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Literature
update: Rodriguez
M, Felsenfeld A. PTH,
FGF-23 and early CKD. Nephrol
Dial Transplant 2008;23(11):3391-3. Bover
J, Andres E, Lloret M, Aguilar A, Ballarin J. Dietary
and Pharmacological Control of Calcium and Phosphate Metabolism in
Dialysis Patients. Blood
Purif 2009;27(4):369-386. Chronic
kidney disease-mineral and bone disorder is a new term defining a
complex syndrome which underlines the need of a systemic approach to
disturbances of calcium and phosphate metabolism in patients with renal
failure. In recent years, the availability of new phosphorus binders and
the appearance of new selective vitamin D receptor activators and
calcimimetics have increased our current armamentarium and have changed
previous paradigms. All these drugs can be used in combination, acting
in distinct yet complementary pathways, with a resultant improvement in
their individual clinical profile and reduction in secondary effects,
while enhancing the achievement of clinical guideline targets. On the
other hand, we should be aware that treatment costs are increasing and
most of our knowledge is opinion-based. In this article, we shall
consider rational recommendations on the control of calcium, phosphorus
and parathyroid hormone while awaiting new evidence. We shall also
briefly review some important related issues such as vascular
calcification, adynamic bone disease, osteoporosis and the need of
parathyroidectomy. Future guidelines may modify current recommendations,
but we believe that the lack of an absolute evidence is not equivalent
to the lack of awareness of the important problem which chronic kidney
disease-mineral and bone disorder represents. Terai
K, Nara H, Takakura K, Mizukami K, Sanagi M, Fukushima S, et al. Vascular
calcification and secondary hyperparathyroidism of severe chronic kidney
disease and its relation to serum phosphate and calcium levels. Br
J Pharmacol [Epub ahead of print] 2009:Mar 19. Background
and purpose: Various complications consequent on disordered calcium and
phosphate homeostasis occur frequently in chronic kidney disease (CKD)
patients. Particularly, vascular calcification has high morbidity and
mortality rates. There is a clear need for a better CKD model to examine
various aspects of this disordered homeostasis. Experimental approach:
Oral dosing with adenine induced CKD in rats in only 10 days. Serum
calcium, phosphate and parathyroid hormone were measured and
calcification in aorta was assessed histologically. The effects of
varying phosphorus content of diet or treatment with phosphate binders
or active vitamin D(3) on these parameters were examined. Key results:
After adenine dosing, significant hyperphosphatemia, hypocalcemia and
secondary hyperparathyroidism (2HPT) were observed during the
experimental period of 15 weeks. Aortic calcification was detected in
only some of the animals even at 15 weeks ( approximately 40%).
Treatment with vitamin D(3) for 18 days, even at a low dose (100 ng.kg(-1),
3-4 times week(-1), p.o), caused aortic calcification in all animals and
increases in serum calcium levels up to the normal range. The vitamin
D(3)-induced calcification was significantly inhibited by phosphate
binders which lowered serum phosphate levels and the calcium x phosphate
product, although serum calcium levels were elevated. Conclusions: These
data suggest that rats dosed orally with adenine provide a more useful
model for analysing calcium/phosphate homeostasis in severe CKD.
