Nephrol Dial Transplant. 2004 May;19(5):1190-7.
Correction of metabolic acidosis improves
thyroid and growth hormone axes in haemodialysis patients.↑ Back To Top
Wiederkehr MR, Kalogiros J, Krapf R.
Baylor University Medical Center, Dallas Nephrology Associates,
3500 Gaston Avenue, Dallas, TX 75246, USA.
BACKGROUND: Chronic metabolic
acidosis (CMA) in normal adults results in complex endocrine
and metabolic alterations including growth hormone (GH)
insensitivity, hypothyroidism, hyperglucocorticoidism,
hypoalbuminaemia and loss of protein stores. Similar
alterations occur in chronic renal failure, a prototypical
state of CMA. We evaluated whether metabolic acidosis contributes
to the endocrine and metabolic alterations characteristic
of end-stage renal disease. METHODS: We
treated 14 chronic haemodialysis patients with daily oral
Na-citrate for 4 weeks, yielding a steady-state pre-dialytic
plasma bicarbonate concentration of 26.7 mmol/l, followed
by 4 weeks of equimolar Na-chloride, yielding a steady-state
pre-dialytic plasma bicarbonate of 20.2 mmol/l.
RESULTS: Blood pressure, body weight and dialysis adequacy
were equivalent in the two protocols. Na-citrate
treatment corrected CMA, improved GH insensitivity, increased
and normalized plasma free T(3) concentration, and improved
plasma albumin. Correction of CMA had no significant
effect on measured cytokines (interleukin-1beta and -6,
tumour necrosis factor-alpha) or acute phase reactants
(C-reactive protein, serum amyloid A, alpha(2)-macroglobulin).
CONCLUSION: CMA contributes to the derangements of the
growth and thyroid hormone axes and to hypoalbuminaemia,
but is not a modulator of systemic inflammation in dialysis
patients. Correcting CMA may improve nutritional and metabolic
parameters and thus lower morbidity and mortality
Kidney Int. 2002 Dec;62(6):2160-6.↑ Back To Top
Bone histology and bone mineral density after correction
of acidosis in distal renal tubular acidosis.
Domrongkitchaiporn S, Pongskul C, Sirikulchayanonta
V, Stitchantrakul W, Leeprasert V, Ongphiphadhanakul B,
Radinahamed P, Rajatanavin R.
Department of Medicine, Faculty of Medicine, Ramathibodi
Hospital, Mahidol University, Bangkok, Thailand.
BACKGROUND: The association between chronic metabolic acidosis
and alterations in bone cell functions has been demonstrated
in vitro and in animal studies. However, the causal role
of acidosis and the effects of alkaline therapy on bone
histology and bone mineral density in chronic metabolic
acidosis have never been systematically demonstrated in
humans. This study was conducted to examine the alterations
in bone mineral density and bone histology before and after
correction of acidosis among patients with distal renal
tubular acidosis (dRTA) METHODS: Correction of metabolic
acidosis by potassium citrate was done in non-azotemic
dRTA patients, 6 females and 4 males, who had never received
long-term alkaline therapy before enrolling into this study.
Blood chemistries, serum intact parathyroid hormone, and
24-hour urine collection for the determination of urinary
calcium, phosphate, sodium, potassium, bone mineral density
determination, and transiliac bone biopsy were done in
all patients at baseline and after one year of potassium
citrate therapy. RESULTS: Significant elevations in serum
bicarbonate (16.5 +/- 3.0 vs. 24.6 +/- 2.8 mEq/L, P < 0.05)
and urinary potassium excretion (35.2 +/- 7.9 vs. 55.4
+/-3.5 mEq/L, P < 0.05) were observed after potassium
citrate therapy. No significant alterations in other serum
and urine electrolytes were found after the therapy. Serum
intact parathyroid hormone level was also significantly
elevated after one year of treatment (12.8 +/- 7.3 vs.
26.2 +/- 8.7 pg/mL, P < 0.05). Bone formation rate was
significantly suppressed at baseline and was normalized
by the treatment (0.02 +/- 0.02 vs. 0.06 +/- 0.03 microm(3)/microm(2)/day,
P < 0.05). There were non-significant elevations in
trabecular bone volume, osteoblastic and osteoclastic numbers.
Bone mineral densities in dRTA patients were also significantly
decreased below normal values in most studied areas at
baseline and were significantly elevated at the trochanter
of femur (0.677 +/- 0.136 vs. 0.748 +/- 0.144 g/c m(2),
P < 0.05) and total femur (0.898 +/- 0.166 vs. 0.976
+/- 0.154 g/c m(2), P < 0.05) after the treatment. CONCLUSIONS:
This study demonstrates that alkaline
therapy corrects abnormal bone cell function and elevates
bone mineral density in dRTA patients, indicating
the causal role of acidosis in the alterations of bone
cell functions and reduction in bone mineral density. Parathyroid
gland activity also may be involved in the adaptation of
the body to chronic metabolic acidosis.
