scholarly journals Two Cases of Hypophosphatemia with Increased Renal Phosphate Excretion in Legionella Pneumonia

2016 ◽  
Vol 6 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Shuhei Watanabe ◽  
Keiji Kono ◽  
Hideki Fujii ◽  
Kentaro Nakai ◽  
Shunsuke Goto ◽  
...  

We encountered 2 cases of hypophosphatemia due to Legionella pneumonia. Both cases showed increased urinary phosphate excretion and renal tubular dysfunction, which ameliorated with recovery from Legionella pneumonia. Serum fibroblast growth factor-23 level was suppressed, whereas serum 1,25(OH)2 vitamin D and parathyroid hormone levels were normal. Delayed elevation of serum 1,25(OH)2 vitamin D levels was observed with improvement in renal tubular function. These findings suggested hypophosphatemia might be mediated by renal tubular dysfunction.

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195682 ◽  
Author(s):  
Xiao Chen ◽  
Yan Dai ◽  
Zhongqiu Wang ◽  
Guoying Zhu ◽  
Xiaoqiang Ding ◽  
...  

PEDIATRICS ◽  
1970 ◽  
Vol 46 (6) ◽  
pp. 871-880
Author(s):  
C. Arnaud ◽  
R. Maijer ◽  
T. Reade ◽  
C. R. Scriver ◽  
D. T. Whelan

Three French-Canadian children in a large inbred pedigree each developed hypocalcemic, hypophosphatemic rickets in the latter half of their first year of life; there were also manifestations of generalized renal tubular dysfunction. These abnormalities, which mimic advanced Vitamin D deficiency, disappeared only when Vitamin D2 or D3 was given at about 100 times the recommended daily allowance; this indicated the diagnosis of Vitamin D dependency. Enamel hypoplasia was a prominent clinical finding; only those teeth which calcify postnatally were affected, indicating that the condition found does not affect Vitamin D-dependent nutrition in utero. The level of parathyroid hormone was elevated in serum before treatment; it fell to normal either after treatment with Vitamin D, or during intravenous infusion with a calcium solution sufficient to produce hypercalcemia. Vitamin D dependency appeared to be inherited as an autosomal recessive trait in this pedigree, but we could observe no phenotypic signs in presumably obligate heterozygotes. One of the three cases in the pedigree arose from outbreeding, suggesting that the mutant allele is probably not particularly rare in the population under our surveillance.


PEDIATRICS ◽  
1960 ◽  
Vol 26 (1) ◽  
pp. 75-85
Author(s):  
Gunnar B. Stickler ◽  
Alvin B. Hayles ◽  
Marschelle H. Power ◽  
John A. Ulrich

Observations on two girls in whom an unusual type of chronic renal insufficiency developed many months after the onset of nephrotic syndrome are reported. Each patient became free of edema in spite of persistent massive proteinuria. Growth was retarded and rickets and attacks of tetany developed. The chemical disturbances of the blood were characterized by hypocalcemia, hypokalemia, azotemia and metabolic acidosis. Hyposthenuria, proteinuria, amino-aciduria, and minimal erythrocyturia, cylindruria and glycosuria were present. Healing of the rickets and cessation of attacks of tetany followed the administration of vitamin D and calcium salts. Prednisone was administered to one patient and thereafter proteinuria decreased and renal tubular function improved. Both girls are relatively asymptomatic 11 and 9 years after the onset of nephrotic syndrome, although they are rather small and still have evidence of renal disease. It is possible that cells of the renal tubules have been damaged as a result of prolonged massive proteinuria.


PEDIATRICS ◽  
1961 ◽  
Vol 28 (1) ◽  
pp. 91-91

An error appeared in the article entitled "Renal Tubular Dysfunction Complicating the Nephrotic Syndrome," by Stickler et al., in Pediatrics, 26:75, 1960. In Figure 7, page 82, the fecal excretion of phosphorus (hatched area) for Period 7 is plotted incorrectly. The value should be 0.109 gm (not 0.6 as shown). The following statement in the text on page 84 is correct: "In Case 2, after the administration of vitamin D (Period 7), 63% of the total intake of phosphorus was excreted in the urine and only 10% of the phosphorus was excreted in the stool."


Nephron ◽  
1996 ◽  
Vol 72 (2) ◽  
pp. 364-364 ◽  
Author(s):  
V. García Nieto ◽  
E. Sánchez Almeida ◽  
M. García García

2020 ◽  
Vol 33 (8) ◽  
pp. 1065-1071
Author(s):  
Marjan Jeddi ◽  
Maryam Heidari ◽  
Neda Hatami ◽  
Gholam Hossein Ranjbar Omrani

AbstractObjectivesPhosphate is essential for skeletal mineralization, which is regulated by parathyroid hormone, calcitriol and fibroblast growth factor 23 (FGF23). Serum phosphate is physiologically higher in younger children, but factors that contribute to this physiological state are poorly understood. This study aimed to evaluate phosphate and its regulators in children compared with adults.Materials and methodsThe participants were children aged 3–11 years and adults older than 20 years of age. Biochemical parameters including calcium, phosphorus, alkaline phosphatase, FGF23, and vitamin D were measured. Fractional excretion of phosphate was calculated, using serum and urine phosphate and creatinine.ResultsThis cross-sectional study was conducted on 45 children (mean age: 9.0 ± 2.1) and 44 adults (mean age: 38.9 ± 11.1). The children had higher serum calcium, phosphate, alkaline phosphatase, and FGF23 (p < 0.001), but fractional excretion of phosphate was greater in adults (14.1 ± 5.7, 11.4 ± 4.4, p = 0.019, 95% confidence interval [CI]: −0.7 to −0.2). Of all individuals, 61.8% had vitamin D deficiency. By multiple regression analysis, entering age, calcium, phosphate, and vitamin D level, the only independent predictor of FGF23 was 1, 25 dihydroxy-vitamin D3 (β: 0.78, p < 0.001, 95% CI: 0.5–1.1, R2: 0.59 for children, and β: 0.59, p < 0.001, 95% CI: 0.5–1.4, R2: 0.45 for adults).ConclusionAs far as we know, there is little information regarding the role of FGF23 in physiologic state. In this cross-sectional study no association was found between FGF23 and urinary phosphate excretion in growing children. Further studies with more detail are essential to evaluate phosphate homeostasis during childhood.


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