Doses Of Sodium Polystyrene Sulfonate Research Articles

Comparison of effectiveness and safety of sodium polystyrene sulfonate and sodium zirconium cyclosilicate for treatment of hyperkalemia in hospitalized patients.

Potassium binders are frequently utilized for the treatment of hyperkalemia in hospitalized patients; however, there is limited data directly comparing individual agents. The purpose of this study was to compare the effectiveness and safety of sodium polystyrene sulfonate (SPS) and sodium zirconium cyclosilicate (SZC) for hyperkalemia treatment in hospitalized patients. This retrospective cohort study evaluated adult patients who were admitted within a 7-hospital health system and received SPS or SZC for a serum potassium level greater than 5.0 mEq/L. Patients receiving dialysis prior to SPS/SZC administration, those receiving other potassium-lowering medications within 6 hours prior to blood sampling for a repeat potassium level, and those started on kidney replacement therapy prior to sampling for a repeat potassium level were excluded. Following evaluation of 3,903 patients, the mean reduction in serum potassium 4 to 24 hours after binder administration was 0.96 mEq/L with SPS and 0.78 mEq/L with SZC (P < 0.0001). The median dose of SPS was 30 g (interquartile range [IQR], 15-30 g) while the median (IQR) dose of SZC was 10 g (10-10 g). Resolution of hyperkalemia within 24 hours was achieved in a higher percentage of patients with use of SPS (74.9%) versus SZC (68.8%) (P < 0.001). One of the largest comparisons of SPS and SZC conducted to date, this study demonstrated the effectiveness and safety of both agents. While a statistically greater reduction in serum potassium was observed with use of SPS, there was significant dosing variability among agents that limited the ability to directly compare specific doses. Further investigation is needed to determine the optimal dose of each agent for acute hyperkalemia management. This data will inform clinical decisions about the choice of potassium binder for acute hyperkalemia.

Single Dose of Sodium Zirconium Cyclosilicate Versus Sodium Polystyrene Sulfonate in Hospitalized Patients With Hyperkalemia.

Sodium zirconium cyclosilicate (SZC) is an inorganic zirconium silicate compound that selectively exchanges potassium for hydrogen and sodium. "Once" doses of SZC (with option to redose) in patients with hyperkalemia in hospitalized settings have not been evaluated. We hypothesized that a once dose of SZC would be non-inferior to sodium polystyrene sulfonate (SPS) in reducing serum potassium. The objective of our study is to evaluate the effect of a "once" dose of SZC when compared with SPS in reducing serum potassium levels. This was a retrospective analysis of patients who received either a "once" dose of SZC or single or repeated doses of SPS for hyperkalemia. The primary endpoint was mean absolute reduction in the first serum potassium value at least 4 hours after administration. The secondary efficacy endpoints were the rate of additional potassium-lowering therapies and the rate of normokalemia within 48 hours. Safety endpoints were the incidence of electrolyte abnormalities, hypoglycemia, hypertension, hypotension, and colonic necrosis. A total of 260 patients were included in the analysis. The mean initial serum potassium was similar between groups (5.6 ± 0.4). The absolute serum potassium reduction was -0.88 ± 0.64 mEq/L and -0.75 ± 0.65 mEq/L with SZC and SPS, respectively. The "once" regimen of SZC demonstrated non-inferiority compared with SPS (P < 0.0001). The proportion of patients achieving normokalemia within 48 hours and the proportion of patients receiving additional potassium-lowering therapies did not differ between groups. The "once" dose regimen (with redose option) of SZC was non-inferior to the "once" or repeated dosing regimen of SPS with regard to absolute potassium reduction. There were no significant differences in the rate of additional potassium-lowering therapies and the rate of normokalemia at 48 hours. The incidence of hypertension was less common among patients who received SZC.

