scholarly journals Relationship of spot urine oxalate to creatinine ratio and 24 hours urinary oxalate excretion in patients with urolithiasis

2020 ◽  
Vol 60 ◽  
pp. 330-333
Author(s):  
Syed Bilal Hashmi ◽  
Lena Jafri ◽  
Hafsa Majid ◽  
Jamsheer Talati ◽  
Wajahat Aziz ◽  
...  
PEDIATRICS ◽  
1994 ◽  
Vol 94 (5) ◽  
pp. 674-678 ◽  
Author(s):  
Thomas Campfield ◽  
Gregory Braden ◽  
Patrecia Flynn-Valone ◽  
Nathaniel Clark

Objective. To study urinary oxalate excretion in infants fed human milk versus formula, and to compare urinary calcium oxalate and calcium phosphate saturation in premature infants with term infants and adults. Methodology. We measured urinary oxalate-to-creatinine ratio and urinary oxalate concentration in 15 premature infants fed human milk compared to 16 formula-fed premature infants, and in eight human milk-fed term infants compared to 17 formula-fed term infants. We then studied urinary calcium oxalate and calcium phosphate saturations based on our observations of elevated urinary oxalate excretion in premature infants. Urinary calcium oxalate and calcium phosphate saturations were calculated from urinary concentrations of oxalate, calcium, sodium, potassium, chloride, uric acid, magnesium, phosphorus, and urinary pH. We calculated urinary calcium oxalate and calcium phosphate saturations in nine healthy adults and nine formula-fed term infants to establish control values for urinary saturation. Urinary calcium oxalate and calcium phosphate saturations were determined in nine premature infants receiving a glucose and electrolyte solution, 11 premature infants receiving parenteral nutrition, nine formula-fed premature infants, and 11 human milk-fed premature infants. Results. Urinary oxalate excretion was higher in formula-fed compared to human milk-fed premature infants whether expressed as oxalate-to-creatinine ratio (0.32 ± 0.04 versus 0.18 ± 0.03, P < .01) or urinary oxalate concentration (0.047 ± 0.007 versus 0.022 ± 0.002 mg/mL, P < .01). Urinary oxalate excretion was higher in formula-fed term infants than in human milk-fed term infants whether expressed as oxalate-to-creatinine ratio (0.14 ± 0.01 versus 0.07 ± 0.01, P < .01) or urinary oxalate concentration (0.022 ± 0.002 versus 0.012 ± 0.002 mg/mL, P < .01). The urinary calcium oxalate saturation in healthy adults was 2.84 ± 0.79; the value in formula-fed term infants was 2.12 ± 0.31. The urinary calcium oxalate saturation was significantly higher in premature infants receiving formula (15.68 ± 3.15), human milk (15.02 ± 2.27), or parenteral nutrition (11.38 ± 2.56) compared to adults or term infants (P < .01). Urinary calcium oxalate saturation in premature infants receiving a glucose and electrolyte solution (2.45 ± 0.36) was not significantly different from that in adults or term infants. In contrast, urinary calcium phosphate saturation in premature infants as well as term infants and adults was less than 1; precipitation of calcium phosphate is not likely to occur under these conditions. Conclusion. Formula-fed infants have higher urinary oxalate excretion than human milk-fed infants. Premature infants receiving standard nutritional regimens may have urinary calcium oxalate saturation levels at which dissolved calcium oxalate may form nuclei of its solid phase.


Author(s):  
J. C. Dijcker ◽  
E. A. Hagen-Plantinga ◽  
D. G. Thomas ◽  
Y. Queau ◽  
V. Biourge ◽  
...  

1995 ◽  
Vol 269 (3) ◽  
pp. E568-E574 ◽  
Author(s):  
R. P. Holmes ◽  
C. H. Hurst ◽  
D. G. Assimos ◽  
H. O. Goodman

Factors that influence hepatic oxalate synthesis are poorly defined. Hormones are important regulators of hepatic metabolism and could potentially be involved. The effects of hyperglucagonemia were examined in guinea pigs injected with either saline or pharmacological doses of glucagon for 4 days. Glucagon treatment increased mean urinary oxalate excretion by 77% in male and 34% in female animals. The levels of hepatic peroxisomal enzymes involved in oxalate synthesis declined with glucagon treatment, but experiments with isolated peroxisomes indicated that oxalate synthesis in vitro was unaffected. Glucagon decreased hepatic alanine levels by 66%, lactate by 69%, and pyruvate by 73%, but glycolate and glyoxylate levels were unaffected. This decrease in alanine would substantially lower the activity of alanine-to-glyoxylate aminotransferase activity in vivo and make more glyoxylate available for oxalate synthesis. The decrease in lactate and pyruvate concentrations would stimulate the enzymatic conversion of glyoxylate to oxalate and may account for the increase in oxalate synthesis without an increase in glyoxylate concentration. These results demonstrate that hepatic oxalate synthesis is influenced by metabolic changes and that alterations in hepatic alanine, lactate, and pyruvate concentrations may be important elements.


1988 ◽  
Vol 15 (3-4) ◽  
pp. 264-270 ◽  
Author(s):  
Teruhiro Nakada ◽  
Isoji Sasagawa ◽  
Hidekatsu Furuta ◽  
Takashi Katayama ◽  
Jun Shimazaki

2002 ◽  
Vol 35 (6) ◽  
pp. 669-675 ◽  
Author(s):  
J.L. Nishiura ◽  
L.A. Martini ◽  
C.O.G. Mendonça ◽  
N. Schor ◽  
I.P. Heilberg

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