End Stage Kidney Disease and Calcium Level

tlc2u · Nov 13, 2009

here is an article that adresses your question. the article is dated 2002 i don't know if you need something more recent or not. and another article below that explains the seesaw levels of calcium versus phosphorous in the blood. when one is up the other is down.

http://www.medscape.com/viewarticle/439639

from [color=#004276]medscape critical care

calcium and vitamin d in end-stage renal disease

geoffrey bihl, md

[color=#004276]authors and disclosures

published: 08/07/2002

question

we need clarification as to whether vitamin d and calcium are required in end-stage renal disease (esrd). i have an esrd patient who has been on dialysis for about 6 months. erythropoietin is being given weekly.

richard ziegler, md

response from geoffrey bihl, md

ideally, correction of the abnormal calcium (ca) and phosphate (po) homeostasis should begin well before patients reach renal failure and dialysis. the primary problem in this regard is the inability of the failing kidney to excrete po. the high serum po results in a raised parathormone (pth), which lowers the ca and results in a vicious cycle. for this reason, management of the serum po is central to the prevention and management of renal bone disease and secondary hyperparathyroidism (hpt).

furthermore, as renal function continues to decline, the activation of vitamin d by the kidney is impaired and the low levels of activated vitamin d fail to suppress pth, thereby compounding the secondary hpt present in chronic and end-stage patients.

unfortunately, dialysis does not adequately remove po, and therapy, therefore, should be aimed at normalizing serum po with po binders and dietary restriction of po intake.[color=#004276][1] this is essential. po binders should be taken with every meal. in order to further suppress the pth level, serum ca should be slowly raised with the use of ca supplements between meals, to a serum level at the upper limit of normal. it is important to note that calcium carbonates are used as po binders, and they have the added advantage of helping to correct hypocalcemia. in some centers, the elevated po is initially reduced with the use of aluminum hydroxide, although the aluminum has long-term problems in its own right.[color=#004276][2]

as levels of activated vitamin d are reduced in chronic and end-stage patients, synthetic vitamin d analogues are used to correct hypocalcemia by increasing ca reabsorption from the gut. unfortunately, they also increase po reabsorption from the gut and, thus, should not be used until po control has been achieved. the vitamin d also lowers the pth level.

close monitoring of response to therapy is essential, remembering that uncontrolled secondary hpt is one of the causes of a poor response to rhuepo therapy,[color=#004276][3] and that poorly controlled ca, po, and pth result in significant renal bone disease.[color=#004276][4]

[color=#705e3e]http://www.webmd.com/a-to-z-guides/phosphate-in-blood

[color=#705e3e]phosphate in blood

a phosphate test measures the amount of [color=#3789b9]phosphate in a blood sample. phosphate is a charged particle (ion) that contains the [color=#3789b9]mineral phosphorus. the body needs phosphorus to build and repair bones and teeth, help nerves function, and make muscles contract. most (about 85%) of the phosphorus contained in phosphate is found in bones. the rest of it is stored in tissues throughout the body.

the [color=#3789b9]kidneys [color=#3789b9] help control the amount of phosphate in the blood. extra phosphate is filtered by the kidneys and passes out of the body in the urine. a high level of phosphate in the blood is usually caused by a kidney problem.

the amount of phosphate in the blood affects the level of [color=#3789b9]calcium in the blood. calcium and phosphate in the body react in opposite ways: as blood calcium levels rise, phosphate levels fall. but this relation between calcium and phosphate may be disrupted by some diseases or infections. for this reason, phosphate and calcium levels are usually measured at the same time.

hope that helps,

tlc2u

al7139, ASN, RN · Nov 13, 2009

Lets see if we can make this simple:

In renal disease the kidneys cannot produce the activated form of vitamin D (Calcitriol), which leads to reduced use of calcium, thus hypocalcemia. This is because phosphate retention and calcitriol deficiency disrupt the calcium/phosphate balance. Normally excessive dietary phosphate is excreted by the kidneys in the urine. PTH controls the amount of phosphate in the blood by causing tubular excretion when there is an excess. A sign of chronic renal failure is reduced phosphate excretion. As levels increase, calcium levels decrease. Chronic hypocalcemia causes stimulation of the parathyroid glands. Calcium is released from storage ares in bone which results in bone density loss. the additional calcium needed to compensate the excess phosphate levels. Hypocalcemia is compounded because decreased renal function causes decresed production of active vitamin D, thus less calcium is absorbed.

Hope this helps, but I guess it's not really that simple.

Amy