An 80-Year-Old Man With Hematochezia and Hyperkalemia

Question: An 80-year-old man with a history of colon cancer with previous resection and a primary anastomosis as well as chronic kidney disease presented to the emergency room with a presyncopal episode. On arrival, he was hypotensive, with a hemoglobin of 9.9 g/dL, blood urea nitrogen of 45 mg/dL, and creatinine of 1.9 mg/dL with a serum potassium of 6.0 mmol/L. The patient’s hyperkalemia was attributed to chronic kidney disease and was managed medically. After treatment for hyperkalemia, on the same day of admission, the patient developed bright red bleeding per rectum. The patient underwent colonoscopy on day 2 of admission, which showed internal hemorrhoids, as well as a dusky appearing mass at the rectosigmoid junction, 13 cm from the anal verge measuring 5 cm in length (Figure A). Biopsies of the mass were obtained, and histologic analysis of the biopsies is shown (Figure B). What is the etiology of these endoscopic and histologic findings? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Histology showed colonic mucosa with ischemic injury, ulceration, acute inflammatory exudates, absence of neoplastic cells, and the presence of sodium polystyrene sulfonate (SPS) crystals (highlighted in the rectangle in Figure B). Immunohistochemical stain for cytomegalovirus was negative (not shown). Upon review of the patient’s medications, 1 dose of SPS (Kayexalate) had been given on the first day of admission before the development of hematochezia. Owing to a suspected sampling error, the patient underwent repeat colonoscopy 5 days after the index endoscopy which showed notable regression of the previously seen pseudotumor (Figure C); biopsies of the remnant lesion showed persistent ischemic type injury with acute inflammatory exudates and SPS crystals (indicated by the blue arrow in Figure D). SPS is a potassium-binding resin used to treat acute hyperkalemia. SPS has been associated with gastrointestinal complications, including ischemic colitis, bleeding, and perforation.1Bui M. Chou S.Y. Faubert P. et al.Resin-induced colonic pseudotumor: rare complication from chronic use of potassium binders in a hemodialysis patient.Case Rep Nephrol. 2016; 20163692086PubMed Google Scholar Ischemic colitis with associated pseudotumor formation is a rare adverse event that can mimic a malignant process, and present as hematochezia or as a radiographically apparent colonic mass.1Bui M. Chou S.Y. Faubert P. et al.Resin-induced colonic pseudotumor: rare complication from chronic use of potassium binders in a hemodialysis patient.Case Rep Nephrol. 2016; 20163692086PubMed Google Scholar These pseudotumors are non-neoplastic, inflammatory, and necrotic lesions that have been reported to occur in the esophagus, colon, and in extraintestinal areas.2Chatila A.T. Bilal M. Merwat S. Kayexalate-induced colonic pseudotumor.Clin Gastroenterol Hepatol. 2019; 17: e73Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar,3Goh L.H. Wong J. Chng T.W. et al.Extra-intestinal sodium polystyrene sulfonate crystal-induced inflammatory pseudotumour in an asymptomatic haemodialysis patient.Int Urol Nephrol. 2021; 53: 1265-1266Crossref PubMed Scopus (1) Google Scholar Although the mechanism is unknown, it is proposed that SPS causes a shift in the osmotic load and, therefore, vascular redirection and then ulceration or ischemia.2Chatila A.T. Bilal M. Merwat S. Kayexalate-induced colonic pseudotumor.Clin Gastroenterol Hepatol. 2019; 17: e73Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar The characteristic pathologic finding includes a fish scale pattern seen on hematoxylin and eosin staining representing SPS crystals. SPS-induced pseudotumor formation does not seem to be dose dependent; investigators have reported the development of SPS-induced ischemic pseudotumor after a wide range of doses, ranging from merely 2 doses to scheduled administration up to 1 year.1Bui M. Chou S.Y. Faubert P. et al.Resin-induced colonic pseudotumor: rare complication from chronic use of potassium binders in a hemodialysis patient.Case Rep Nephrol. 2016; 20163692086PubMed Google Scholar, 2Chatila A.T. Bilal M. Merwat S. Kayexalate-induced colonic pseudotumor.Clin Gastroenterol Hepatol. 2019; 17: e73Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar, 3Goh L.H. Wong J. Chng T.W. et al.Extra-intestinal sodium polystyrene sulfonate crystal-induced inflammatory pseudotumour in an asymptomatic haemodialysis patient.Int Urol Nephrol. 2021; 53: 1265-1266Crossref PubMed Scopus (1) Google Scholar Recognition of this entity is therefore important irrespective of the SPS dose and duration to avoid unnecessary interventions.1Bui M. Chou S.Y. Faubert P. et al.Resin-induced colonic pseudotumor: rare complication from chronic use of potassium binders in a hemodialysis patient.Case Rep Nephrol. 2016; 20163692086PubMed Google Scholar SPS-induced ischemic pseudotumor regresses with discontinuation of the drug. This case highlights the potential for mistaking SPS-induced pseudotumor formation for malignancy. In addition, in the absence of a dose response, a single dose of SPS can lead to the development of ischemic pseudotumor.