DGHS Chron. 1985 Jan-Mar;21(1):1, 3.
Dehydration: W.H.O. has a new solution.
PIP: The World Health Organization (WHO)
has developed an improved formula for oral rehydration
solution (ORS) that is based on trisodium citrate dihydrate
rather than sodium bicarbonate. The new preparation will
be easier and cheaper to package, have a longer shelf-life,
and be more effective against diarrhea. Clinical trials
have shown that the new formula corrects acidosis at a
similar rate to sodium bicarbonate and is far more effective
in reducing the amount of diarrhea, especially in diseases
such as cholera. Although the citrate solution costs slightly
more than the earlier preparation, packaging costs can
be reduced by up to 50% through local production, making
the end product cheaper. Local production of ORS-citrate
does not require new investment or changes in equipment.
WHO is recommending that countries with supplies of ORS-bicarbonate
should use up these stocks and then decide whether to switch
to the new formula. Research is also being carried out
on other improved ORS formulas, e.g. glycine-fortified
and rice powder-based ORS.
Eur J Nutr. 2001 Oct;40(5):200-13.↑ Back To Top
Diet, evolution and aging--the pathophysiologic effects
of the post-agricultural inversion of the potassium-to-sodium
and base-to-chloride ratios in the human diet.
Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian
University of California, San Francisco 94143, USA.
we humans should be better adapted physiologically to the
diet our ancestors were exposed to during millions of years
of hominid evolution than to the diet we have been eating
since the agricultural revolution a mere 10,000 years ago,
and since industrialization only 200 years ago. Among the
many health problems resulting from this mismatch between
our genetically determined nutritional requirements and
our current diet, some might be a consequence in part of the deficiency
of potassium alkali salts (K-base), which are amply present
in the plant foods that our ancestors ate in abundance,
and the exchange of those salts for sodium chloride (NaCl), which
has been incorporated copiously into the contemporary diet,
which at the same time is meager in K-base-rich plant foods.
Deficiency of K-base in the diet increases the net systemic
acid load imposed by the diet. We know that clinically-recognized
chronic metabolic acidosis has deleterious effects on the
body, including growth retardation in children, decreased
muscle and bone mass in adults, and kidney stone formation,
and that correction of acidosis can ameliorate those conditions.
Is it possible that a lifetime of eating diets that deliver
evolutionarily superphysiologic loads of acid to the body
contribute to the decrease in bone and muscle mass, and
growth hormone secretion, which occur normally with age?
That is, are contemporary humans suffering from the consequences
of chronic, diet-induced low-grade systemic metabolic acidosis?
Our group has shown that contemporary net acid-producing
diets do indeed characteristically produce a low-grade
systemic metabolic acidosis in otherwise healthy adult
subjects, and that the degree of acidosis increases with
age, in relation to the normally occurring age-related
decline in renal functional capacity. We
also found that neutralization of the diet net acid load
with dietary supplements of potassium bicarbonate (KHCO3)
improved calcium and phosphorus balances, reduced bone
resorption rates, improved nitrogen balance, and mitigated
the normally occurring age-related decline in growth hormone
secretion--all without restricting dietary NaCl. Moreover,
we found that co-administration of an alkalinizing salt
of potassium (potassium citrate) with NaCl prevented NaCl
from increasing urinary calcium excretion and bone resorption,
as occurred with NaCl administration alone. Earlier studies
estimated dietary acid load from the amount of animal protein
in the diet, inasmuch as protein metabolism yields sulfuric
acid as an end-product. In cross-cultural epidemiologic
studies, Abelow found that hip fracture incidence in older
women correlated with animal protein intake, and they suggested
a causal relation to the acid load from protein. Those
studies did not consider the effect of potential sources
of base in the diet. We considered that estimating the
net acid load of the diet (i. e., acid minus base) would
require considering also the intake of plant foods, many
of which are rich sources of K-base, or more precisely
base precursors, substances like organic anions that the
body metabolizes to bicarbonate. In following up the findings
of Abelow et al., we found that plant food intake tended
to be protective against hip fracture, and that hip fracture
incidence among countries correlated inversely with the
ratio of plant-to-animal food intake. These findings were
confirmed in a more homogeneous population of white elderly
women residents of the U.S. These findings support affirmative
answers to the questions we asked above. Can we provide
dietary guidelines for controlling dietary net acid loads
to minimize or eliminate diet-induced and age-amplified
chronic low-grade metabolic acidosis and its pathophysiological
sequelae. We discuss the use of algorithms to predict the
diet net acid and provide nutritionists and clinicians
with relatively simple and reliable methods for determining
and controlling the net acid load of the diet. A more difficult
question is what level of acidosis is acceptable. We argue
that any level of acidosis may be unacceptable from an
evolutionarily perspective, and indeed, that a low-grade
metabolic alkalosis may be the optimal acid-base state
for humans.↑ Back To Top
Urol Res. 2001 Oct;29(5):295-302.↑ Back To Top
A comparison of the effects of potassium citrate and
sodium bicarbonate in the alkalinization of urine in homozygous
Fjellstedt E, Denneberg T, Jeppsson JO, Tiselius HG.
