Hyperphosphatemia in CKD

HYPERPHOSPHATEMIA
In Chronic Kidney Disease
Rehab Aly Rayan & Doaa Ali Hegy
Rehab.a.rayan@gmail.com

23-May-14
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HYPERPHOSPHATEMIA | In Chronic Kidney Disease
Table of Contents
INTRODUCTION ......................................................................................................................................................................2
THE CAUSES OF HYPERPHOSPHATEMIA................................................................................................................................2
Acute or chronic kidney disease ........................................................................................................................................3
Phosphate Retention..............................................................................................................................................................3
GUIDELINE TARGET LEVELS....................................................................................................................................................4
Treatment of Hyperphosphatemia........................................................................................................................................4
1- Phosphate restriction :...............................................................................................................................................5
2- Phosphate binders: categorized as:............................................................................................................................5
1. Aluminum hydroxide :............................................................................................................................................5
2. Magnesium-containing antacids:...........................................................................................................................5
3. Calcium salts :.........................................................................................................................................................5
4. Non-calcium binders ..............................................................................................................................................6
3- NOVEL THERAPIES ......................................................................................................................................................7
 Nicotinamide : ........................................................................................................................................................7
 Polynuclear iron (III)-oxyhydroxide phosphate (PA21) :.......................................................................................7
 Increased and/or extended hemodialysis :...........................................................................................................7
Managing hyperphosphatemis in CKD Patients’...................................................................................................................7
Among dialysis patients:...................................................................................................................................................7
Stage 3 to 5 CKD not yet on dialysis: ..............................................................................................................................7
Summery.................................................................................................................................................................................8
References..............................................................................................................................................................................9

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INTRODUCTION
Phosphate is an inorganic molecule consisting of a central phosphorus atom and four oxygen atoms. In the
steady state, the serum phosphate concentration is determined by the ability of the kidneys to excrete dietary
phosphate.
THE CAUSES OF HYPERPHOSPHATEMIA
Phosphate intake above 4000 mg/day (130 mmol/day) causes small elevations in serum phosphate
concentrations as long as the intake is distributed over the course of the day. If, however, an acute phosphate
load is given over several hours, transient hyperphosphatemia will occur.
The diagnostic approach to hyperphosphatemia involves elucidating why phosphate entry into the
extracellular fluid exceeds the degree to which it can be excreted or why the renal threshold for phosphate
excretion is increased above normal.
 There are four general circumstances in which this occurs:

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Acute or chronic kidney disease
The filtered load of phosphate is approximately 4 to 8 g/day (130 to 194 mmol/day). If, for example, the
glomerular filtration rate (GFR) is 180 L/day (125 mL/min) and the phosphate concentration is 4 mg/dL (1.3
mmol/L), then the filtered load will be 7.2 g/day. Only 5 to 20 percent of the filtered phosphate is normally
excreted, with most being reabsorbed in the proximal tubule. The normal physiologic regulation of renal
phosphate excretion, the following factors are involved:
 Serum phosphate concentration – Hyperphosphatemia can directly diminish proximal tubular
phosphate reabsorption via suppression of sodium-phosphate cotransporters in the luminal membrane
that mediate reabsorption of filtered phosphate.
 Parathyroid hormone – Parathyroid hormone (PTH) increases phosphate excretion by diminishing
activity of sodium-phosphate cotransporters.
 Phosphatonins – Phosphatonins such as fibroblast growth factor 23 (FGF23) and secreted frizzled
related protein-4 (sFRP-4) decrease phosphate reabsorption by suppressing the luminal expression of
sodium phosphate cotransporters.
An acute or chronic reduction in GFR will initially diminish phosphate filtration and excretion. Nevertheless,
phosphate balance can initially be maintained in such patients by decreasing proximal phosphate reabsorption
under the influence of increased secretion of PTH and FGF23. Once the GFR falls below 20 to 25 mL/min,
however, phosphate reabsorption is thought to be maximally suppressed, and urinary excretion may no longer
keep pace with phosphate intake. At this point, hyperphosphatemia occurs, increasing the filtered load and
reestablishing phosphate balance.
Phosphate Retention
A tendency toward phosphate retention begins early in renal disease due to the reduction in the filtered
phosphate load. Although this problem is initially mild, with hyperphosphatemia being a relatively late event,
phosphate retention is intimately related to the common development of cardiovascular disease risk in
chronic kidney disease (CKD), increased fibroblast growth factor (FGF)-23 levels, and secondary
hyperparathyroidism. These adaptive endocrine alterations are a potential concern because high circulating
levels of parathyroid hormone (PTH) play an important role in the development of renal osteodystrophy, and
elevated circulating FGF-23 concentrations are strongly associated with increased cardiovascular mortality and
renal failure.