Exemple d’un cas d’hyperkaliémie du nourrisson : proposition d’un circuit pour le prétraitement du lait infantile par résine de polystyrène sulfonate de sodium à l’hôpital

Sodium polystyrene sulfonate (SPS) is used to reduce intestinal potassium absorption in hyperkalemia during conservative management of chronic renal failure in infants. Milk can be pretreated by SPS to reduce the risk of enteropathy associated with oral or rectal administration. We report the case of an infant for whom this pre-treatment has been implemented. The objective of this work was to define the hospital procedure for the pre-treatment of milk by the SPS. This pre-treatment involves both a drug and infant milk. Each product has its own regulation and their processes do not normally cross each other. The roles of each contributor were therefore defined: prescription of pre-treated milk (dose of SPS and volume of milk) by the physician, dispensing of SPS by the pharmacist, delivery of milk by the milk kitchen staff, pre-treatment by a nurse and administration by a nursing auxiliary. The preparation of the bottles is as follows: placing approximately 1g of SPS per 100mL of milk in contact, stirring, resting in the refrigerator for one hour, taking the supernatant to be administered. In the reported case, serum potassium levels were reduced from 5.57mmol/L before treatment to 4.53mmol/L after treatment, in line with the 20% decrease found in the literature. This method of administration is beneficial in terms of tolerance and acceptability. The preparation is simple and allows going back home under treatment.

An Evaluation of the Pharmacodynamics, Safety, and Tolerability of the Potassium Binder RDX7675.

Hyperkalemia is common in patients with heart failure or chronic kidney disease, particularly those taking renin-angiotensin-aldosterone system inhibitors, and can cause arrhythmias and sudden cardiac death. The most widely used treatment, sodium polystyrene sulfonate (SPS), limits gastrointestinal potassium absorption, but has poor palatability. RDX7675 (RDX227675) is the calcium salt of a reengineered polystyrene sulfonate-based resin with improved palatability over SPS. The pharmacodynamic effects and safety of RDX7675 were assessed in a phase 1, single-center, randomized, active-controlled study. Healthy volunteers received nominal active doses of RDX7675 4.6g twice a day (BID), 4.6g 3 times a day (TID), 6.9g BID, 13.7g daily (QD), 9.2g TID, or 13.7g BID (n=12 each), or equivalent doses of SPS (n=3 each), for 4days. RDX7675 dosing increased stool potassium excretion and decreased urinary potassium excretion from baseline. Stool potassium excretion increased by up to 1481mg/day with RDX7675 (6.9g BID), and urinary potassium excretion decreased by up to 939mg/day (13.7gBID). Similar levels of potassium excretion were observed using QD, BID, or TID dosing of a 13.7g total daily RDX7675 dose. Few adverse events were reported. In conclusion, repeated oral dosing with RDX7675 over 4days reduced potassium absorption in healthy volunteers; the results support QD dosing of RDX7675 in future clinical studies.

Evaluation of Sodium Polystyrene Sulfonate Dosing Strategies in the Inpatient Management of Hyperkalemia.

Hyperkalemia occurs frequently in an inpatient setting, for which sodium polystyrene sulfonate (SPS) is a common treatment modality. Few studies have investigated the dose-response of SPS. To quantify the change in serum potassium after 15-, 30-, and 60-g oral and 30-g rectal doses of SPS. Secondary objectives were to compare the proportion of patients attaining post-SPS dose normokalemia between dosing groups and to investigate the effect of certain characteristics on SPS dose-response. The reduction in serum potassium after 15-, 30-, and 60-g oral and 30-g rectal doses of SPS administered to adult inpatients was evaluated through a retrospective chart review. Ottawa Hospital Research Ethics Board approval was obtained prior to data collection. A total of 118 patients were included in the analysis. Serum potassium levels were reduced by 0.39, 0.69, 0.91, and 0.22 mEq/L following 15-, 30-, and 60-g oral doses and a 30-g rectal dose of SPS, respectively. A greater proportion of patients (50% vs 23%) remained hyperkalemic in the 15-g versus the 60-g group (P = 0.018), and all patients in the rectal group remained hyperkalemic. No patient in any group experienced postdose hypokalemia. The influence of all studied interindividual characteristics on SPS dose-response was clinically nonsignificant. Mild hyperkalemia can be effectively treated with a single 60-g oral dose of SPS as monotherapy, with minimal risk of hypokalemia. Moderate to severe hyperkalemic episodes warrant alternative therapy. The potassium-lowering effect is correlated to SPS dose and is independent of interindividual characteristics.