Department of Internal Medicine, Motala Hospital, Sweden.
For many years, urine alkalinization has been one of the
cornerstones in the treatment of homozygous cystinuria.
Because of the relationship found between the excretion
of urinary sodium and cystine, potassium citrate has emerged
as the preferred sodium-free alkalizing agent. To evaluate the
usefulness of potassium citrate for urine alkalization in
cystinuric patients, sodium bicarbonate and potassium citrate
were compared in 14 patients (10 on tiopronin treatment
and four without treatment with sulfhydryl compounds).
The study started with 1 week without the use of any alkalizing
agents (Period 0) followed by 2 weeks with sodium bicarbonate
(Period 1) and 2 weeks with potassium citrate (Period 2).
Urinary pH, volume, excretion of sodium, potassium, citrate
and free cystine, as well as the plasma potassium concentration,
were recorded. Potassium citrate was shown to be effective
as an alkalizing agent and, in this respect, not significantly
different from sodium bicarbonate. Even though a normal
diet was used, a significant increase in urinary sodium
excretion was observed with sodium bicarbonate (Period
1). Urinary potassium and citrate excretion increased with
potassium citrate (Period 2). A significant correlation
was found between urinary sodium and cystine in the tio-pronin-treated
patients. No significant differences in cystine excretion
were recorded in Periods 0, 1 and 2. Plasma potassium was
significantly higher during Period 2, but only one patient
developed a mild hyperkalemia (5.0 mmol/l). The
use of potassium citrate for urine alkalization in homozygous
cystinuria is effective and can be recommended in
the absence of severe renal impairment.
Am J Kidney Dis. 2001 Nov;38(5):979-87.
Simplified citrate anticoagulation for high-flux hemodialysis.
Apsner R, Buchmayer H, Lang T, Unver B, Speiser W, Sunder-Plassmann
G, Horl WH.
Department of Internal Medicine III, Division of Nephrology
and Dialysis, and Institute of Laboratory Medicine, General
Hospital and Medical School of Vienna, Austria.
In a randomized crossover trial, we compared
a simple citrate anticoagulation protocol for high-flux
hemodialysis with standard anticoagulation by low-molecular-weight
heparin (dalteparin). Primary end points were urea reduction
rate (URR), Kt/V, and control of electrolyte and acid-base
homeostasis. Secondary end points were bleeding time at
vascular puncture sites and markers of activation of platelets,
coagulation, and fibrinolysis. Solute removal during citrate
dialysis was excellent (URR, 0.71 +/- 0.06; Kt/V, 1.55
+/- 0.3) and similar to results of conventional bicarbonate
hemodialysis anticoagulation with dalteparin (URR, 0.72
+/- 0.04; Kt/V, 1.56 +/- 0.2). Electrolyte
control was effective with both anticoagulation regimens,
and total and ionized calcium, sodium, potassium, and phosphate
concentrations at the end of dialysis did not differ. Alkalemia
was less frequent after citrate than conventional dialysis
(pH 7.5 in 25% versus 62% of patients; mean pH at end of
dialysis, 7.46 +/- 0.06 versus 7.51 +/- 0.07; P < 0.01).
Bleeding time at puncture sites was shorter by 30% after
citrate compared with dalteparin anticoagulation (5.43
+/- 2.80 versus 7.86 +/- 2.93 minutes; P < 0.001). Activation
of platelets, coagulation, and fibrinolysis was modest
for both treatments and occurred mainly within the dialyzer
during dalteparin treatment and in the vascular-access
region during citrate anticoagulation. Citrate-related
adverse events were not observed. We conclude that citrate
anticoagulation for high-flux hemodialysis is feasible
and safe using a simple infusion protocol. ↑ Back To Top
Respir Care. 2001 Apr;46(4):354-65.
Metabolic alkalosis.↑ Back To Top
Khanna A, Kurtzman NA.
Department of Internal Medicine, Texas Tech University
Health Sciences Center, Lubbock, TX, USA.
Metabolic alkalosis is a primary pathophysiologic event
characterized by the gain of bicarbonate or the loss of
nonvolatile acid from extracellular fluid. The kidney preserves
normal acid-base balance by two mechanisms: bicarbonate
reclamation, mainly in the proximal tubule, and bicarbonate
generation, predominantly in the distal nephron. Bicarbonate
reclamation is mediated mainly by a Na(+)-H(+) antiporter
and to a smaller extent by the H(+)-ATPase (adenosine triphosphate-ase).