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From the viewpoint of calcium and phosphate balance, the hyper secretion of FGF-23 and PTH reflect the
development of phosphate retention and are initially appropriate. FGF-23 appears to be the initial hormonal
abnormality leading to increased urinary phosphate excretion and suppression of 1, 25-
dihydroxycholecalciferol (1, 25(OH) D). PTH increases in response to reductions in 1, 25(OH) D. By increasing
bone turnover and calcium phosphate release from bone and enhancing urinary phosphate excretion (via a
decrease in proximal reabsorption), PTH can correct both the hypocalcaemia and the hyperphosphatemia.
FGF-23 is also important in the renal adaptation to maintain phosphate excretion. The effect on renal
phosphate handling is manifested by a progressive reduction in the fraction of the filtered phosphate that is
reabsorbed, from the normal value of 80 to 95 percent to as low as 15 percent in advanced renal failure. As a
result, phosphate balance and a normal serum phosphate concentration are generally maintained (at the price
of elevated FGF-23 and hyperparathyroidism) until the glomerular filtration rate (GFR) falls below 25 to 40
mL/min.
Hyperphosphatemia alone or in combination with a high serum calcium has been associated with increased
mortality in dialysis patients.
When both calcium and phosphate levels are high (due in part to the increased intake of calcium [via calcium-
based phosphate binders]), heterotopic deposition of hydroxyapatite in arteries, joints, soft tissues, and the
viscera develops; when small arterioles are affected, tissue ischemia and calciphylaxis may occur .
Tumoral collections of calcium phosphate crystals may also be a consequence of hyperphosphatemia and
increased calcium levels.
Increased coronary arterial calcification is associated with coronary atherosclerosis and is related to the
presence and/or consequences of elevated serum phosphorus, calcium, FGF-23, and PTH levels. If the oral
phosphate binders described below are ineffective, parathyroidectomy may be required to control both the
hyperparathyroidism and that part of the hyperphosphatemia that is due in part to PTH-induced release from
bone.
However, calcitriol and other vitamin D analogs also increase intestinal phosphate absorption and can
exacerbate the hyperphosphatemia, unless bone remodeling is reduced, due to inhibition of PTH secretion.
High doses of vitamin D analogs also stimulate vascular calcification. Thus, such therapy should not be started
until the serum phosphate concentration is under reasonable control.
GUIDELINE TARGET LEVELS
1. K/DOQI guidelines — The 2003 Kidney Disease Outcomes Quality Initiative (K/DOQI) practice guidelines
made the following recommendations for goal serum phosphate at different levels of severity of
chronic kidney disease (CKD):
o At an estimated glomerular filtration rate (eGFR) between 15 and 59 mL/min per 1.73 m (stage 3
and 4 CKD), the serum phosphate should be between 2.7 and 4.6 mg/dL (0.87 and 1.49 mmol/L).
o At an eGFR <15 mL/min per 1.73 m (stage 5 CKD), the serum phosphate should be between 3.5 and
5.5 mg/dL (1.13 and 1.78 mmol/L).
Treatment of Hyperphosphatemia
Both the (K/DOQI) and (KDIGO) have published guidelines concerning the management of hyperphosphatemia
in patients with (CKD).Two principal modalities are used in an attempt to prevent and/or reverse the
hyperphosphatemia of renal failure:

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1- Phosphate restriction :
- Approximately 900 mg/day is a level that at least some patients will find acceptable. Phosphate
restriction should primarily include processed foods, colas, and not high biologic value foods such as
meat and eggs.
- A large fraction of dialyzed patients has either overt or borderline malnutrition. Thus, protein
supplementation rather than protein restriction is the goal. In this setting, the patient should be
encouraged to avoid unnecessary dietary phosphate (as in phosphorus-containing food additives, dairy
products, certain vegetables, many processed foods, and colas), while increasing the intake of high
biologic value sources of protein (such as, meat and eggs).
2- Phosphate binders: categorized as:
 calcium containing (mostly calcium carbonate and calcium acetate)
 Non-calcium containing (including sevelamer and lanthanum).
o Use of calcium-containing phosphate binders become less frequent because of concerns about
toxicity of calcium accumulation. We generally use non-calcium-containing phosphate binders
for:
 normocalcemic CKD patients
 CKD patients who are receiving active vitamin D analogs for parathyroid hormone (PTH)
suppression (non-calcium-based phosphate binders decrease mortality among CKD
patients).
1. Aluminum hydroxide :
 The phosphate binder of choice, forming insoluble and nonabsorbable aluminum phosphate
precipitates in the intestinal lumen.
 -It has been avoided due to Aluminum intoxication due to the gradual tissue accumulation of
absorbed aluminum , The major manifestations of this problem develop in the bone, skeletal muscle,
and the central nervous system (CNS), leading to vitamin D-resistant osteomalacia; a refractory,
microcytic anemia; bone and muscle pain; and dementia.
 There appears to be no safe dose of aluminum in CKD that is also large enough to control the serum
phosphate concentration.
2. Magnesium-containing antacids:
 Generally avoided in patients with kidney dysfunction because of the risk of hypermagnesemia and
the frequent development of diarrhea.
3. Calcium salts :
 The problems with aluminum led to the preferential administration of calcium salts to bind intestinal
phosphate they include calcium carbonate and calcium acetate.
o Calcium acetate may be a more efficient phosphate binder than calcium carbonate as calcium
carbonate dissolves only at an acid pH, and many patients with advanced renal failure have
achlorhydria or are taking H2-blockers. Calcium acetate, on the other hand, is soluble in both
acid and alkaline environments. The net effect is that only one-half as much calcium is required
with calcium acetate, however, this difference does not appear to be clinically important, since
the incidence of hypercalcemia is similar to that seen with higher doses of calcium carbonate.
o Calcium citrate should be avoided in patients with renal failure since citrate can markedly
increase intestinal aluminum absorption and possibly induce aluminum neurotoxicity or the
rapid onset of symptomatic osteomalacia.
o Sodium bicarbonate is preferred in advanced kidney disease, even if the patient is not being
treated with aluminum, since many foods and medications contain some aluminum. However,
if such items are avoided, sodium citrate can be used in some patients unable to tolerate

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sodium bicarbonate since it does not produce the bloating associated with bicarbonate
therapy.
 The dose of calcium-containing phosphate binders is generally increased until the serum phosphate
falls to normal values for patients with stage 3 to 5 CKD not yet on dialysis, or between 4.5 and 5.5
mg/dL for dialysis patients, or until hypercalcemia ensues.
 One potential complication of calcium therapy is that absorption of some of the administered calcium
may promote the development of coronary arterial calcification, which is postulated to be associated
with coronary atherosclerosis.
 To help decrease this possibility, the total dose of elemental calcium (including dietary sources)
should not exceed 2000 mg/day, and the amount of elemental calcium should be no more than 1.5
grams per day. In addition, the dose of active vitamin D sterols should be lowered or therapy should
be discontinued until calcium levels return to 8.4 to 9.5 mg/dL.
 Phosphate binders are most effective if taken with meals. This regimen has the advantages of binding
dietary phosphate and, therefore, of leaving less free calcium available for absorption. In comparison,
administration between meals only binds the phosphate present in intestinal secretions and results in
a greater degree of calcium absorption.
 This problem is most likely to occur if a vitamin D preparation is also given or if the patient has
decreased bone turnover due to osteomalacia or adynamic bone disease, thereby limiting uptake of
the extra calcium by bone.
 Adynamic bone disease can be suspected in patients with a low plasma PTH level who develop
hypercalcemia on calcium-based phosphate binders or active vitamin D therapy. A bone biopsy is the
only way to definitively diagnose this disorder. Thus, careful monitoring of the serum calcium
concentration is essential with the chronic administration of calcium salts, particularly in patients on
hemodialysis where the dialysate calcium concentration can vary and therefore affect the ability to
administer calcium-containing phosphate binders.
4. Non-calcium binders
a. Sevelamer :
o Sevelamer hydrochloride (Renagel®) and sevelamer carbonate (Renvela®) are nonabsorbable
agents that contain neither calcium nor aluminum.
o These drugs are cationic polymers that bind phosphate through ion exchange.
o Relatively less progression of vascular calcification with sevelamer versus calcium-containing
phosphate binders among patients with CKD.However, it is unclear whether this benefit is
associated with improvements in morbidity and mortality from cardiovascular disease.
o There appears to be no major difference between sevelamer and calcium-based phosphate
binders in terms of bone histology, although the evidence is somewhat inconsistent, there
appears to be a correlation between increased calcium intake and an increased incidence of
both adynamic bone disease and vascular calcification.
o One problem associated with sevelamer hydrochloride is the possible induction of metabolic
acidosis. As a result, sevelamer carbonate has been developed. It is associated with higher
serum bicarbonate levels than sevelamer hydrochloride, it is likely that it will become the
preferred binder in this class, but these agents appear to be equivalent in their ability to control
phosphate levels.
o Sevelamer is much more expensive than calcium-based phosphate binders are.
b. Lanthanum :
o It is a rare earth element, has significant phosphate-binding properties.
o The risk of lanthanum accumulation and toxicity, however, appears to be quite low with short-
term use.

