Talletin vuonna 2002 artikkelin :Fernandes I et al. Sulfate homeostasis, NaSi-1 cotransporter, and SAT-1 exhancer expression in chronic renal failure in rats. Kidney Int 2001 Jan ; 59(1):210-21. Jouduin K-vitamiinityöni yhteydessä katsomaan rikkiaineenvaihduntaa, koska osa K-vitamiinifunktioista toimi sillä alueella ( sulfotransferaasien ja arylsulfataasien tarvitsemana cofaktorina ja lipidisynteesien alueella myös sulfatidien synteesin varhaisvaihe vaati Kvitamiinia kuten päätösvaihekien. samoin myös B6-vitamiini. Rikistä oli varsin vähän tietoa ravinto-opin kirjoissa ja kuitenkin sen osuus proteiineissa on yhtä konventionelli kuin typen niin että niillä on proteiinistruktuurissa tietty normaali suhteensa N:S. Tässä artikkelissa jonka säästin, mainittiin viime lauseessa, että "kroonisessa munuaisviassa hypersulfatemia aiemmin kuin hyperfosfatemia". Kirjoitin joskus paperin reunaan: "Katso tämä asia!".
Tänään etsin PubMed hakulaitella sanalla Hypersulfatemia ja saan 8 vastausta, joisa on juuri tämä artikkeli numero 2.
Katson näitä nyt.
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Tänään etsin PubMed hakulaitella sanalla Hypersulfatemia ja saan 8 vastausta, joisa on juuri tämä artikkeli numero 2.
Katson näitä nyt.
Search results
Items: 8
1.
Pelham RW, Alcorn H Jr, Cleveland Mv.
J Clin Pharmacol. 2010 Mar;50(3):350-4. doi: 10.1177/0091270009339741. Epub 2010 Jan 12.
The pharmacokinetics (PK) of an oral sulfate solution (OSS) for bowel
cleansing preparation was studied. OSS (30 g of sulfate) was split
between 2 doses, 12 hours apart. Safety measures included
electrocardiography, vital signs, adverse events, hematology, blood
chemistry, and urinalysis. Six adult patients with moderate renal
disease (MRD), 6 with mild-moderate hepatic disease (M/MHD), and 6
normal healthy volunteers (NHVs) completed the study. Adverse events
were mild to moderate in severity and were mainly limited to headache
and expected gastrointestinal symptoms. Serum sulfate levels were highly
variable at all times, even after adjusting for baseline. Sulfate was
higher in MRD in comparison to the other groups. The C(max) and AUC were
higher in the patients, but no statistically significant differences
emerged.
Sulfate levels returned to predose values within 54 hours after
dosing. No electrolyte disturbances occurred. Urinary sulfate excretion
was approximately 20% of the dose. OSS was well tolerated. The types
and severity of adverse events were similar to those seen in large phase
III trials. While patients with MRD had elevated sulfate, the levels
were less than those in renal failure and did not alter biochemical
parameters that are associated with hypersulfatemia.
2.
Fernandes I, Laouari D, Tutt P, Hampson G, Friedlander G, Silve C.
Kidney Int. 2001 Jan;59(1):210-21.
It is known that hypersulfatemia, like hyperphosphatemia, occurs in
chronic renal failure (CRF). The aim of this study was to assess the
effects of CRF on sulfate homeostasis and on sodium sulfate cotransport
(NaSi-1) and sulfate/oxalate-bicarbonate exchanger (Sat-1) expression in
the kidney. In addition, sulfate homeostasis was compared with
phosphate homeostasis...Free Article
3.
Cole DE, Evrovski J.
Crit Rev Clin Lab Sci. 2000 Aug;37(4):299-344. Review.
Although inorganic sulfate is an essential and ubiquitous anion in human
biology, it is infrequently assayed in clinical chemistry today.
Serum
sulfate is difficult to measure accurately without resorting to
physicochemical methods, such as ion chromatography, although many other
techniques have been described.
It is strongly influenced by a variety
of physiological factors, including age, diet, pregnancy, and drug
ingestion.
Urinary excretion is the principal mechanism of disposal for
the excess sulfate produced by sulfur amino acid oxidation, and the
kidney is the primary site of regulation.
In renal failure, sulfoesters
accumulate and hypersulfatemia
contributes directly to the unmeasured anion gap characteristic of the
condition.
In contrast, sulfate in urine is readily assayed by a number
of means, particularly nephelometry after precipitation as a barium
salt.
Sulfate is most commonly assayed today as part of the clinical
workup for nephrolithiasis, because sulfate is a major contributor to
the ionic strength of urine and alters the equilibrium constants
governing saturation and precipitation of calcium salts.
Total sulfate
deficiency has hitherto not been described, although genetic defects in
sulfate transporters have been associated recently with congenital
osteochondrodystrophies that may be lethal.
New insights into sulfate
transport and its hormonal regulation may lead to new clinical
applications of sulfate analysis
in the future.