The principal factors affecting HCO3(-) reabsorption include
effective arterial blood volume, glomerular filtration
rate, chloride, and potassium. Bicarbonate
regeneration is primarily affected by distal Na(+) delivery
and reabsorption, aldosterone, arterial pH, and arterial
partial pressure of carbon dioxide. To generate
metabolic alkalosis, either a gain of base or a loss of
acid must occur. The loss of acid may be via the gastrointestinal
tract or via the kidney. Excess base may be gained by oral
or parenteral HCO3(-) administration or by lactate, acetate,
or citrate administration. Factors
that help maintain metabolic alkalosis include decreased
glomerular filtration rate, volume contraction, hypokalemia,
hypochloremia, and aldosterone excess. Clinical
states associated with metabolic alkalosis are vomiting,
mineralocorticoid excess, the adrenogenital syndrome, licorice
ingestion, diuretic administration, and Bartter's and
Gitelman's syndromes. The effects of metabolic alkalosis
on the body are variable and include effects on the central
nervous system, myocardium, skeletal muscle, and liver.
Treatment of this disorder is simple, once the pathophysiology
of the cause is delineated. Therapy consists of reversing
the contributory factors that are promoting the alkalosis
and, in severe cases, administration of carbonic anhydrase
inhibitors, acid infusion, and low bicarbonate dialysis.
J Am Diet Assoc. 1999 Dec;99(12):1536-41.
Alterations in taste thresholds in men
with chronic obstructive pulmonary disease.↑ Back To Top
Chapman-Novakofski K, Brewer MS, Riskowski J, Burkowski
C, Winter L.
Department of Food Science and Human Nutrition, University
of Illinois, Urbana 61801, USA.
OBJECTIVE: Weight loss is a common occurrence in chronic
obstructive pulmonary disease (COPD), and efforts to increase
energy intake are often unsuccessful. The objectives of
this study were to determine if there were any taste threshold
differences between normal-weight and underweight men with
COPD, and to determine if there was any association between
absolute and recognition taste thresholds and biochemical
data associated with COPD. DESIGN: Cross-sectional comparative.
SUBJECTS/SETTING: Potential subjects were identified by
their physicians. Forty-six men were willing and eligible
to participate. Subjects were given sets of triangle taste
tests for 4 tastants: sweet, salty, bitter, and sour. Additional
information collected included health history data and
biochemical data. Subjects were classified as underweight
or normal weight for comparison. STATISTICAL ANALYSES PERFORMED:
Independent t tests and one-way analysis of variance were
used to determine differences between persons in the underweight
(n = 17) and normal-weight (n = 29) groups, and the influence
of confounding variables. Bivariate correlations were used
to determine associations between tastant thresholds and
biochemical indexes for the entire group (N = 46). Stepwise
regression analysis was used to determine significant variables
in prediction of thresholds of the 4 tastants for the entire
group (N = 46). RESULTS: Underweight subjects had a significantly
higher bitter taste threshold than normal-weight subjects
(5.76 vs 5.10, P = .016). A significant negative correlation
was found between absolute bitter and bicarbonate (r =
-.39, P = .01) and PCO2 (r = -.34, P = .02). A significant
regression equation for absolute bitter taste threshold
was determined (P = .011) on the basis of bicarbonate values;
and upon body mass index for bitter taste recognition threshold
(P = .031). APPLICATIONS: Recognition that patients with
COPD may have alterations in taste that are associated
with weight status and/or biochemical status can guide
dietitians in their recommendations for meal plans targeting
individual weight goals.
J Nutr. 1999 Nov;129(11):2043-7.
Dietary potassium bicarbonate and potassium
citrate have a greater inhibitory effect than does potassium
chloride on magnesium absorption in wethers.↑ Back To Top
Schonewille JT, Beynen AC, Van't Klooster AT, Wouterse
H, Ram L.
Department of Nutrition, Faculty of Veterinary Medicine,
Utrecht University, 3508 TD Utrecht, The Netherlands.
We addressed the question whether the type of anion in
potassium salts affects magnesium absorption and the transmural
potential difference by using wethers (n = 8) fed a control
diet and diets supplemented with equimolar amounts of KHCO(3),
KCl or K-citrate according to a Latin-square design. The
control diet contained 10.9 g K/kg dry matter and the high
K diets contained 41.3 g K/kg dry matter. Compared with
the control diet, KHCO(3) and K-citrate significantly reduced
apparent Mg absorption by 9.5 and 6.5%, respectively. Supplemental
KCl tended to reduce (P = 0.070) group mean magnesium absorption
by 5.5%. Consumption of supplemental KHCO(3) and K-citrate
produced a significant increase in the transmural potential
difference (serosal side = positive) by 17.1 and 20.7 mV,
respectively, whereas the addition of KCl to the diet did
not. The individual values for the four diets tended to
show a negative correlation (r = -0.336, n = 32, P = 0.060)
between the transmural potential difference and apparent
magnesium absorption. We conclude that different
potassium salts have different effects on magnesium absorption
in ruminants as caused by different effects on the
transmural potential difference.
Artif Organs. 1998 Jul;22(7):614-7.↑ Back To Top
Heparin-induced hyperkalemia in chronic hemodialysis
patients: comparison of low molecular weight and unfractionated
Hottelart C, Achard JM, Moriniere P, Zoghbi F, Dieval
J, Fournier A.