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o The lower pill burden is one consideration that may favor the use of lanthanum.
o Sevelamer is commonly initially used over lanthanum since, although equally effective in lowering
phosphate, as the long-term data on safety of lanthanum are more limited.
3- NOVEL THERAPIES
The current approach to management of hyperphosphatemia is not optimal; a number of alternative therapies
are undergoing evaluation.
 Nicotinamide :
o Nicotinamide, a metabolite of nicotinic acid (niacin, vitamin B3), inhibits the Na/Pi co-transport
system in the gastrointestinal tract and kidneys and may be effective in lowering phosphate
levels in dialysis patients by reducing gastrointestinal tract phosphate absorption
 Polynuclear iron (III)-oxyhydroxide phosphate (PA21) :
o Various doses of polynuclear iron (III)-oxyhydroxide phosphate (PA21) were compared with
sevelamer in a randomized, multicenter open-label study, PA21 at doses of 5 and 7.5 g/day
produced similar decreases in serum phosphorus to sevelamer dosed at 4.8 g/day.
o Further study is required to better understand the efficacy and safety of these and related
agents in this setting.
 Increased and/or extended hemodialysis :
o Standard dialysis is limited in its ability to remove phosphate. Although dialysis membranes are
relatively efficient, there is only a slow efflux of phosphate from the large intracellular stores
into the extracellular fluid, which is undergoing dialysis. Thus, lengthening dialysis (within
standard dialysis regimens) or using larger, high-efficiency dialyzers is unlikely to substantially
increase phosphate removal.
o The average standard dialysis removes approximately 900 mg of phosphate. By comparison,
extremely long and/or frequent dialysis clears a larger amount of phosphate.
o For patients with refractory hyperphosphatemia who are willing to accept this form of dialysis,
this form of dialysis may be the best approach.
Managing hyperphosphatemis in CKD Patients’
 Calcium, and parathyroid hormone (PTH) levels initially and then on an ongoing basis, particularly after
changes in therapeutic measures.
 Among all patients with CKD, we avoid aluminum hydroxide except for short-term therapy (four
weeks for one course only) of severe hyperphosphatemia.
Among dialysis patients:
 we aim to maintain serum phosphate levels between 3.5 and 5.5 mg/dL
1- Restrict dietary phosphate to 900 mg/day.
2- Among dialysis patients with elevated phosphate levels that are refractory to maintenance dialysis
therapy and diet, we recommend the administration of phosphate-binding agents.
3- More frequent and more intensive dialysis can also lower phosphate levels. Extremely long and/or
frequent dialysis, such as that provided by nocturnal hemodialysis, clears a large amount of
phosphate; it is an option among those who are willing to accept this form of dialysis.
Stage 3 to 5 CKD not yet on dialysis:
1- Restrict dietary phosphate to 900 mg/day.
2- Among patients with serum phosphate levels greater than target levels despite dietary phosphorus
restriction after one month, we suggest the administration of phosphate binders.