Controlling serum calcium/phosphate levels with phosphate binders may be
better than vitamin D(3) treatment in hyperphosphatemia and 2HPT, to
avoid vascular calcification. Chen
Y, Su C, Wang S, Lee H, Lin S. A
Preliminary Investigation of the Association between Serum Uric Acid and
Impaired Renal Function. Chang
Gung Med J 2009;32(1):66-71. Background:Hemodialysis
for end-stage renal disease (ESRD) incurs huge medical costs in Roman-Garcia
P, Carrillo-Lopez N, Cannata-Andia J. Pathogenesis
of bone and mineral related disorders in chronic kidney disease: key
role of hyperphosphatemia. J
Ren Care 2009;35 Suppl 1:34-8. This
paper reviews the pathogenesis of hyperphosphataemia and its role in the
regulation of parathyroid hormone synthesis and parathyroid cell
proliferation in chronic kidney disease. The association between
hyperphosphaemia and vascular calcification, and the interventions that
can be used to control plasma phosphate are also discussed. Sigrist
M, Chiarelli G, Lim L, Levin A. Early
initiation of phosphate lowering dietary therapy in non-dialysis chronic
kidney disease: a critical review. J
Ren Care 2009;35 Suppl 1:71-8. Dietary
management of hyperphosphatemia and hyperparathyroidism have long been
important elements in the clinical management of CKD stage 4 and 5 for
the prevention of mineral bone disease. The rationale for phosphate
lowering has been further justified, given the accumulating data to
support the association of phosphate with vascular damage, in this
population who are at high risk of cardiovascular (CV) death. Phosphate
is a novel CV risk factor in both CKD and in the general population, and
a growing body of literature suggests that high normal serum phosphate
may be a risk factor for progression of CKD. Few studies have examined
hard outcomes after phosphate lowering. Nonetheless, given the balance
of data both in cell, animal and human studies, the use of phosphate
lowering strategies at earlier stages of CKD, perhaps even prior to
serum phosphate level rising, may well be justified. This review will
discuss the complications associated with higher serum phosphate, the
potential benefits of early phosphate intervention, practical
considerations of low phosphate diets and novel strategies for
evaluating these strategies in clinical practice. Kariyawasam
D. Phosphate
management-a dietitian's perspective. J
Ren Care 2009;35 Suppl 1:79-83. Hyperphosphataemia
is a complication of renal failure which can lead to vascular
calcification and hyperparathyroidism. Many factors influence phosphate
levels, e.g. adherence to a low phosphate diet, adequate dialysis,
hyperparathyroidism and concordance with phosphate binders. This article
looks at the issues to consider and provides a dietitian's perspective
on phosphate management. Cannata-Andia
J, Naves-Diaz M. Phosphorus
and survival: key questions that need answers. J
Am Soc Nephrol 2009;20(2):234-6. Goldstein-Fuchs
J, Fouque D. The
ubiquitous nature and elusive role of phosphorus and vascular
calcification. Am
J Kidney Dis 2009;53(3):363-5. Kanbay
M, Goldsmith D, Akcay A, Covic A. Phosphate
- the silent stealthy cardiorenal culprit in all stages of chronic
kidney disease: a systematic review. Blood
Purif 2009;27(2):220-30. BACKGROUND
AND AIM: Due to increasing evidence suggesting a link between
hyperphosphatemia and cardiovascular disease (CVD), mediated through
vascular calcification in patients on dialysis, the following question
arises: At what stage of chronic kidney disease (CKD) does the
relationship between elevated phosphate levels, vascular calcification
and increased cardiovascular mortality begin? Therefore, the purpose of
the current study was to critically review the current literature
regarding this issue. METHODS: We performed a systematic search of the
National Library of Medicine and the Cochrane Library databases from
January 1985 to February 2008 to identify clinical studies examining the
effects of plasma phosphate on cardiovascular outcome, mortality and
progression of kidney disease in subjects with and without CKD who have
not yet received dialysis. The primary outcome measure was the
development of CVD, mortality and progression of kidney disease. RESULTS:
Twelve clinical trials investigated the role of serum phosphate levels
and adverse outcome (9 studies examining CVD outcome and 3 examining
progression of kidney disease). After adjustment for risk factors for
mortality, adverse cardiovascular outcome and progression of kidney
disease, all studies found a graded independent significant association
between phosphate levels and mortality, development of CVD and
progression of kidney disease. There was no such association with plasma
calcium levels. CONCLUSIONS: There is a graded independent association
between serum phosphate levels and mortality, mainly cardiovascular
events, and the progression of renal disease in subjects with and
without definable (loss of glomerular filtration rate) CKD. Savica
V, Calo L, Monardo P, Caldarera R, Cavaleri A, Santoro D, et al. High
phosphate content beverages in dialysis patients: relevance for
hyperphosphatemia and cardiovascular risk. Nutr
Metab Cardiovasc Dis 2008;18(8):e39-40. Bellasi
A, Kooienga L, Block G, Veledar E, Spiegel D, Raggi P. How
long is the warranty period for Nil or low coronary artery calcium in
patients new to hemodialysis? J
Nephrol 2009;22(2):255-62. Background:
Coronary artery calcification (CAC) is common in patients with advanced
chronic kidney disease on dialysis. A sizeable proportion of patients
has no or minimal CAC at the inception of dialysis, but it is unclear
how long they remain free of it. Methods: For the purpose of this study,
36 incident hemodialysis patients were submitted to sequential chest
computed tomography to quantify CAC at baseline, 6, 12, 18 and 30 months.