Service de Nephrologie, Medecine Interne, CHU Amiens, France.
and subsequent hyperkalemia are well described reversible
side effects of prolonged treatment with heparin.
This study was designed to examine whether the discontinuous
use of heparin three times a week to prevent thrombosis
formation during hemodialysis sessions could also induce
hypoaldosteronism and might contribute to increased predialysis
kalemia in hemodialysis patients. Two different heparinization
regimens were prospectively compared in a crossover study
of 11 chronic hemodialysis patients. During 2 consecutive
weeks, the patients were dialyzed each week with either
their usual doses of unfractionated heparin (UH) (6,160
IU +/- 1,350 IU) or low molecular weight heparin (LMWH)
(15 anti-Xa activity [aXa] U/kg + 5 aXa U/kg/h). In all
but 2 patients, the predialysis level of plasma K+ was
higher with UH than with LMWH, and the mean value was higher
(5.66+/-0.83 versus 5.15+/-0.68 mM, p = 0.01) while no
differences in the predialysis plasma concentrations of
creatinine, phosphate, urea, and bicarbonate were observed,
excluding the potential role of differences in diet and
dialysis efficacy in explaining the higher plasma K+ concentration
with UH. The mean plasma aldosterone to plasma renin activity
(pRA) ratio was higher with LMWH than with UH (149.54+/-123.1
versus 111.91+/-86.22 pg/ng/ h, p < 0.05). Individual
plasma aldosterone values were found to be correlated to
pRAs both during the UH period and the LMWH period, and
the slope of the positive linear relation between plasma
aldosterone and pRA was lower during the UH treatment period
(63 versus 105 pg/ng/h). Finally, a negative linear correlation
was found between the differences in individual predialysis
plasma K+ observed during the 2 protocols and the differences
in the corresponding plasma aldosterone levels, suggesting
a link between the higher kalemia and the lower aldosterone
responsiveness to angiotensin with unfractionated heparin.
Although it cannot be concluded whether or not LMWH inhibits
aldosterone synthesis, should LMWH decrease aldosterone
production, this side effect is 33% less marked than that
of UH so that the predialysis plasma K+ levels are 10%
lower. This property makes
LMWH use preferable to that of UH in patients with elevated
Arch Dis Child. 1977 Apr;52(4):255-67.↑ Back To Top
Congenital chloride diarrhoea. Clinical analysis of
21 Finnish patients.
Holmberg C, Perheentupa J, Launiala K, Hallman
Clinical findings in 21 Finnish children with congenital
chloride diarrhoea are reported. Inheritance of this disease
by the autosomal recessive mode is established. All children
were born 1-8 weeks prematurely. Hydramnios was present
in every case and no meconium was observed; intrauterine
onset of diarrhoea is thus apparent. In most cases the
diarrhoea or passing of large volumes of "urine" was
noted on the first day of life and the abdomen was usually
large and distended. The neonatla weight loss was abnormally
large, and was associated with hypochloraemia and hyponatraemia.
Some infants survived the neonatal period without adequate
therapy. They presented later with failure to thrive and
usually had hypochloraemia, hypokalaemia, and metabolic
alkalosis associated with hyperaldosteronism. However,
these features may be absent and the diagnosis is based
on a history of hydramnios and diarrhoea, and a faecal
Cl- concentration which always exceeds 90 mmol/l when fluid
and electrolyte deficits have been corrected. Lower faecal
Cl- concentrations were seen only in chronic hypochloraemia,
which is also associated with achloriduria. Adequate
treatment consists of full continuous replacement of the
faecal losses of water, NaCl, and KCl. This should
be given intravenously in the early neonatal period; later
a solution can be taken orally with meals. The dose has
to be adjusted to maintain normal serum electrolyte concentrations,
normal blood pH, and some chloriduria. This therapy prevents
the renal lesions and the retarded growth and psychomotor
development which were seen in the children who were diagnosed
late and in those who received inadequate replacement therapy.
The watery diarrhoea persists and increases slightly with
age, though patients learn to live with their disease and
to make an adequate social adjustment.
Acta Med Scand Suppl. 1986;707:33-6.↑ Back To Top
Intracellular electrolytes in cardiac failure.
Wester PO, Dyckner T.
In congestive heart failure (CHF) there are several compensatory
mechanisms operating which may influence electrolyte metabolism.
The activation of the renin-angiotensin-aldosterone system
causes retention of sodium (Na) and losses of potassium
(K) and magnesium (Mg). The secondary hyperaldosteronism
may give rise to high intracellular Na and low intracellular
K through a direct permeability effect on the cell membrane. The
Mg deficiency may lead to a further increase of intracellular
Na and decrease of intracellular K since Mg is a necessary
ion for the function of the Na-K pump. In 297 patients
with diuretic treated CHF we found that 42% had hypokalemia,
37% hypomagnesemia and 12% hyponatremia. We
also found that 57% had excess muscle Na, 52% had depletion
of muscle K and 43% had low muscle Mg. We have also shown
that the low muscle K cannot be corrected by K supplementation
when there is a concomitant Mg deficiency and that
Mg infusions may change the disturbed relation between
extra-and intracellular electrolytes towards normal.
