Evaluating the associations between urinary excretion of magnesium and that of other components in calcium stone-forming patients

2018 ◽  
Vol 51 (2) ◽  
pp. 279-284 ◽  
Author(s):  
Sanaz Tavasoli ◽  
Maryam Taheri ◽  
Fatemeh Taheri ◽  
Abbas Basiri ◽  
Fahimeh Bagheri Amiri
Keyword(s):  
Urinary Excretion ◽  
Calcium Stone

The Influence of Glucose and Crude Fibre (Wheat Bran) on the Rate of Intestinal 47Ca Absorption The Influence of Glucose and Wheat Bran on Calcium Absorption

1979 ◽  
Vol 65 (3) ◽  
pp. 143-146
Author(s):  
M. A. Macleod ◽  
N. J. Blacklock
Keyword(s):  
Urinary Excretion ◽  
Wheat Bran ◽  
Calcium Absorption ◽  
Normal Subjects ◽  
Calcium Balance ◽  
Theoretical Possibility ◽  
Crude Fibre ◽  
Calcium Stone ◽  
Negative Calcium Balance ◽  
Stone Formers

AbstractWith evidence of induction of increased urinary excretion of calcium by the ingestion of glucose and sucrose there is the theoretical possibility in these circumstances of at least a transient negative calcium balance. In this study the ingestion of glucose or glucose equivalent was found to stimulate 47Ca absorption from the intestine both in normal subjects and in idiopathic calcium stone formers. This induced increase in the rate of 47Ca absorption by glucose can be negated by the addition of crude fibre in the form of wheat bran.

Excretion of urine extracellular vesicles bearing markers of activated immune cells and calcium/phosphorus physiology differ between calcium kidney stone formers and non-stone formers

2020 ◽  
Author(s):  
Jiqing Zhang ◽  
Sanjay Kumar ◽  
Muthuvel Jayachandran ◽  
Stanley Wang ◽  
Elena M. Wilson ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Extracellular Vesicles ◽  
Immune Cells ◽  
Kidney Stone ◽  
Fibroblast Growth Factor 23 ◽  
Pathogenic Mechanisms ◽  
Calcium Stone ◽  
Phosphorus Excretion ◽  
Stone Formers ◽  
Calcium Phosphorus

Abstract Backgrounds: Previous studies have demonstrated that excretion of urinary extracellular vesicles (EVs) from different nephron segments differs between kidney stone formers and non-stone formers (NSFs), and could reflect pathogenic mechanisms of urinary stone disease. In this study we quantified selected populations of specific urinary EVs carrying protein markers of immune cells and calcium/phosphorus physiology in calcium stone formers (CSFs) compared to non-stone formers (NSFs). Methods Incident CSFs (n = 24) and age- and sex- matched NSFs (n = 21) were studied. Clinical data were abstracted and biobanked cell-free urine samples were used to quantify specific urinary EV populations. EVs carrying proteins related to renal calcium/phosphorus physiology (phosphorus transporters (PiT1 and PiT2), Klotho, and fibroblast growth factor 23 (FGF23)); markers associated with EV generation (anoctamin-4 (ANO4) and Huntington interacting protein 1 (HIP1)), and markers shed from activated immune cells were quantified by standardized and published method of digital flow cytometry. Results The urine pH of CSFs was lower than NSFs (P < 0.05), whereas urine excretion of calcium, phosphorus, and calcium oxalate and uric acid supersaturation (SS) were significantly higher in CSFs compared to NSFs (P < 0.05). Urinary excretion of EVs with markers of total leukocytes (CD45), neutrophils (CD15), macrophages (CD68), Klotho, FGF23, PiT1, PiT2, and ANO4 were each markedly lower in CSFs than NSFs (P < 0.05) whereas excretion of those with markers of monocytes (CD14), T-Lymphocytes (CD3), B-Lymphocytes (CD19), plasma cells (CD138 plus CD319 positive ) were not different between the groups. Urinary excretion of EVs expressing PiT1 and PiT2 negatively (P < 0.05) correlated with urinary phosphorus excretion whereas excretion of EVs expressing FGF23 correlated negatively (P < 0.05) with both urinary calcium and phosphorus excretion. Conclusions Urinary excretion of EVs derived from specific types of activated immune cells and EVs with proteins related to calcium/phosphorus regulation were different between CSFs and NSFs. Thus, further validation of these and other populations of urinary EVs could identify biomarkers that elucidate novel pathogenic mechanisms of calcium stone formation in specific subsets of patients.