Results: Among them, 15 had absent or minimal CAC score (CACS 0 to 30)
and 21 had a CACS >30 at baseline. Overall, the median baseline CACS
was 129 (interquartile range [IQR] = 0-709) and it increased to 364 (IQR=8.3-1683)
at study completion (182% increase). Among the 15 patients with minimal
CACS, only 3 progressed and the median CACS increase was 20, as opposed
to 15 of 21 patients with a baseline CACS >30 whose median
progression was 431 (p<0.02). The 18 patients who had CACS
progression were older (68.5 vs. 57.3 years, p=0.0081) and exhibited a
poorer control of mineral metabolism (phosphorus 5.2 vs. 4.9 mg/ dL,
p=0.048; corrected calcium x phosphorus product [CaxP] 49.3 vs. 46.2
mg2/dL2, p=0.001) than the patients without progression. On
multivariable analysis, independent predictors of progression were
baseline CACS (p=0.038) and time-averaged Cax;P (p=0.077). Conclusion:
These data suggest that absent or low CAC at baseline is associated with
minimal progression even up to 30 months. Careful management of mineral
metabolism appears to be one of the main factors that limit progression
of CAC. Giachelli
C. The
emerging role of phosphate in vascular calcification. Kidney
Int 2009;75(9):890-7. Vascular
calcification is recognized as a major contributor to cardiovascular
disease (CVD) in end stage renal disease (ESRD) patients. Susceptibility
to vascular calcification is genetically determined and actively
regulated by diverse inducers and inhibitors. One of these inducers,
hyperphosphatemia, promotes vascular calcification and is a
nontraditional risk factor for CVD mortality in ESRD patients. Vascular
smooth muscle cells (SMCs) respond to elevated phosphate levels by
undergoing an osteochondrogenic phenotype change and mineralizing their
extracellular matrix through a mechanism requiring sodium-dependent
phosphate cotransporters. Disease states and cytokines can increase
expression of sodium-dependent phosphate cotransporters in SMCs, thereby
increasing susceptibility to calcification even at phosphate
concentrations that are in the normal range. Kapustin
A, Shanahan C. Targeting
vascular calcification: softening-up a hard target. Curr
Opin Pharmacol 2009;9(2):84-9. Widespread
vascular calcification is a ubiquitous feature of aging and is prevalent
in association with a number of common pathologies including
atherosclerosis, renal failure, and diabetes. Once thought of as
innocuous, emerging evidence suggests that calcification is causal in
precipitating vascular events and mediating chronic cardiovascular
damage, independent of disease context. Importantly, a large body of
data has shed light on the factors that favor the formation of
calcification in vivo, as well as on the complex mechanisms that
initiate and promote it. This has identified some novel targets and
allowed for the possibility that calcification can potentially be
blocked and ultimately regressed. Targets include local and circulating
inhibitors of calcification as well as factors that may ameliorate
vascular smooth muscle cell (VSMC) apoptosis. Despite this, the
vasculature remains a difficult tissue to target and currently there are
no effective treatments in general use. More crucially, any potential
treatments will need to be carefully evaluated as they may impinge on
bone metabolism. Our best hope for the near future is to normalize
factors associated with accelerated calcification in pathologies such as
renal failure where, aberrant mineral metabolism, as well as treatment
regimes, may contribute to the initiation and progression of
calcification. Inaba
M. [Chronic
kidney disease (CKD) and bone. Impact
of diabetes mellitus on the development of CKD-MBD]. Clin
Calcium 2009;20(4):502-7. Chronic
kidney disease-mineral and bone disorder (CKD-MBD) develops as renal
function deteriorates. The presence of diabetes mellitus as comorbidity
modulates the severity of CKD-MBD. The prevalence of vascular
calcification, which becomes higher in diabetic CKD patients than in
non-CKD counterparts, increases cardiovascular mortality in diabetic
patients. The main factor which causes vascular calcification in
diabetic CKD patients is poor glycemic control, in contrast to
hyperphosphatemia in non-diabetic CKD patients. Diabetes directly
impairs osetoblasts to decrease bone mass, suppresses bone turnover to
impair bone quality by impairing secretion of parathyroid hormone and
increase AGE-modification of bone collagen. Therefore, therapeutic
regimens for CKD-MBD should be considered specifically for diabetic CKD
patients since the mode of its development differs between diabetic and
non-diabetic CKD patients. Yokoyama
K. [Chronic
kidney disease (CKD) and bone.
