scholarly journals Renal Tubular Dysfunction of Vitamin-D Deficiency Rickets

Nephron ◽  
1996 ◽  
Vol 72 (2) ◽  
pp. 364-364 ◽  
Author(s):  
V. García Nieto ◽  
E. Sánchez Almeida ◽  
M. García García
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Deficiency Rickets ◽  
Renal Tubular

scholarly journals The association between serum vitamin D levels and renal tubular dysfunction in a general population exposed to cadmium in China

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195682 ◽  
Author(s):  
Xiao Chen ◽  
Yan Dai ◽  
Zhongqiu Wang ◽  
Guoying Zhu ◽  
Xiaoqiang Ding ◽  
...  
Keyword(s):  
Vitamin D ◽  
General Population ◽  
Serum Vitamin ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Serum Vitamin D ◽  
Vitamin D Levels ◽  
Renal Tubular

VITAMIN D DEPENDENCY: AN INHERITED POSTNATAL SYNDROME WITH SECONDARY HYPERPARATHYROIDISM

PEDIATRICS ◽  
1970 ◽  
Vol 46 (6) ◽  
pp. 871-880
Author(s):  
C. Arnaud ◽  
R. Maijer ◽  
T. Reade ◽  
C. R. Scriver ◽  
D. T. Whelan
Keyword(s):  
Vitamin D ◽  
Autosomal Recessive ◽  
Hypophosphatemic Rickets ◽  
First Year ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Recessive Trait ◽  
Daily Allowance ◽  
Renal Tubular ◽  
First Year Of Life

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.

RENAL TUBULAR DYSFUNCTION COMPLICATING THE NEPHROTIC SYNDROME

PEDIATRICS ◽  
1960 ◽  
Vol 26 (1) ◽  
pp. 75-85
Author(s):  
Gunnar B. Stickler ◽  
Alvin B. Hayles ◽  
Marschelle H. Power ◽  
John A. Ulrich
Keyword(s):  
Vitamin D ◽  
Nephrotic Syndrome ◽  
Metabolic Acidosis ◽  
Renal Insufficiency ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Renal Tubules ◽  
Renal Tubular ◽  
Amino Aciduria ◽  
Unusual Type

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.

Correction

PEDIATRICS ◽  
1961 ◽  
Vol 28 (1) ◽  
pp. 91-91
Keyword(s):  
Vitamin D ◽  
Nephrotic Syndrome ◽  
Fecal Excretion ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Total Intake ◽  
Renal Tubular

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."

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 ◽  
...  
Keyword(s):  
Vitamin D ◽  
Fibroblast Growth Factor 23 ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Fibroblast Growth ◽  
Phosphate Excretion ◽  
Legionella Pneumonia ◽  
Vitamin D Levels ◽  
Renal Tubular ◽  
Renal Phosphate Excretion

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.

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