Eur J Clin Nutr. 2004 Feb;58(2):270-6.
Influence of a mineral water rich in
calcium, magnesium and bicarbonate on urine composition
and the risk of calcium oxalate crystallization.↑ Back To Top
Siener R, Jahnen A, Hesse A.
Division of Experimental Urology, Department of Urology,
University of Bonn, Bonn, Germany.
OBJECTIVE: To evaluate the effect of a mineral water rich
in magnesium (337 mg/l), calcium (232 mg/l) and bicarbonate
(3388 mg/l) on urine composition and the risk of calcium
oxalate crystallization. DESIGN: A total of 12 healthy
male volunteers participated in the study. During the baseline
phase, subjects collected two 24-h urine samples while
on their usual diet. Throughout the control and test phases,
lasting 5 days each, the subjects received a standardized
diet calculated according to the recommendations. During
the control phase, subjects consumed 1.4 l/day of a neutral
fruit tea, which was replaced by an equal volume of a mineral
water during the test phase. On the follow-up phase, subjects
continued to drink 1.4 l/day of the mineral water on their
usual diet and collected 24-h urine samples weekly. RESULTS:
During the intake of mineral water, urinary pH, magnesium
and citrate excretion increased significantly on both standardized
and normal dietary conditions. The mineral water led to
a significant increase in urinary calcium excretion only
on the standardized diet, and to a significantly higher
urinary volume and decreased supersaturation with calcium
oxalate only on the usual diet. CONCLUSIONS: The
magnesium and bicarbonate content of the mineral water
resulted in favorable changes in urinary pH, magnesium
and citrate excretion, inhibitors of calcium oxalate stone
formation, counterbalancing increased calcium excretion.
Since urinary oxalate excretion did not diminish, further
studies are necessary to evaluate whether the ingestion
of calcium-rich mineral water with, rather than between,
meals may complex oxalate in the gut thus limiting intestinal
absorption and urinary excretion of calcium and oxalate.
J Med Assoc Thai. 2002 Nov;85 Suppl 4:S1143-9.
The optimal dose of potassium citrate
in the treatment of children with distal renal tubular
Tapaneya-Olarn W, Khositseth S, Tapaneya-Olarn
C, Teerakarnjana N, Chaichanajarernkul U, Stitchantrakul
W, Petchthong T.
Department of Pediatrics, Faculty of Medicine,
Ramathibodi Hospital, Mahidol University, Bangkok 10400,
BACKGROUND: Distal renal tubular acidosis
(RTA) is a common cause of intractable calcium nephrolithiasis.
In adults, the use of potassium citrate (PC) in distal
RTA effectively decreases metabolic acidosis and the risk
of calcium oxalate stone but it cannot decrease the risk
of calcium phosphate stone. However, there is no report
for the optimal dose of PC and the risk of calcium stone
in distal RTA in children. OBJECTIVE: To evaluate the optimal
dose of PC that minimizes the risk of calcium nephrolithiasis
in children with distal RTA. METHOD: Prospective study
PATIENTS: Children who have distal RTA and were followed-up
for 4 months. Patients were studied in a control phase,
1 month of PC 2 mEq/kg/day, 2 months of PC 3 mEq/kg/day
and 1 month of PC 4 mEq/kg/day. The urine specimens of
41 normal children were measured for the reference value
of the parameters determining the risk of calcium stone.
RESULTS: Eight children (mean age of 10 +/- 3.7 years,
female : male = 6: 2) with distal RTA were studied during
the control phase and after receiving PC 2 mEq/kg/day for
I month. Treatment with PC 2 mEq/kg/day was not able to
normalize serum bicarbonate and caused no significant change
in the urine citrate/creatinine ratio, and activity production
of calcium phosphate stone but it caused a significant
decrease in the urine calcium/citrate ratio. Although PC
3 mEq/kg/day for I month normalized plasma bicarbonate,
only this dose given for 2 months caused a significant
increase in the urine citrate/creatinine ratio and urine
calcium/ citrate ratio to values that were not different
from normal children, while the activity production of
calcium phosphate stone did not decrease to normal level.
The effect of PC 4 mEq/kg/day was similar to that of 3
mEq/kg/day. CONCLUSION: Potassium
citrate 3 mEq/kg/day for 2 months effectively normalized
serum bicarbonate and decreased the risk of calcium oxalate
stone but this treatment was theoretically unable
to reduce the risk of calcium phosphate stone in children
with distal RTA.↑ Back To Top
J Ren Nutr. 1998 Jul;8(3):127-31.↑ Back To Top
Potassium and sodium intake and excretion in calcium
stone forming patients.