Vascular calcification in CKD.]. Clin
Calcium 2009;20(4):552-8. Vascular
calcification is associated with the mortality of patients with chronic
kidney disease (CKD) . Susceptibility to vascular calcification is
genetically determined and actively regulated by diverse inducers and
inhibitors. One of these inducers, hyperphosphatemia, promotes vascular
calcification and is a nontraditional risk factor for CVD mortality in
CKD patients. Hyperphosphatemia promotes vascular calcification in part
by promoting VSMCs to undergo an osteochondrogenic phenotype change
through a mechanism requiring sodium-dependent phosphate cotransporters.
Recent randomized clinical trials showed that lowering serum phosphate
levels with a non-calcium containing phosphate binder slows progression
of vascular calcification in ESRD patients. Moreover, calcimimetics
reduce arterial remodeling and calcification in rats with subtotal
nephrectomy. Whether this difference will also be found in humans and
will ultimately translate into less CV events in calcimimetics treated
uremic patients is for a matter for speculation. Calcium and phosphate
load are an important driver of vascular calcification. Levey
AS. A
new equation to estimate glomerular filtration rate. Ann
Intern Med 2009;150(9):604-612. The
objective of this study was to develop and validate a new estimating
equation, the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration)
equation, based on the serum creatinine level that would be as accurate
as the MDRD Study equation at a GFR <60 mL/min per 1.73 m2 and more
accurate at a higher GFR. ·
This was a cross-sectional analysis with
separate pooled data sets for equation development and validation and a
representative sample of US population for prevalence estimates
(n=8,254). The authors utilized an additional data set to validate there
analysis (n=3896). ·
The new CKD-EPI equation estimates the
NHANES median eGFR at 9.5 ml/min per 1.73 m² higher and therefore would
estimate the prevalence in the ·
The overall burden of the disease would be
reduced and more accurate dosing of medications critical to patients
early CKD health could continue. renal newsletter n° 2 Taylor
J, Bushinsky D. Calcium
and phosphorus homeostasis. Blood Purif
2009;27(4):387-94. Calcium
and phosphorus homeostasis relies on a complex, tightly regulated system
involving many ions and hormones. The regulation of calcium and
phosphorus is controlled by the actions of these ions and hormones on
the intestine, kidneys and bone. Disturbances in the serum level of
calcium and/or phosphorus can lead to significant pathology, including
kidney stones and bone disease. In addition to parathyroid hormone and
vitamin D, recently identified factors such as fibroblast growth factors
and klotho play an important role in
maintaining mineral ion homeostasis. The identification of subfamily V
transient receptor potential cation channels
(TRPV channels), Na/P(i)
cotransporters, the vitamin D receptor and
the calcium-sensing receptor have further advanced our understanding of
this complex physiology. In this review we discuss the current
understanding of the relationships between the ions, hormones, and
transporters that maintain calcium and phosphorus homeostasis. Frazao
J, Martins P. Adynamic
bone disease: clinical and therapeutic implications. Curr
Opin Nephrol Hypertens
[Epub ahead of print] 2009:May
6. PURPOSE
OF REVIEW: Adynamic bone disease has
recently been associated with increased risk of vascular calcification.
