Figure 1, it is unlikely that any single factor will be sufficient to explain the development of diabetic glomerulosclerosis. Ultimately, the origin of diabetic nephropathy in IDDM must be traced to insulin lack, with its associated derangements in cellular metabolism. Therefore, the importance of tight glucose control should not be underemphasized.(ABSTRACT TRUNCATED AT 400 WORDS)" @default.
• W159999462 created "2016-06-24" @default.
• W159999462 creator A5028011804 @default.
• W159999462 creator A5085001520 @default.
• W159999462 creator A5091912602 @default.
• W159999462 date "1990-05-01" @default.
• W159999462 modified "2023-09-23" @default.
• W159999462 title "Hyperfiltration and diabetic nephropathy: is it the beginning? Or is it the end?" @default.
• W159999462 cites W1261423890 @default.
• W159999462 cites W1269748144 @default.
• W159999462 cites W141724131 @default.
• W159999462 cites W1519162988 @default.
• W159999462 cites W1590233037 @default.
• W159999462 cites W1964377393 @default.
• W159999462 cites W1964676918 @default.
• W159999462 cites W1967429137 @default.
• W159999462 cites W1969495982 @default.
• W159999462 cites W1970672884 @default.
• W159999462 cites W1978891183 @default.
• W159999462 cites W1980244877 @default.
• W159999462 cites W1980575557 @default.
• W159999462 cites W1982291941 @default.
• W159999462 cites W1983790228 @default.
• W159999462 cites W1984861596 @default.
• W159999462 cites W1985085196 @default.
• W159999462 cites W1985133368 @default.
• W159999462 cites W1987101515 @default.
• W159999462 cites W1989721148 @default.
• W159999462 cites W1990708942 @default.
• W159999462 cites W1992286264 @default.
• W159999462 cites W1996485736 @default.
• W159999462 cites W1996618703 @default.
• W159999462 cites W2000958826 @default.
• W159999462 cites W2006473120 @default.
• W159999462 cites W2009251691 @default.
• W159999462 cites W2009974525 @default.
• W159999462 cites W2010451625 @default.
• W159999462 cites W2013073525 @default.
• W159999462 cites W2014606909 @default.
• W159999462 cites W201899596 @default.
• W159999462 cites W2021813090 @default.
• W159999462 cites W2022230104 @default.
• W159999462 cites W2023377229 @default.
• W159999462 cites W2027318170 @default.
• W159999462 cites W2031534703 @default.
• W159999462 cites W2032931290 @default.
• W159999462 cites W2036294140 @default.
• W159999462 cites W2040724816 @default.
• W159999462 cites W2042204992 @default.
• W159999462 cites W2043184584 @default.
• W159999462 cites W2044102243 @default.
• W159999462 cites W2044731824 @default.
• W159999462 cites W2045134192 @default.
• W159999462 cites W2045261889 @default.
• W159999462 cites W2052865379 @default.
• W159999462 cites W2053221035 @default.
• W159999462 cites W2059343329 @default.
• W159999462 cites W2059571085 @default.
• W159999462 cites W2063928700 @default.
• W159999462 cites W2069142242 @default.
• W159999462 cites W2069375794 @default.
• W159999462 cites W2077255594 @default.
• W159999462 cites W2081955935 @default.
• W159999462 cites W2083314447 @default.
• W159999462 cites W2084523333 @default.
• W159999462 cites W2086234557 @default.
• W159999462 cites W2087129314 @default.
• W159999462 cites W2090893037 @default.
• W159999462 cites W2091802771 @default.
• W159999462 cites W2094100703 @default.
• W159999462 cites W2127172990 @default.
• W159999462 cites W2136898798 @default.
• W159999462 cites W2143006777 @default.
• W159999462 cites W2145989568 @default.
• W159999462 cites W2152582537 @default.
• W159999462 cites W2153708025 @default.
• W159999462 cites W2168234252 @default.
• W159999462 cites W2170707143 @default.
• W159999462 cites W2174290215 @default.
• W159999462 cites W2175650968 @default.
• W159999462 cites W2186098454 @default.
• W159999462 cites W2216421071 @default.
• W159999462 cites W2231812784 @default.
• W159999462 cites W2260136722 @default.
• W159999462 cites W2264139579 @default.
• W159999462 cites W2268804050 @default.
• W159999462 cites W2270243128 @default.
• W159999462 cites W2326515685 @default.
• W159999462 cites W2332239235 @default.
• W159999462 cites W2337023833 @default.
• W159999462 cites W2400965286 @default.
• W159999462 cites W2405081937 @default.
• W159999462 cites W2407838112 @default.
• W159999462 cites W2411576775 @default.
• W159999462 cites W2414146551 @default.
• W159999462 cites W2414324190 @default.
• W159999462 cites W2429630160 @default.
• W159999462 cites W2439650917 @default.

• next