Pseudohypoaldosteronism type 1 due to novel variants of SCNN1B gene.

SummaryAutosomal recessive pseudohypoaldosteronism type 1 (PHA1) is a rare disorder characterized by sodium wasting, failure to thrive, hyperkalemia, hypovolemia and metabolic acidosis. It is due to mutations in the amiloride-sensitive epithelial sodium channel (ENaC) and is characterized by diminished response to aldosterone. Patients may present with life-threatening hyperkalemia, which must be recognized and appropriately treated. A 32-year-old female was referred to the National Institutes of Health (NIH) for evaluation of hyperkalemia and muscle pain. Her condition started in the second week of life, when she was brought to an outside hospital lethargic and unresponsive. At that time, she was hypovolemic, hyperkalemic and acidotic, and was eventually treated with sodium bicarbonate and potassium chelation. At the time of the presentation to the NIH, her laboratory evaluation revealed serum potassium 5.1 mmol/l (reference range: 3.4–5.1 mmol/l), aldosterone 2800 ng/dl (reference range: ≤21 ng/dl) and plasma renin activity 90 ng/ml/h (reference range: 0.6–4.3 ng/ml per h). Diagnosis of PHA1 was suspected. Sequencing of the SCNN1B gene, which codes for ENaC, revealed that the patient is a compound heterozygote for two novel variants (c.1288delC and c.1466+1 G>A), confirming the suspected diagnosis of PHA1. In conclusion, we report a patient with novel variants of the SCNN1B gene causing PHA1 with persistent, symptomatic hyperkalemia.Learning points PHA1 is a rare genetic condition, causing functional abnormalities of the amiloride-sensitive ENaC.PHA1 was caused by previously unreported SCNN1B gene mutations (c.1288delC and c.1466+1 G>A).Early recognition of this condition and adherence to symptomatic therapy is important, as the electrolyte abnormalities found may lead to severe dehydration, cardiac arrhythmias and even death.High doses of sodium polystyrene sulfonate, sodium chloride and sodium bicarbonate are required for symptomatic treatment.

Apparent lisinopril overdose requiring hemodialysis

A case of apparent overdose of angiotensin-converting-enzyme inhibitors requiring hemodialysis is reported. A 51-year-old white man (weight, 85 kg; height, 178 cm; body mass index, 28) with a history of hypertension, low back pain, and anxiety apparently took 27 lisinopril 10-mg tablets (3.18 mg/kg body weight) over a period of 3 or fewer days. The friend who brought him to the emergency department reported that the patient was hard to rouse and was speaking incoherently on the day of admission. Over the previous few days, the patient reportedly had visual hallucinations, incoherence, and inarticulate speech. Laboratory tests, electrocardiography, and computed tomography were performed. The patient was judged to have high-anion-gap metabolic acidosis, acute kidney injury, severe hyperkalemia, and rhabdomyolysis. He was given three doses of albuterol via a nebulizer, three doses of calcium gluconate 1 g i.v., two doses of sodium bicarbonate 100 meq i.v., two doses of sodium polystyrene sulfonate 30 g orally, three doses of insulin 10 units i.v., and three doses of dextrose 25 g (as 50% dextrose injection) i.v. He then underwent emergent hemodialysis and was admitted to the intensive care unit. The patient's confusion abated, kidney function improved, and acid-base and electrolyte imbalances resolved. The patient was discharged after 15 days. A man who had evidently taken an overdose of lisinopril had multiorgan dysfunction in the absence of hypotension. The abnormalities resolved after he was treated for acidosis and hyperkalemia and received hemodialysis to remove the lisinopril.