This review focuses on the emerging data in adynamic
bone disease, its clinical consequences and therapeutic implications.
RECENT FINDINGS: There is a lack of good biochemical markers of
parathyroid status, bone formation and reabsorption
to allow a secure diagnosis of bone disease. Recent data have suggested
a possible link between bone activity and vascular calcification.
Cardiovascular calcification is an independent predictor of mortality. Adynamic
bone is associated with a very low capacity of bone to incorporate
calcium in the bone compartment and inability to handle an extra calcium
load. A positive association between vascular calcifications and low
bone turnover has been suggested. Calcium-containing phosphate binders,
active vitamin D therapy and high calcium dialysate
may enhance vascular calcifications in the presence of adynamic
bone disease. SUMMARY: There is recent evidence suggesting a negative
impact of calcium load in the progression of vascular calcification in
dialysis patients with chronic kidney disease stage 5 with adynamic
bone disease. The current therapeutic approach to these patients should
focus on reduction of calcium and vitamin D load to restore parathyroid
activity. Ketteler
M, Biggar P. Dietary
and pharmacological control of calcium and phosphate metabolism in
predialysis stages of chronic kidney disease. Blood Purif
2009;27(4):345-9. Data on
calcium and phosphate metabolism in the predialysis stages of chronic
kidney disease (CKD) are scarce when compared with the available
information on patients on dialysis. Visible derangements of calcium and
phosphate levels start to become apparent when GFR falls below 40
ml/min. In some but not all patients, hyperphosphatemia
may be a mortality risk predictor in CKD stages 4-5. There are only few
treatment studies targeting hyperphosphatemia
in these CKD stages. However, the RIND study, evaluating progression of
coronary artery calcification in incident hemodialysis
patients, demonstrated that vascular calcification processes manifest in
predialysis stages in the majority of patients, which may well be linked
to deranged calcium and phosphate homeostasis. Novel insights into the pathophysiology
of calcium and phosphate handling, especially the discovery of the phosphatonin
FGF23, suggest that a more complex assessment of phosphate balance is
warranted. This assessment should include measurements of fractional
phosphate excretion and phosphatonin levels
to objectively judge and effectively correct phosphate overload. Nikolov
I, Mozar A, Drueke
T, Massy Z. Impact
of disturbances of calcium and phosphate metabolism on vascular
calcification and clinical outcomes in patients with chronic kidney
disease. Blood Purif
2009;27(4):350-9. Chronic
kidney disease (CKD) is frequently complicated by arterial calcification.
The latter is part of the associated mineral and bone disorder (CKD-MBD).
Hypercalcemia and hyperphosphatemia
have long been known to play a major role in the occurrence of vascular
and other soft tissue calcification in patients with CKD, together with
endocrine disturbances including vitamin D, parathyroid hormone,
fibroblast growth factor-23, and klotho. In
addition, many other systemic and local promoters, including
inflammation and uremic toxins, contribute to the occurrence of vascular
calcification, despite a powerful defense system made up of systemic and
local inhibitors, as demonstrated in elegant experimental studies done
in vitro and in vivo. Most importantly, several reports have shown that
both hyperphosphatemia and hypophosphatemia,
and to a lesser degree hypercalcemia and hypocalcemia,
are associated with an increased relative risk of mortality in patients
with CKD. However, all these reports were observational in nature and
must therefore be considered as hypothesis generating. It remains to be
demonstrated in prospective randomized trials whether normalization of
serum phosphorus and/or calcium leads to better patient outcome. In
order to improve outcome in patients with CKD-MBD, early medical
intervention is of utmost importance. Articolo
su Sevelamer e infiammazione:
Sevelamer
hydrochloride use and circulating endotoxin
in hemodialysis patients: a pilot
cross-sectional study Phyllis P.
Sun, MS, RD, Mary C. Perianayagam, PhD, and
Bertrand L. Jaber, MD, MS Objective:
There is a growing interest in the potential anti-inflammatory
properties of sevelamer hydrochloride, a
commonly used phosphate binder for patients with chronic kidney failure.
