Hyperphosphatemic tumoral calcinosis caused by FGF23 compound heterozygous mutations: what are the therapeutic options for a better control of phosphatemia
? Pediatr Nephrol 2018;33:1263-1267.
Nevertheless, after 5 months of TDF-treatment, normoglycemic glycosuria (glycemia 88 mg/dl, glycosuria 70 mg/dl), phosphaturia with hypophosphatemia (reduced tubular absorption of phosphorus (56%), phosphatemia
1.9 mg/dl, proteinuria (albuminuria 100 mg/dl at dipstick, proteinuria: 0.2 g/24 h), glomerular filtration rate (GFR) 70 ml/min/1.73 [m.sup.2], and urine creatinine 0.47 g/day were detected, leading to diagnosis of Fanconi Syndrome associated with TDF-therapy.
The protein fibroblast growth factor-23 (FGF-23) (5) and its coreceptor Klotho have attracted great attention in recent years and are currently recognized as playing a key role in the regulation of phosphatemia. FGF-23, a bone-derived hormone secreted in response to dietary phosphate intake, acts in the kidneys, increasing urinary phosphate excretion in a Klotho-dependent manner to maintain healthy phosphorus homeostasis.
These increases may represent a compensatory response to maintain normal phosphatemia or reflect an end organ resistance to the phosphaturic stimulus due to a renal Klotho deficiency.
Both alterations contributed to the increased CV risk observed in CKD patients with secondary hyperparathyroidism, a frequent complication resulting from the loss of the ability of the kidney to regulate phosphatemia
and synthesize calcitriol, the active form of vitamin D [4-6].
In poststroke subjects, even small increases in phosphatemia
are associated with increased bone resorption and decreased BSI, despite higher serum osteocalcin and calcium concentrations, both of which are negatively associated with eGFR.
There is evidence that in chronic dialysis patients haemodiafiltration (HDF) induces better control of phosphatemia
[1, 2] and lower [beta]2-microglobulin ([beta]2-m) blood levels [2, 3] with observed better clinical outcomes [4, 5].
In this stage patient has most of the manifestations of renal failure like hypertension, acidosis and hyper phosphatemia
. In end stage renal failure creatinine clearance is less than 5ml /min.
is closely connected with the content of urea in blood, the change of buffer base, the displacement of urine pH.
Certain cat's biochemical parameters such as glucemia (0.75-1.03 g/l), calcemia (8.2-10.7 mg/dl) and phosphatemia
(3.9-6.1 mg/dl) (5) were similar to the parameters found in P.
would be higher to those published on mammals (3-6 mg/dL, Kolb 1987; 3-8 mg/dL, Coles 1989; 2.6-6.9 mg/dL, Kaneko 1989, and 3-5.2 mg/dL, Coppo 2001).