Secondary Prevention of Hyperkalemia With Sodium Polystyrene Sulfonate in Cardiac and Kidney Patients on Renin‐Angiotensin‐Aldosterone System Inhibition Therapy

Hyperkalemia, induced by renin-angiotensin-aldosterone system inhibition (RAAS-I) in patients with chronic kidney disease (CKD), or cardiac disease often leads to withdrawal of RAAS-I therapy. Sodium polystyrene sulfonate (SPS) is a potassium-binding resin used for the treatment of hyperkalemia. Recently, concerns about the safety and efficacy of SPS were raised. We report here a follow-up of 14 patients with CKD and heart disease on RAAS-I treatment who were treated with low-dose daily SPS to prevent recurrence of hyperkalemia. Daily SPS is safe and effective for secondary prevention of hyperkalemia induced by RAAS-I therapy in CKD patients with heart disease. We reviewed the medical charts of the patients with CKD (nondialysis patients) and heart disease treated in our CKD clinic from 2005 to 2010 and identified all patients on RAAS-I therapy who were treated with daily SPS (sorbitol-free) after episodes of hyperkalemia. Data on hospitalizations, symptoms that may be attributed to SPS therapy, and electrolyte concentration levels were obtained. Fourteen patients were treated with low-dose SPS therapy for a total of 289 months (median length of follow-up, 14.5 months). None of the patients developed colonic necrosis or life-threatening events that could be attributed to SPS use. Mild hypokalemia was noted in 2 patients and responded to reducing the dose of SPS. No further episodes of hyperkalemia were recorded while patients were on the therapy. SPS was well-tolerated during the follow-up without need for withdrawal or reduction of the dose of RAAS-I therapy by any patients. Low-dose SPS was safe and effective as a secondary preventive measure for hyperkalemia induced by RAAS-I in CKD patients with heart disease.

The use of sodium polystyrene sulfonate in the inpatient management of hyperkalemia

Limited data exist on the precise dose of sodium polystyrene sulfonate (SPS) needed for specific potassium concentrations in the management of mild to moderate hyperkalemia in an inpatient hospital setting. A retrospective cohort study involving a review of electronic medical records of inpatients receiving SPS for the treatment of hyperkalemia was conducted at the Jesse Brown Veteran Affairs Medical Center, between January 1, 2006 and December 31, 2006. Hyperkalemia was defined as a serum potassium concentration >5.1 mmol/L. The primary endpoint was the mean change in potassium concentration associated with specific SPS dosage administration. A total of 122 patients were selected for inclusion in the analysis. The mean potassium concentrations before SPS administration were 5.40 ± 0.18 mmol/L, 5.51 ± 0.30, 5.83 ± 0.46, and 5.92 ± 0.30 in the 15, 30, 45, and 60 gm groups, respectively. The mean potassium concentration decreased by 0.82 ± 0.48 mmol/L in the 15 gm group, 0.95 ± 0.47 in the 30 gm group, 1.11 ± 0.58 in the 45 gm group, and 1.40 ± 0.42 in the 60 gm group. After a single dose of SPS, the mean potassium concentration was within normal range in 115 patients (94%). A possible direct dose response relationship between SPS and the reduction in serum potassium concentration was found and should be evaluated prospectively.