This study explores the hypothesis that sevelamer
hydrochloride binds bacterial endotoxin in
the intestinal tract, leading to lower circulating endotoxin
levels, and offering a novel anti-inflammatory mechanism. Methods:
We performed a cross-sectional study in medically stable patients with
chronic kidney failure undergoing maintenance hemodialysis.
Blood samples were collected before 2 consecutive dialysis sessions, and
plasma was tested for endotoxin,
interleukin-6 and C-reactive protein. Linear regression analyses were
used to examine patient-related and dialysis-related factors associated
with plasma endotoxin level. Results:
Forty-six patients met our eligibility criteria. Their mean age was 62
years, 41% were diabetic, and 65% reported the use of sevelamer
hydrochloride. The mean plasma endotoxin
level was significantly lower in patients using sevelamer
hydrochloride compared with those who were not (0.2360.01 vs. 0.3060.01
EU/mL, P5.001). However, plasma
interleukin-6 and C-reactive protein levels were not significantly
different between the two groups. According
to multivariate analysis, the use of sevelamer
hydrochloride was associated with a lower plasma endotoxin
level after adjustment for race, gender, age, dialysis vintage, total
cholesterol level, and white blood cell count. Conclusions:
This proof-of-concept pilot study demonstrates that the use of sevelamer
hydrochloride is associated with a lower plasma endotoxin
level, supporting the hypothesis that this agent binds to endotoxin
in the intestinal lumen. Although this may be an important mechanism by
which sevelamer hydrochloride attenuates
systemic inflammation, a clinical trial is required to test this
hypothesis. renal newsletter n° 3
Ketteler
M. The
control of hyperphosphatemia in chronic
kidney disease: which phosphate binder? Int
J Artif Organs 2009;32(2):95-100. Hyperphosphatemia
is currently regarded as a key mortality risk predictor in late CKD
stages and especially in patients on dialysis. Fortunately, the armatorium
to effectively treat hyperphosphatemia in
end-stage renal disease has grown in recent years, and we gained an
improved understanding of potential benefits and harms of specific
compounds. Most interestingly, novel insights into the pathophysiology
of calcium and phosphate handling, especially, the discovery of the phosphatonin
FGF23, suggest a more complex assessment of phosphate balance especially
in predialysis stages is warranted. This assessment should probably
include measurements of fractional phosphate excretion and phosphatonin
levels to objectively judge and effectively correct phosphate overload,
however, clinical data on calcium and phosphate metabolism in CKD stages
3 - 4 are still scarce. This overview will both discuss aspects of pathophysiology
of phosphate regulation and current and future clinical treatement
approaches. Bellotti
G, Presta P, Panzino T, Capria
M, Caglioti A, Riccio M, et
al. [Multiple
peritrochanteric and pubic calcifications in
a young woman on hemodialysis with severe
renal osteodystrophy successfully treated
with sevelamer+cinacalcet+paracalcitol
combination therapy.]. G Ital Nefrol
2009;26(3):372-6. Secondary
hyperparathyroidism is a frequent complication of chronic renal failure
that can induce severe bone disease and negatively influence the
cardiovascular outcome. Therefore, nephrologists should attempt to reach
the targets recommended by national and international guidelines using
all the available therapeutic strategies. We describe the case of a
37-year-old woman affected by spina bifida
and myelomeningocele who had been on hemodialysis
since 1993. In July 2006 she developed secondary hyperparathyroidism
complicated by peritrochanteric
calcifications which did not respond to standard therapy. Because it was
impossible to perform a parathyroidectomy,
we started medical therapy with a combination of sevelamer
hydrochloride, paracalcitol and cinacalcet,
which resulted in progressive improvement of laboratory data and osteodystrophy.
A diagnosis of mixed secondarytertiary
hyperparathyroidism was made, but a progressive increase in iPTH
to very high levels suggested a rapid evolution toward a pure tertiary
form. Imanishi
Y. [Clinical
aspect of recent progress in phosphate metabolism.