Martini LA, Cuppari
L, Cunha MA, Schor N, Heilberg IP.
Master in Science, Universidade Federal de Sao Paulo-EPM,
Sao Paulo, Brazil.
OBJECTIVE: To determine mean potassium (K) intake and its
correlation with urinary calcium (uCa) and citrate excretion,
as well as uCa, sodium (Na), and K levels of calcium stone
forming patients. We determined the K-rich foods most commonly
consumed by these patients. DESIGN: Case-control. SETTING:
University-affiliated outpatient renal Lithiasis Unit.
PATIENTS AND CONTROLS: One hundred hypercalciuric calcium
stone forming patients (CSF, 54 men/46 women), 37 with
associated hypocitraturia, were sequentially enrolled in
the study that was performed before the initiation of any
care for their renal stones. The control group consisted
of 100 age-matched healthy subjects (HS, 47 men/53 women)
who were laboratory employees with no history of renal
stones. INTERVENTION: The analyses consisted of a 3-day
dietary record to determine the mean K and calcium (Ca)
intakes, and a 24-hour urine sample with measurements of
K, Ca, Na, and citrate. MAIN OUTCOME MEASURE: K and Na
intake determined by dietary record. RESULTS: uCa and Na
levels and the Na/K ratio were significantly higher for
CSF versus HS (238 +/- 118 v 148 +/- 74 mg/24 hours, 238
+/- 100 v 181 +/- 68 mEq/24 hours, 6.6 +/- 3.5 v 5.1 +/-
2.3, respectively, P < .05). The mean citrate excretion
was lower in CSF than in HS patients (410 +/- 265 v 530
+/- 240 mg/24 hours). Mean uCa did not differ between groups.
CSF patients showed a higher sodium chloride intake compared
with HS (14 +/- 4 vs 8 +/- 3 g/day). The mean Ca intake
of CSF and HS were 559 +/- 327 and 457 +/- 363 mg/day,
respectively. The mean K intake of CSF and HS were 58 +/-
17 and 51 +/- 27 mEq/day. A positive correlation was observed
between uCa and urinary sodium (r = .40 and r = .65, P < .05),
urinary potassium and urinary citrate (r = .25 and r =
.53, P <
.05), uCa and Na/K (r = .33 and r = .56, P < .05) respectively
for CSF and HS. The following were the K-rich foods consumed
at least once a day by these groups: beans (by 70% of CSF
and 75% of HS), tomatoes (by 42% of CSF and 50% of HS),
oranges (by 30% of CSF and 55% of HS), and bananas (by
42% of CSF and 23% of HS). CONCLUSION: Despite the consumption
of K-rich foods at least once a day, the mean
K intake by CSF patients was 58 mEq/day. This intake can
still be considered to be low, although
it meets recommended daily dietary allowance requirements.
Therefore, we describe herein a population of CSF with
high-Na intake and normal- to low-K intake, which may contribute
to stone formation.
J Am Coll Nutr. 1998 Apr;17(2):148-54.
Calciuric effects of short-term dietary
loading of protein, sodium chloride and potassium citrate
in prepubescent girls.↑ Back To Top
Duff TL, Whiting SJ.
College of Pharmacy and Nutrition, University of Saskatchewan,
OBJECTIVE: Studies using adult human subjects indicate
that dietary protein and sodium chloride have negative
effects on the retention of calcium by increasing urinary
calcium excretion, while alkaline
potassium improves calcium retention along with
decreasing urinary calcium losses. This study investigated
the effect of these dietary factors on acute urinary calcium
excretion in 14 prepubescent girls age 6.7 to 10.0 years.
METHODS: Subjects provided a fasting urine sample then
consumed a meal containing one of five treatments: moderate
protein (MP) providing 11.8 g protein, moderate protein
plus 26 mmol sodium chloride (MP+Na), high protein (HP)
providing 28.8 g protein, high protein plus 26 mmol sodium
chloride (HP+Na), or high protein plus 32 mmol potassium
as tripotassium citrate (HP+K). Urine was collected at
1.5 and 3.0 hours after the meal. Supplemental protein
was given as 80:20 casein:lactalbumin. Test meals were
isocaloric, and unless intentionally altered, components
of interest except phosphate were equal between treatments.
Each subject completed all five treatments. RESULTS: Urinary
calcium excretion rose after the meal, peaking at 1.5 hours.
There were no significant differences in calcium excretion
between treatments at any time point. The high protein
treatments did not result in a significant increase in
either net acid or sulfate excretion at 1.5 hours compared
to moderate protein. Dietary sodium chloride had no effect
on urinary sodium or calcium excretion over the 3 hours. After
the potassium treatment, sodium excretion increased (p< or
=0.002) and net acid excretion decreased (p<0.001) compared
to other treatments at 1.5 hours. CONCLUSIONS: In
children, a simultaneous increase in protein and phosphorus
due to increased milk protein intake did not increase acute
urinary calcium excretion. An effect of dietary
sodium chloride on acute urinary calcium excretion was
not observed. Both these findings were similar to those
of adult studies previously conducted in the same laboratory
using similar format and treatments. Potassium
citrate was not hypocalciuric in children, a response differing
from that for adults, who have shown a decrease
in acute urinary calcium excretion in response to alkaline
potassium treatment. Further characterization of calciuric
responses to dietary factors is required for children,
who may differ from adults in many respects.