4.
Kirschbaum B.
ASAIO J. 1998 Jul-Aug;44(4):314-8.
Concentrations of sulfate can increase eightfold in the blood of
patients with severe reductions in glomerular filtration rate. Sulfate
enters the body almost exclusively as the amino acids cysteine and
methionine, and leaves in the urine predominantly as inorganic sulfate.
Concentrations in plasma may exceed 2.5 mol/L in renal failure, and
raise the anion gap by 5 mEq/L.
In studies by the author and colleagues,
hemodialysis using large dialyzers and brisk blood flow rates
effectively lowered the concentrations of sulfate in plasma to normal in
the immediate post dialysis period; the sulfate reduction ratio
actually exceeded the urea reduction ratio.
Significant correlation was
observed between the two ratios.
Concentrations of sulfate, in
conjunction with other data, may prove useful for estimating dietary
intake of protein and monitoring control of acid-base balance.
5.
Martínez-Piñeiro L, Mateos Antón F, Martínez-Piñeiro JA.
Arch Esp Urol. 1992 Nov;45(9):875-89. Review. Spanish.
- PMID:
- 1337244
6.
Ricci J, Oster JR, Gutierrez R, Schlessinger FB, Rietberg B, O'Sullivan MJ, Clerch AR, Vaamonde CA.
Am J Nephrol. 1990;10(5):409-11.
Although hypermagnesemia purportedly lowers the anion gap (AG), we have
shown previously that increases in the serum concentration of the
unmeasured cation (UC) Mg due to therapeutic infusion of MgSO4 are not
associated with AG reduction. To assess our hypothesis that increases in
serum SO4 (unmeasured anion, UA) offset the effect of elevated serum Mg
on the AG, we prospectively studied 11 patients receiving MgSO4
intravenously for toxemia of pregnancy. After 6 h of MgSO4 infusion,
serum Mg increased by 2.1 +/- 0.2 (SE) mEq/l (p less than 0.001) without
a significant decrease in the AG. Concomitantly, serum SO4 increased by
1.4 +/- 0.2 mEq/l. Comparison of the renal handling of SO4 versus Mg
showed a higher fractional excretion of the former, probably accounting
in part for the smaller increment of serum SO4 than of Mg. Comparison of
the change in serum SO4 minus that of Mg indicated that, on the
average, 70% of the observed 1.0 +/- 0.7 mEq/l reduction in AG was
accounted for by the observed changes in the two pertinent unmeasured
ions. A small decrement in serum Ca probably was a quantitatively minor
factor tending to obviate a greater decrease in AG. We conclude that hypersulfatemia attenuates the reduction in AG that would otherwise accompany MgSO4-induced hypermagnesemia.
7.
Friedlander MA, Lemke JH, Johnston MJ, Freeman RM.
Am J Kidney Dis. 1983 May;2(6):660-3.
Serum sulfate concentrations may reach five to ten times normal in renal
failure patients dialyzed on a sorbent cartridge system, and these
patients have elevated alkaline phosphatase levels suggesting an
increased incidence of renal oseodystrophy. We studied the effect of
adding sulfate on ionized calcium (Ca2+) in human serum in vitro and in
rat serum in vivo. K2SO4 or Na2SO4:NaCl mixtures were added to aliquots
of serum from normal subjects to reproduce the observed biologic range
of sulfate concentrations up to 10 mmol. Serum Ca2+ concentration was
found to decrease linearly as serum sulfate concentration increased, for
each subject. The weighted mean slope estimates of the effect of
sulfate on ionized calcium in two experiments were -.0197 and -.0181.
Rats were infused through the inferior vena cava with 2 mL of either 200
mmol NaCl (N = 5) or 100 mmol Na2SO4 (N = 6), after ligation of the
renal arteries and veins and withdrawal of 2 mL blood for baseline
studies. The animals were killed by exsanguination from the aorta after a
five-minute equilibration period. In rats administered NaCl, no
difference in Ca2+ or sulfate concentration was found between pre- and
postinfusion sera. In the Na2SO4 treated rats, however, a significant
mean increase of 0.635 mmol (p less than .005) in serum sulfate
concentration was associated with a significant mean decrease of -0.062
mmol (p less than .01) in serum Ca2+ concentration. We conclude that the
acute in vitro and in vivo addition of sulfate results in a decrease in
serum Ca2+ concentration. Thus, hypersulfatemia,
which is present chronically in patients on sorbent dialysis systems,
may contribute to elevated alkaline phosphatase levels in these
patients.
8.
LESTRADET H, FREDERICH A, RODRIGUEZ-SORIANO J.
Presse Med. 1962 Jan 27;70:211-2. French. No abstract available.
- PMID:
- 14464375
jatko: haen näsitä entsyymeistä tietoa NaSi1-cotransporter, SAT-1 exhancer jos löytyy ortologit ihmisestä.
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