High calcium level-help!

[Guest guest]

Hi, my child at age of 10, have persistent high in calcium in last year. But

this calcium level is tested under element-erythrocytes with ION profile from

Metametrix.

Calcium raised from 46ppm to 55ppm (ref is 24-65ppm)from Mar 2011 to Aug 2011 in

5 months.

There is a remark indicating :

**Relevant to membrane permeability,not nutritional status.

But in Mar 2011, we also tested Calcium, Ionized at 5.1mg/dL April2011

ref4.8-5.5mg/dL

Now i am very worried about, as she is taking 400mg of mg, but no calcium,

though she is drinking daily bone soup. Wonder if too much for her. What ways

can we do to lower the calcium level?

Appreciate any help!

thanks much,

Corinna

[Guest guest]

Corrina,

This could reflect high levels of calcium oxalate in the red blood cells.

There are genetic differences in how much oxalate is imported into red blood

cells via the Band 3 protein, so we know it is there and that in other

conditions where oxalate is high (like patients on a certain type of dialysis)

calcium gets high in erythrocytes.

So that might explain it. Are you doing a high oxalate diet or have you been

shifting into a higher oxalate diet than before?

For info, see www.lowoxalate.info and Trying_Low_Oxalates .

J Gen Physiol. 1996 Jan;107(1):145-59.

Characterization of oxalate transport by the human erythrocyte band 3 protein.

Jennings ML, Adame MF.

Source

Department of Physiology and Biophysics, University of Texas Medical Branch,

Galveston 77555, USA.

Abstract

This paper describes characteristics of the transport of oxalate across the

human erythrocyte membrane. Treatment of cells with low concentrations of H2DIDS

(4,4'-diisothiocyanatostilbene-2,2'-disulfonate) inhibits Cl(-)-Cl- and

oxalate-oxalate exchange to the same extent, suggesting that band 3 is the major

transport pathway for oxalate. The kinetics of oxalate and Cl- self-exchange

fluxes indicate that the two ions compete for a common transport site; the

apparent Cl- affinity is two to three times higher than that of oxalate. The net

exchange of oxalate for Cl-, in either direction, is accompanied by a flux of H+

with oxalate, as is also true of net Cl(-)-SO4(2-) exchange. The transport of

oxalate, however, is much faster than that of SO4(2-) or other divalent anions.

Oxalate influx into Cl(-)-containing cells has an extracellular pH optimum of

approximately 5.5 at 0 degrees C. At extracellular pH below 5.5 (neutral

intracellular pH), net Cl(-)-oxalate exchange is nearly as fast as Cl(-)-Cl-

exchange. The rapid Cl(-)-oxalate exchange at acid extracellular pH is not

likely to be a consequence of Cl- exchange for monovalent oxalate (HOOC-COO-;

pKa = 4.2) because monocarboxylates of similar structure exchange for Cl- much

more slowly than does oxalate. The activation energy of Cl(-)-oxalate exchange

is about 35 kCal/mol at temperatures between 0 and 15 degrees C; the rapid

oxalate influx is therefore not a consequence of a low activation energy. The

protein phosphatase inhibitor okadaic acid has no detectable effect on oxalate

self-exchange, in contrast to a recent finding in another laboratory (Baggio,

B., L. Bordin, G. Clari, G. Gambaro, and V. Moret. 1993. Biochim. Biophys. Acta.

1148:157-160.); our data provide no evidence for physiological regulation of

anion exchange in red cells.

PMID:

8741736

Clin Lab. 2011;57(7-8):551-7.

Lipid peroxidation and parathyroid hormone influence the cytosolic calcium

levels of erythrocytes in peritoneal dialysis patients.

Sahin E, Goçmen AY, Gümü & #351;lü S, Sahin M, Koçak H, Tuncer M.

Source

Department of Central Laboratory, Clinical Biochemistry Unit, Faculty of

Medicine, Akdeniz University, 07070 Antalya, Turkey.

Abstract

BACKGROUND:

The aim of this study was to examine the alterations in calcium and lipid

peroxidation in red blood cells (RBCs) and serum samples of continuous

ambulatory peritoneal dialysis (CAPD) patients. We also investigated the

relationship between parathyroid hormone (PTH) and calcium homeostasis in this

study.

METHODS:

For this purpose, routine blood counts and blood chemistry were analyzed by

standard laboratory procedures in serum samples. The concentration of TBARS was

measured in erythrocytes and serum samples. RBC calcium was measured by Fura-2AM

in a spectrofluorometer.

RESULTS:

In CAPD patients, hemoglobin, albumin, and high density lipoprotein cholesterol

levels were lower, but glucose, very low density lipoprotein cholesterol,

triglyceride, magnesium, PTH, sensitive C-reactive protein, and uric acid levels

were higher than the controls. Thiobarbituric acid-reactive substance (TBARS)

levels in RBCs and serum samples and cytosolic calcium in RBCs were all found to

be significantly increased in CAPD patients compared to control subjects.

Multiple regression analysis showed that RBC TBARS and serum PTH were the

independent predictors of RBC calcium in our study.

CONCLUSIONS:

Our results confirm that oxidative stress is an important risk factor for CAPD.

The results of multiple regression analysis suggest that RBC calcium was

affected by both increased levels of TBARS and PTH.

PMID:

21888020

>

> Hi, my child at age of 10, have persistent high in calcium in last year. But

this calcium level is tested under element-erythrocytes with ION profile from

Metametrix.

>

> Calcium raised from 46ppm to 55ppm (ref is 24-65ppm)from Mar 2011 to Aug 2011

in 5 months.

> There is a remark indicating :

> **Relevant to membrane permeability,not nutritional status.

>

> But in Mar 2011, we also tested Calcium, Ionized at 5.1mg/dL April2011

ref4.8-5.5mg/dL

>

> Now i am very worried about, as she is taking 400mg of mg, but no calcium,

though she is drinking daily bone soup. Wonder if too much for her. What ways

can we do to lower the calcium level?

>

> Appreciate any help!

> thanks much,

> Corinna

>

[Guest guest]

Corinna, One reason for this may be mitochondrial dysfunction (and cell membrane permeability (problems)). It is being better understood that mitochondria control "calcium homeostasis" in OXPHOS disorders. As a result of cellular dysfunction, extracellular calcium accumulates, in some kids, because the cells are not functioning properly. Is her calcium outside the reference range?Calcium raised from 46ppm to 55ppm (ref is 24-65ppm)... this looks to still be within the reference rangeCalcium, Ionized at 5.1mg/dL April2011 ref4.8-5.5mg/dL To: mb12valtrex Sent: Tuesday, September 13, 2011 1:09 AMSubject: High calcium level-help!

Hi, my child at age of 10, have persistent high in calcium in last year. But this calcium level is tested under element-erythrocytes with ION profile from Metametrix.

Calcium raised from 46ppm to 55ppm (ref is 24-65ppm)from Mar 2011 to Aug 2011 in 5 months.

There is a remark indicating :

**Relevant to membrane permeability,not nutritional status.

But in Mar 2011, we also tested Calcium, Ionized at 5.1mg/dL April2011 ref4.8-5.5mg/dL

Now i am very worried about, as she is taking 400mg of mg, but no calcium, though she is drinking daily bone soup. Wonder if too much for her. What ways can we do to lower the calcium level?

Appreciate any help!

thanks much,

Corinna