Phosphate retension, a
powerful risk factor for mortality in chronic kidney disease (CKD)]. Clin
Calcium 2009;19(6):828-35. Higher
levels of serum phosphate are associated not only with progression of
secondary hyperparathyroidism but also adverse cardiovascular outcomes,
such as ectopic calcifications, cardiovascular events its death. The
treatments of hyperphosphatemia with
phosphate binders were shown to be effective on a risk factor for
cardiovascular disease and mortality on hemodialysis
patients. Reddy
V, Symes F, Sethi
N, Scally A, Scott J, Mumtaz
R, et al. Dietitian-led
education program to improve phosphate control in a single-center hemodialysis
population. J Ren
Nutr 2009;19(4):314-20. OBJECTIVE:
We sought to analyze the effect of a structured, dietitian-led education
program on patients' general knowledge of phosphate and phosphate
binders, and its impact on serum phosphate concentrations in a
single-center hemodialysis population.
DESIGN: We compared subjects before and after intervention. SETTING:
This study involved two dialysis units operated by a single center.
PATIENTS: One hundred and fifteen hemodialysis
patients consented to participate in this study (54% male; mean age,
61.1 years; 32% Asian). Patients acted as their own controls. One
hundred and eight patients completed the study. INTERVENTION: All
patients completed a questionnaire to assess their knowledge of
phosphate and phosphate-binder therapy. Small group teaching sessions
were then delivered to patients by a single dietitian, with the aid of a
hospital interpreter as required. Patients also received information
booklets or audio cassettes translated into Urdu. A second identical
questionnaire was completed a month later. MAIN OUTCOME MEASURES:
Outcome measures involved pre-education and posteducation
knowledge scores, monthly measurements of serum phosphate, calcium, and
mean Kt/V, and parathyroid hormone concentrations every 3 months during
the 5 month run-in period and subsequent 5-month study period. RESULTS:
The education program significantly improved patients' general knowledge
of phosphate and of phosphate-binders (P < .001), especially in
patients with a low pretest score and those of South Asian origin. This
result was associated with a significant reduction in serum phosphate in
patients with hyperphosphatemia (P = .032).
CONCLUSIONS: These findings suggest that a combination of educational
initiatives is effective in enhancing patients' knowledge of phosphate
and phosphate-binders, and consequently in improving serum phosphate
levels in patients with hyperphosphatemia. David
S, Kumpers P, Eisenbach
G, Haller H, Kielstein J. Prospective
evaluation of an in-centre conversion from conventional haemodialysis
to an intensified nocturnal strategy. Nephrol
Dial Transplant 2009;24(7):2232-40. INTRODUCTION:
Under physiological conditions kidneys work continuously, 168 h/week. In
contrast, patients with end-stage renal disease are usually dialyzed
only 12-15 h/ week. This unphysiological
dialysis dose, even if considered adequate by current Kt/V-based dose
estimates, is just capable to maintain the alterations of multiple
metabolic parameters at a level that permits an unacceptable annual
mortality rate of 10-20%, mainly due to cardiovascular events, protein
energy wasting and infections. PATIENTS AND METHODS: Thirteen haemodialysis
patients were converted from conventional (3 x 4 h/week) to an
intensified nocturnal (3 x 8 h/week) dialysis and were longitudinally
followed up for 12 months. Different parameters were evaluated before
treatment conversion and quarterly during the follow-up period [i.e.
dialysis efficacy (eKt/V), mean arterial
pressure (MAP), antihypertensive drug score, extra-cellular volume (ECV),
haemoglobin, transferrin
saturation, ferritin, dose of erythropoiesis-stimulating
agents (ESA), iron requirement, parameters of nutrition (body weight (BW),
albumin, protein, normalized protein catabolic rate (nPCR),
bioelectrical impedance analysis (BIA)), C-reactive protein,
calcium-phosphate product, alkaline phosphatase
(AP), intact parathyroid hormone (iPTH) and
amount of phosphate-binding pharmacotherapy]. RESULTS: The calculated
dialysis efficacy rose after switching the treatment mode (eKt/V
1.87 versus 2.7, P < 0.0001). Further, a significantly decreased MAP
in the pre- (100 versus 89 mmHg) and postdialytic
period (97 versus 83 mmHg), and a decreased ECV (13.8 versus 13.2 L; P =
0.03) even though antihypertensive pharmacotherapy could be
substantially reduced (P < 0.0001), was found. Concomitant with a
reduction of ESA (66.5 versus 45.2 IU/ kg/week; P = 0.006), the haemoglobin
level rose significantly (11.4 versus 12.5 g/dL, P = 0.01). Nutritional
status assessed by BW (70.9 +/- 20.2 versus 72.1 +/- 19.8 kg, P = 0.02),
nPCR (1.39 versus 2.25 g/kg/day, P = 0.02)
and BIA (phase angle: 6.2 versus 6.9 degrees, P < 0.001) improved.
