scholarly journals Testosterone increases urinary calcium excretion and inhibits expression of renal calcium transport proteins

2010 ◽  
Vol 77 (7) ◽  
pp. 601-608 ◽  
Author(s):  
Yu-Juei Hsu ◽  
Henrik Dimke ◽  
Joost P.H. Schoeber ◽  
Shih-Che Hsu ◽  
Shih-Hua Lin ◽  
...  
Keyword(s):  
Calcium Transport ◽  
Urinary Calcium ◽  
Transport Proteins ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Renal Calcium Transport

scholarly journals Effects of furosemide on renal calcium handling

2007 ◽  
Vol 293 (4) ◽  
pp. F1231-F1237 ◽  
Author(s):  
Chien-Te Lee ◽  
Hung-Chun Chen ◽  
Li-Wen Lai ◽  
Kim-Chong Yong ◽  
Yeong-Hau H. Lien
Keyword(s):  
Calcium Transport ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Immunofluorescent Staining ◽  
Calcium Excretion ◽  
Mrna Levels ◽  
Calbindin D9k ◽  
Calbindin D28k ◽  
Transport Molecules ◽  
Renal Calcium Excretion

Furosemide is a loop diuretic agent that has been used to treat hypercalcemia because it increases renal calcium excretion. The effect of furosemide on calcium transport molecules in distal tubules has yet to be investigated. We conducted studies to examine the effects of furosemide on renal calcium excretion and expression of calcium transport molecules in mice. Mice were administered with a single dose of furosemide (15 mg/kg) and examined 4 h later or were given twice-daily furosemide injections for 3 days. To evaluate the effects of volume depletion, drinking water was supplemented with salt. Our results showed that, in acute experiments, furosemide enhanced urinary calcium excretion, which was associated with a significant increase in mRNA levels of TRPV5, TRPV6, and calbindin-D28k but not calbindin-D9k as measured by real-time PCR (TRPV5 and TRPV6 are transient receptor potential vanilloid 5 and 6). Chronic furosemide administration induced three- to fourfold increases in urinary calcium excretion and elevated mRNA levels of TRPV5, TRPV6, calbindin-D28k, and calbindin-D9k without or with salt supplement. Similar upregulation of calcium transport molecules was observed in mice with gentamicin-induced hypercalciuria. Coadministration of chlorothiazide decreased furosemide-induced calciuria, either acutely or chronically, although still accompanied by upregulation of these transport molecules. Immunofluorescent staining studies revealed comparably increased protein abundance in TRPV5 and calbindin-D28k. We conclude that furosemide treatment enhances urinary calcium excretion. Increased abundance of calcium transport molecules in the distal convoluted tubule represents a solute load-dependent effect in response to increased calcium delivery and serves as a compensatory adaptation in the downstream segment.

Effects of excess protein, sodium and potassium on acute and chronic urinary calcium excretion in young women

1998 ◽  
Vol 18 (3) ◽  
pp. 475-487 ◽  
Author(s):  
Susan J Whiting ◽  
Timothy J Green ◽  
Evelyn P MacKenzie ◽  
Shawna J Weeks
Keyword(s):  
Young Women ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Sodium And Potassium

Adolescents with anorexia nervosa have decreased calcium absorption and increased urinary calcium excretion

1991 ◽  
Vol 12 (2) ◽  
pp. 171
Author(s):  
Steven A. Abrams ◽  
Tomas J. Silber ◽  
Nora V. Esteban ◽  
Nancy E. Vieira ◽  
Mansoud Majd ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Calcium Absorption ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion

Determinants and outcomes associated with urinary calcium excretion in chronic kidney disease

2021 ◽  
Author(s):  
Jing Liu ◽  
Maria Clarissa Tio ◽  
Ashish Verma ◽  
Insa M Schmidt ◽  
Titilayo O Ilori ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Atherosclerotic Cardiovascular Disease ◽  
Clinical Events ◽  
Males And Females ◽  
End Stage ◽  
Egfr Decline

Abstract Context Abnormalities in calcium metabolism are common in chronic kidney disease (CKD). Diminished urinary calcium excretion may promote vascular calcification, and increased urinary calcium excretion may lead to nephrolithiasis and nephrocalcinosis, conditions associated with CKD. Objective To study predictors of urinary calcium excretion and its association with adverse clinical outcomes in CKD. Design, Setting and Patients This study assessed 3,768 non-dialysis participants in the Chronic Renal Insufficiency Cohort study from April 2003 to September 2008. Participants were followed up to October 2018. Exposure Clinically plausible predictors of urinary calcium excretion and 24-hour urinary calcium excretion at baseline. Main Outcome Measures Urinary calcium excretion; incident end stage kidney disease (ESKD), CKD progression (50% estimated glomerular filtration rate (eGFR) decline or incident ESKD), all-cause mortality, and atherosclerotic cardiovascular disease events. Results eGFR was positive correlated with 24-hour urinary calcium excretion. The variables most strongly associated with 24-hour urinary calcium excretion were 24-hour urinary sodium (β=0.19 and 0.28 in males and females), serum parathyroid hormone (β=-0.22 and -0.20), loop diuretics (β=0.36 and 0.26), thiazide diuretics (β=-0.49 and -0.53), and self-identified black race (β=-0.23 and -0.27). Lower urinary calcium excretion was associated with greater risks of outcomes, but these associations were greatly attenuated or nullified after adjustment for baseline eGFR. Conclusion Urinary calcium excretion is markedly lower in individuals with CKD compared to general population. Determinants of urinary calcium excretion differed between sexes and levels of CKD. Significant associations between urinary calcium excretion and adverse clinical events were substantially confounded by eGFR.

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