THE RELATION BETWEEN THE URINARY EXCRETION OF CITRIC ACID AND CALCIUM; ITS IMPLICATIONS FOR URINARY CALCIUM STONE FORMATION

Science ◽  
1942 ◽  
Vol 96 (2504) ◽  
pp. 587-588 ◽  
Author(s):  
E. SHORR ◽  
T. P. ALMY ◽  
M. H. SLOAN ◽  
H. TAUSSKY ◽  
V. TOSCANI
Keyword(s):  
Citric Acid ◽  
Urinary Excretion ◽  
Stone Formation ◽  
Urinary Calcium ◽  
Calcium Stone

Urinary Excretion of Urate in Renal Calcium Stone Disease and in Renal Tubular Acidification Disturbances

1982 ◽  
Vol 127 (3) ◽  
pp. 589-592 ◽  
Author(s):  
Bengt Fellström ◽  
Ulla Backman ◽  
Bo G. Danielson ◽  
Gunnar Johansson ◽  
Sverker Ljunghall ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Stone Disease ◽  
Calcium Stone ◽  
Renal Tubular

Tryptophan-Niacin Metabolism in Rat with Puromycin Aminonucleoside-Induced Nephrosis

2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Enzyme Activities ◽  
Treated Group ◽  
Control Group ◽  
Puromycin Aminonucleoside ◽  
Low Level ◽  
Key Enzyme

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.

Cigarette Smoking Increases Thromboxane A2 Formation without Affecting Platelet Survival in Young Healthy Females

1992 ◽  
Vol 68 (05) ◽  
pp. 583-588 ◽  
Author(s):  
Annika Dotevall ◽  
Christina Rångemark ◽  
Elsa Eriksson ◽  
Jack Kutti ◽  
Hans Wadenvik ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cigarette Smoking ◽  
Blood Cell ◽  
Urinary Excretion ◽  
Life Span ◽  
Cell Count ◽  
Thromboxane A2 ◽  
Blood Cell Count ◽  
Platelet Activity ◽  
Pai 1

SummarySmoking is a risk factor for the development of atherosclerotic cardiovascular disease, in men as well as in women. An increased urinary excretion of the thromboxane metabolite 2,3-dinor-thromboxane B2 (Tx-M) has been observed in smokers of both genders, suggesting that cigarette smoking may facilitate cardiovascular disease via an action on the platelets. The present study addressed the hypothesis that the increased Tx-M excretion in female smokers reflects a true facilitation of platelet reactivity in vivo, rather than an increased destruction of the platelets. In healthy female volunteers (aged 20–46 years, 18 smokers and 17 non-smokers) platelet life-span and indices of platelet activity were determined, together with plasma levels of plasminogen activator inhibitor-1 (PAI-1), fibrinogen, peripheral blood cell counts and hematocrit. The urinary excretion of Tx-M was higher in smokers than in non-smokers (361 vs. 204 pg/mg creatinine, respectively, p <0.05), while plasma and urinary β-thromboglobulin, plasma platelet factor 4, platelet mean life-span and platelet production rate did not differ between the groups. PAI-1 activity, white blood cell count and hematocrit were higher in smokers than in non-smokers (p <0.05). These data indicate that smoking facilitates platelet formation of thromboxane A2 without affecting platelet survival; i.e. it increases the activity of platelets without affecting their viability to a measurable extent. Such an increase in platelet activity, operating in parallel to a reduced fibrinolytic activity and a higher hematocrit and white blood cell count, may play an etiological role in smoking-induced cardiovascular disease in women.

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