Renal Handling of Salt and Water, Discussed on the Basis of �a Central Dogma�

Author(s):  
E. Bojesen
Keyword(s):  
Diabetes ◽  
1997 ◽  
Vol 46 (5) ◽  
pp. 868-875 ◽  
Author(s):  
C. Catalano ◽  
E. Muscelli ◽  
A. Quinones Galvan ◽  
S. Baldi ◽  
A. Masoni ◽  
...  
Keyword(s):  

Neuron ◽  
2013 ◽  
Vol 80 (3) ◽  
pp. 648-657 ◽  
Author(s):  
Christine E. Holt ◽  
Erin M. Schuman

2016 ◽  
pp. 25-31
Author(s):  
David S. Goodsell
Keyword(s):  

1983 ◽  
Vol 72 (4) ◽  
pp. 440-443 ◽  
Author(s):  
Akira Kamiya ◽  
Katsuhiko Okumura ◽  
Ryohei Hori

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1959
Author(s):  
Flora O. Vanoni ◽  
Gregorio P. Milani ◽  
Carlo Agostoni ◽  
Giorgio Treglia ◽  
Pietro B. Faré ◽  
...  

Chronic alcohol-use disorder has been imputed as a possible cause of dietary magnesium depletion. The purpose of this study was to assess the prevalence of hypomagnesemia in chronic alcohol-use disorder, and to provide information on intracellular magnesium and on its renal handling. We carried out a structured literature search up to November 2020, which returned 2719 potentially relevant records. After excluding non-significant records, 25 were retained for the final analysis. The meta-analysis disclosed that both total and ionized circulating magnesium are markedly reduced in chronic alcohol-use disorder. The funnel plot and the Egger’s test did not disclose significant publication bias. The I2-test demonstrated significant statistical heterogeneity between studies. We also found that the skeletal muscle magnesium content is reduced and the kidney’s normal response to hypomagnesemia is blunted. In conclusion, magnesium depletion is common in chronic alcohol-use disorder. Furthermore, the kidney plays a crucial role in the development of magnesium depletion.


1995 ◽  
Vol 14 (6) ◽  
pp. 494-499 ◽  
Author(s):  
CJ Lote ◽  
JA Wood ◽  
A. Thewles ◽  
M. Freeman

The known toxicity of aluminium, and the toxicity of agents (such as desferrioxamine) used to remove alumini um from the body, has prompted us to investigate whether there may be ways of enhancing aluminium excretion by exploiting the normal renal handling of aluminium. Aluminium (as sulphate or citrate) was administered intravenously to conscious rats at doses ranging from 25 μg (0.93 μmol) to 800 μg (29.6 μmol) aluminium, and alu minium excretion was monitored over the following 2 h. Measurements of the filterability of aluminium from the rat plasma, and the glomerular filtration rate (inulin clearance), enabled us to calculate the filtered load of alu minium, and hence determine aluminium reabsorption. At all doses of administered aluminium, that adminis tered as sulphate was excreted less effectively than that administered as citrate. This difference was attributable to the much greater filterability of aluminium administered as citrate. However, for any given filtered load, the excre tion of aluminium administered as citrate was not signifi cantly different (in either fractional or absolute terms) from the excretion of aluminium administered as sulphate. It seems likely that, following aluminium sulphate administration, the filtered aluminium may be an alumini um citrate form which is then reabsorbed in the same way as aluminium administered as citrate. It is thus apparent that aluminium removal from the body could be further enhanced if it were possible to pre vent the tubular reabsorption of the aluminium species which is so effectively filtered following aluminium citrate administration.


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