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Summery
 Hyperphosphatemia results when phosphate entry into the extracellular fluid exceeds the rate at
which it can be excreted. This occurs when there is a large phosphate load over a short period of time
(which may be from endogenous or exogenous sources), cellular shift of phosphate from the cells to
the extracellular fluid, acute or chronic kidney disease, and because of a primary increase in proximal
phosphate reabsorption.
 Renal failure is a common cause of diminished phosphate excretion. Urinary excretion may not keep
pace with phosphate intake when the glomerular filtration rate (GFR) falls below 20 to 25 mL/min.
 A tendency toward phosphate retention begins early in renal disease. However, phosphate balance
and a normal serum phosphate concentration are generally maintained (at the price of elevated
parathyroid hormone [PTH] and fibroblast growth factor [FGF]-23 levels) until the glomerular filtration
rate (GFR) falls below 25 to 40 mL/min. At this relatively late stage, dietary phosphate restriction may
still minimize positive phosphate balance and may reduce the serum concentration of both phosphate
and PTH, although not usually to normal. As a result, oral phosphate binders are frequently required.
 Both the Kidney Disease Outcomes Quality Initiative (K/DOQI) and Kidney Disease: Improving Global
Outcomes (KDIGO) have published guidelines concerning the management of hyperphosphatemia in
patients with chronic kidney disease (CKD).
 Restricting dietary phosphate intake and the administration of phosphate binders are the two principal
modalities used to reverse the hyperphosphatemia of CKD. To optimally manage elevated phosphate
levels in all patients with CKD, it is important to first assess the presence or absence of other mineral
abnormalities, to assess vascular calcifications, and note the administration of concurrent therapies,
particularly vitamin D and vitamin D analogs.
 Dialysis
o It is suggested maintaining serum phosphate levels between 3.5 and 5.5 mg/dL (1.13 and 1.78
mmol/L) among dialysis patients (Grade 2C).
o Among dialysis patients with phosphate levels above target levels, we first suggest restricting
dietary phosphate (Grade 2C). Our initial step is to restrict dietary phosphate to 900 mg/day.
The patient should be encouraged to avoid unnecessary dietary phosphate (as in phosphorus-
containing food additives, dairy products, certain vegetables, many processed foods, and colas),
while maintaining the intake of high biologic value sources of protein. Among dialysis patients
with elevated phosphate levels that are refractory to maintenance dialysis therapy and diet, we
suggest the administration of phosphate-binding agents (Grade 2B). Our approach varies based
upon calcium levels and the presence of comorbid conditions.
o Despite dietary restriction, optimal doses of phosphate binders, and conventional dialysis, some
dialysis patients do not achieve the recommended serum phosphate goals. This may be due in
part to the use of various agents to help control PTH levels, particularly vitamin D analogs, as
well as other issues. The approach in these patients is discussed in detail separately.
o Among dialysis patients with persistent hyperphosphatemia, we suggest increasing phosphate
removal via hemodialysis (Grade 2C). Among patients with refractory hyperphosphatemia,
nocturnal hemodialysis is an option for those who are willing to accept this form of dialysis.
o Among all patients with CKD, we recommend not administering aluminum hydroxide, except
for short-term therapy (four weeks for one course only) of severe hyperphosphatemia (Grade
1B).
 Stage 3 to 5 CKD not yet on dialysis
o We suggest maintaining serum phosphate levels in the normal range among patients with stage
3 to CKD not yet on dialysis (Grade 2C).

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o Among patients with stage 3 to 5 CKD, not yet on dialysis with hyperphosphatemia, we first
suggest restricting dietary phosphate (Grade 2C). Our initial step is to restrict dietary phosphate
to 900 mg/day. Among patients with serum phosphate levels greater than target levels despite
dietary phosphorus restriction after four weeks, we suggest the administration of phosphate
binders (Grade 2C). Our specific approach varies based upon calcium levels and the presence of
comorbid conditions.
o Among all patients with CKD, we recommend not administering aluminum hydroxide, except
for short-term therapy (four weeks for one course only) of severe hyperphosphatemia (Grade
1B).
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18. Kestenbaum B, Sampson JN, Rudser KD, et al. Serum phosphate levels and mortality risk among people
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