Magnesium. 1984;3(4-6):324-38.↑ Back To Top
Influence of intravenous Mg++ solutions on renal excretion
of potassium, sodium, calcium, chloride, intraleukocytic
potassium and peripheral vascular resistance: a metabolic
and hemodynamic study in normal volunteers.
Glanzer K, Schlebusch H, Sorger M, Pannenbecker
D, Kruck F.
In an open randomized crossover trial 8 healthy male volunteers
received an intravenous infusion of potassium chloride,
potassium/magnesium chloride, potassium-(D,L)-aspartate,
and potassium/magnesium-(D,L)-aspartate. Equimolar amounts
of potassium (27.75 mmol) and magnesium (13.9 mmol) were
given in a 500-ml volume during 24 h. During two 9-day
periods subjects were maintained on a constant diet with
a daily intake of 80 mmol potassium and 60 mmol magnesium.
Infusions were administered on day 5 and 7 of each period.
Serum and urine electrolyte concentrations as well as intraleukocyte
potassium were measured before, during, and after the tests;
cardiac output and systemic vascular resistance were determined
by impedance cardiography. Potassium and magnesium containing
solutions did not influence renal elimination of potassium,
and also the circadian rhythm of potassium excretion did
not show any change. The
elimination of sodium, calcium, potassium, and chloride
rose significantly over the corresponding control values
during magnesium infusions, but not when potassium salts
were given. The
increase of calcium excretion after Mg++ is most probably
due to suppression of parathyroid hormone. Intraleukocyte
potassium was not affected significantly by the various
infusions, indicating that intracellular compartments are
completely filled. There was no evidence that the anion
(D,L-aspartate or chloride) had a significant effect on
all measured variables. Mean arterial blood pressure and
peripheral vascular resistance were not altered significantly
during the infusions.
Am J Kidney Dis. 1998 Jan;31(1):19-27.↑ Back To Top
On the mechanism of the effects of potassium restriction
on blood pressure and renal sodium retention.
Gallen IW, Rosa RM, Esparaz DY, Young
JB, Robertson GL, Batlle D, Epstein
FH, Landsberg L.
Department of Medicine, Northwestern University Medical
School, Chicago, IL, USA.
Dietary potassium restriction
increases sodium and chloride retention, whereas potassium
administration promotes both diuresis and natriuresis. In
epidemiologic and clinical studies, potassium intake is
inversely related to blood pressure and is lower in blacks
than in whites. The present studies examined the mechanism
by which potassium restriction fosters sodium conservation
and the impact of race on this response. Twenty-one healthy
black and white men and women ingested an isocaloric, potassium-restricted
diet (20 mmol/d) containing 180 mmol/d of sodium with and
without a potassium supplement (80 mmol/d) for 9 days on
two occasions. Additionally, eight of these subjects ingested
the same diets for 3 days followed by a water load to determine
free water clearance before and during the early phase
of dietary potassium restriction. During
potassium restriction, mean arterial pressure (MAP)
derived from 24-hour blood
pressure measurements was higher (85.7 +/- 1.6 mm
Hg v 82.0 +/- 1.3 mm Hg; P < 0.001), cumulative sodium
excretion lower (984 +/- 59 mmol/d v 1,256 +/- 58 mmol/d;
P < 0.001), and weight greater (71.1 +/- 2.1 kg v 69.3
+/- 2.2 kg; P < 0.001). Blacks displayed no greater
increase in MAP, although they excreted less sodium overall
and less potassium on the potassium-supplemented diet.
After a water load, minimum urine osmolality (Uosm) was
lower (53.0 +/- 3.0 mOsm/L v 65.6 +/- 3.5 mOsm/L; P = 0.01)
and free water clearance greater (4.44 +/- 0.59 mL/min
v3.72 +/- 0.58 mL/min; P = 0.009) during potassium restriction.
In conclusion, in healthy, normotensive subjects, potassium
restriction was associated with an increase in blood pressure
and volume expansion effected by increased renal sodium
and chloride retention. Potassium restriction was also
associated with increased free water clearance and enhanced
diluting capacity consistent with augmentation of Na+,
K+:2Cl- cotransporter activity in the thick ascending limb
of Henle. This mechanism may play an important role in
the renal adaptation required for potassium conservation,
but at the expense of sodium chloride retention and an
elevation in blood pressure.
• The E-Lyte Story:
Why You Need Electrolytes!
• Why No Carbs In ElyteSport
• Compare ElyteSport with
other "Sports" drinks
• Pickle Juice
• Taking A Peek Inside a Muscle
• ElyteSport Preloading