Lithium use in special populations

Byline: E. Mohandas, V. Rajmohan Lithium, a monovalent cation, was first used for the treatment of mania in the 1940s. Half a century into its use, the drug continues to be the preeminent choice for bipolar disorder with antimanic, antidepressant (modest) and antisuicidal property. Lithium is the "gold standard" mood stabilizer against which potential mood stabilizer agents are judged. The therapeutic uses of lithium also include use as an augmenting agent in depression, schizoaffective disorder, aggression, impulse control disorder, eating disorders, attention deficit disorder and in certain subsets of alcoholism. Lithium has been used in many medical disorders, especially cluster headache and dermatological disorders (seborrheic dermatitis, eczematoid dermatitis, genital herpes).[sup] [1] The drug is however associated with neurologic, endocrine, cardiovascular, renal, dermatologic and gastrointestinal adverse effects and possible teratogenicity. History Lithium was first discovered and defined by Johan August Arfvedson in 1817 when he did an analysis of the mineral petalite [LiAl(Si2O5)2]. Petalite was first found by Brazilian scientist Jose Bonifacio Andrade e Silva in 1800. Lepidolite, spodumene, petalite and amblygonite are the more important minerals containing lithium. It was Arfwedson's laboratory chief John Jacob Berzelius who named this alkali metal "lithion." Arfvedson was never able to fully isolate lithium, and it wasn't until 1855 that it was isolated by William Thomas Brande. Brande and Sir Humphrey Davy earlier had done electrolysis on lithium oxide in 1818. Lithium was first produced commercially in 1923 by Metallgesellschaft AG.[sup] [2] The use of lithium for medicinal purposes can be traced back 1,800 years to the Greek physician Galen, who treated patients with mania by having them bathe in alkaline springs and drink the water, which probably contained lithium. In 1843 Alexander Ure introduced lithium into modern medicine, and he showed the in vitro reduction of weight of a uric acid bladder stone in a lithium carbonate solution. Sir Alfred Garrod later discovered that gouty uric acid deposits also were soluble in lithium solution. The view in that time was that uric acid imbalances caused a wide range of diseases, and Armand Trousseau and Alexander Haig proposed that mania and depression also may result from this imbalance and lithium may be effective in these conditions. In the 1840s, lithium was mixed with carbonate or citrate to form a salt and was used to treat gout, epilepsy, diabetes, cancer and insomnia. In the 1870s, the then American Surgeon General William Hammond had provided anecdotal evidence for the use of lithium bromide in the treatment of acute mania. In the 1880s and 1890s the Lange brothers Carl and Fritz used lithium in depression, and Carl Lange was the first to systematically use lithium in the acute and prophylactic treatment of depression.[sup] [2] The introduction of lithium preparations and tablets in the 1900s brought to the fore the toxic effects of the drug; and there were reports of weakness, tremor, diarrhea, vomiting and deaths. The drug disappeared from the British Pharmacopoeia by 1932, but later in the 1940s it was used as a sodium substitute in low sodium diets; but the reports of severe intoxication led to its removal from American markets in 1949. [sup] [1] The appearance in 1949 in the Medical Journal of Australia of a paper entitled "Lithium salts in the treatment of psychotic excitement" by John F. J. Cade was an unspectacular entry into a new era of psychiatry. Manic patients showed improvement, with the patient becoming calmer after four to five days. There was no improvement in the excited schizophrenic patients, though there was a calming effect. There was no improvement or deepening of depression. The paper also gave details of initial dosage, maintenance doses, appearance of toxic symptoms and warning about lithium over-dosage. …

Use of Sodium Polystyrene Sulfonate for Reduction of Plasma Lithium Concentrations After Chronic Lithium Dosing in Mice

Previous studies have shown that oral sodium polystyrene sulfonate lowers plasma lithium concentrations after acutely administered oral doses of lithium chloride. However, a significant proportion of lithium overdose cases resulting in morbidity and mortality are those in which exposure to lithium is chronic. This study was designed to determine whether multiple oral doses of sodium polystyrene sulfonate are effective in reducing plasma lithium concentrations after chronic dosing. Placebo-controlled animal study. One hundred thirty mice were given 75 mM lithium chloride in their drinking water for a period of 14 days. At the end of that period, half of the animals were given orogastric sodium polystyrene sulfonate at 5 g/kg/dose 0, 60, 120, 180, and 360 minutes after the cessation of lithium chloride; the remaining half received orogastric water at equivalent times. Subgroups of each group were sacrificed at 90, 150, 330, 480, 1440, and 2880 minutes after lithium chloride cessation and plasma analyzed for lithium content. Lithium concentrations were compared by analysis of variance and single degree of freedom contrasts. Significance was set at an alpha level of 0.05. Lithium concentration was lower overall in the animals treated with sodium polystyrene sulfonate (p < .0001) and specifically at 150, 330, and 480 minutes after lithium chloride cessation (p < .05). Repetitive oral doses of sodium polystyrene sulfonate effectively lowered plasma lithium concentrations. Further study may ultimately define a role for the use of sodium polystyrene sulfonate in the treatment of patients with chronic lithium toxicity.