The calcium-phosphate product slightly declined, without changes in the
dose of any phosphate binders. Surprisingly, iPTH
of those patients with intact parathyroid glands (n = 7) increased
approximately 3-fold (27.9 versus 59.35 pmol/L,
P = 0.009), while the AP was found stable. CONCLUSION: This study
demonstrates improvements in numerous dialysis-associated metabolic
variables after intensification of HD time. Of note, an increase of iPTH
was detected in those patients with intact parathyroid glands. Schlieper
G, Risk
factors for cardiovascular calcifications in non-diabetic caucasian
haemodialysis patients. Kidney
Blood Press Res 2009;32(3):161-168. Background/Aims:
Dialysis patients display an increased mortality which is associated
with cardiovascular calcifications. Diabetes mellitus and ethnicity are
known factors that affect the extent of cardiovascular calcifications.
However, most studies have investigated mixed cohorts with diabetics
and/or mixed ethnicity. Methods: Cardiovascular calcifications were
assessed in non-diabetic Caucasian haemodialysis
patients by the semiquantitative Adragao
calcification score (X-ray pelvis and hands) and a novel composite
calcification score encompassing the Adragao
score as well as calcifications detected by X-ray of the fistula arm,
echocardiography of heart valves and carotid ultrasound. Results: Using
multivariate analysis, age, male gender, dialysis vintage, lower Kt/V,
calcium-phosphate product, smoking and high-sensitivity CRP were
independent risk factors for cardiovascular calcifications as assessed
by the Adragao or the composite score. Pulse
wave velocity was independently related to both calcification scores.
Body mass index, cholesterol, triglycerides, iPTH
and serum levels of fetuin-A and uncarboxylated
matrix Gla protein were not associated with
cardiovascular calcifications. Conclusions: In our cohort of
non-diabetic Caucasian haemodialysis
patients, age, male gender, dialysis vintage, smoking, calcium-phosphate
product, high-sensitivity CRP and lower Kt/V were independent risk
factors for cardiovascular calcifications. Whether lowering the
calcium-phosphate product and increasing dialysis efficiency can reduce
cardiovascular calcifications in dialysis patients remains to be
determined. Petrovic
D, Obrenovic R, Stojimirovic B. Risk
factors for aortic valve calcification in patients on regular hemodialysis. Int
J Artif Organs 2009;32(3):173-9. Introduction:
Aortic valve calcification (AVC) accelerates development of aortic valve
stenosis and cardiovascular complications. Hyperphosphatemia
is one of the key risk factors for aortic valve calcification. Aim: The
aim of this study was to evaluate the prevalence of AVC in patients on
regular hemodialysis and to assess the
impact of different factors on its appearance. Method: The study
investigated a total of 115 patients treated in the Hemodialysis
Department of the Urology and Nephrology Clinic at the
CME/CE
Programs Online: ·
ASN
Renal Week 2008 Official Symposia
now available to view (click on title for link):
Managing
CKD-MBD Through the Disease Continuum
(H.
Malluche, MD; R. Thadhani, MD; B. Kestenbaum, MD, MS)
New
Frontiers in Phosphorus Homeostasis in CKD (H. Malluche, MD; D. ·
A Summary of Key Insights from ASN
Renal Week 2008: All-Stage
Management of CKD-MBD: Insights From Renal Week 2008 (C.
Langman, MD;
B.
Kestenbaum, MD, MS Anjay Rastogi, MD, PhD)
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