Renal Handling of Calcium

Author(s):  
Wadi N. Suki
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):  

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.


2004 ◽  
Vol 93 (2) ◽  
pp. 262-272 ◽  
Author(s):  
Qing Li ◽  
Yoshimichi Sai ◽  
Yukio Kato ◽  
Hiromi Muraoka ◽  
Ikumi Tamai ◽  
...  

2021 ◽  
Vol 22 (11) ◽  
pp. 5809
Author(s):  
Jakub Gburek ◽  
Bogusława Konopska ◽  
Krzysztof Gołąb

Albumin is the main protein of blood plasma, lymph, cerebrospinal and interstitial fluid. The protein participates in a variety of important biological functions, such as maintenance of proper colloidal osmotic pressure, transport of important metabolites and antioxidant action. Synthesis of albumin takes place mainly in the liver, and its catabolism occurs mostly in vascular endothelium of muscle, skin and liver, as well as in the kidney tubular epithelium. Long-lasting investigation in this area has delineated the principal route of its catabolism involving glomerular filtration, tubular endocytic uptake via the multiligand scavenger receptor tandem—megalin and cubilin-amnionless complex, as well as lysosomal degradation to amino acids. However, the research of the last few decades indicates that also additional mechanisms may operate in this process to some extent. Direct uptake of albumin in glomerular podocytes via receptor for crystallizable region of immunoglobulins (neonatal FC receptor) was demonstrated. Additionally, luminal recycling of short peptides into the bloodstream and/or back into tubular lumen or transcytosis of whole molecules was suggested. The article discusses the molecular aspects of these processes and presents the major findings and controversies arising in the light of the research concerning the last decade. Their better characterization is essential for further research into pathophysiology of proteinuric renal failure and development of effective therapeutic strategies.


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