Enhancement of lithium elimination by multiple-dose sodium polystyrene sulfonate.

To determine whether multiple doses of sodium polystyrene sulfonate (SPS) enhance the elimination of IV-administered lithium (Li). The study was a placebo-controlled, investigator-unblinded, murine trial of multiple doses of SPS on serum Li concentrations. Seventy-five male CD-1 mice were given IV pretreatment with LiCl (125 mg/ kg) followed by gavage treatments with SPS (5 g/kg/dose) 20, 40, 90, 150, and 210 minutes after LiCl (experimental group) or deionized water at equivalent times (control group). Subgroups of each treatment group were sacrificed at 1, 2, 4, and 6 hours after LiCl administration and blood was collected for Li analysis. Statistical analyses indicated that the SPS group had lower serum Li concentrations overall than did the control animals. This difference was apparent at the 2-, 4-, and 6-hour time points. In this murine model, repetitive doses of orogastric SPS enhanced the elimination of parenterally administered Li.

Effect of Delayed Treatment with Sodium Polystyrene Sulfonate on Serum Lithium Concentrations in Mice

To determine the efficacy of sodium polystyrene sulfonate (SPS) in lowering serum lithium (Li) concentrations. Specifically, to determine the effects of both different doses of SPS and different times to treatment with SPS on serum Li levels. The study was a controlled, single-dose murine trial of SPS on serum Li levels. Male CD-1 mice (n = 525) were given orogastric LiCl and then divided into three main treatment groups: group SPS received a single orogastric administration of SPS in a dose of 5 gm/kg body weight at either 0, 15, 30, 45, or 90 minutes after LiCl; group half-SPS received a single orogastric administration of SPS in a dose of 2.5 gm/kg body weight at times equivalent to those of group SPS; and the control group received orogastric deionized water in a volume equivalent to that of group SPS at 0, 15, 30, 45, or 90 minutes after LiCl. Subgroups of seven to ten mice in each of the four treatment groups were sacrificed at one, two, four, and eight hours after administration of LiCl, and their blood was analyzed for Li concentration. 1) Single doses of SPS significantly lowered serum Li concentrations; 2) this effect was dose-related; 3) the delays in administration of SPS used in this study did not significantly reduce its ability to lower serum Li concentrations; and 4) even when administered after peak serum Li concentrations had been achieved, a single dose of SPS was effective in lowering serum Li levels. SPS may be efficacious in the treatment for Li toxicity under certain circumstances, even when there is delay to treatment. Additional study is warranted to further characterize the ability of SPS to alter Li kinetics.

Effect of sodium polystyrene sulfonate on lithium bioavailability

To examine the effect of a single dose of sodium polystyrene sulfonate and sorbitol on lithium absorption. Prospective, randomized, crossover. University teaching hospital. Healthy volunteers. Subjects ingested 600 mg lithium carbonate on two occasions, with and without 30 g concomitant sodium polystyrene sulfonate. Blood samples were drawn up to 24 hours after ingestion and assayed for serum lithium concentration. Compared with control, sodium polystyrene sulfonate and sorbitol reduced the area under the lithium serum concentration-time curve by 11.33%, reduced the mean observed peak serum lithium concentration 0.07 +/- 0.08 mmol/L, and delayed the time to the mean observed peak serum lithium concentration by 2.04 +/- 2.40 hours. Sodium polystyrene sulfonate and sorbitol may be used in patients immediately or shortly after ingestion of a significant acute overdose of lithium in situations in which hemodialysis cannot be instituted promptly.

Multiple-dose sodium polystyrene sulfonate in lithium intoxication: an animal model.

Previous work in our laboratory has demonstrated that sodium polystyrene sulfonate (SPS) significantly lowered serum lithium (Li) concentrations when administered in a single oral dose after an oral dose of lithium in a mouse model. The present study was designed to determine whether: 1) repetitive doses of SPS are effective in lowering serum lithium concentrations, 2) the effect of SPS on lithium concentration is dose related and 3) SPS enhances the elimination of lithium. Mice (N = 144) were given orogastric LiCl (250 mg/kg) and then divided into 4 groups: Controls received water 0, 30, 90, 180, and 360 min. after LiCl; the Full-Dose SPS Group received SPS (5 g/kg/dose) at equivalent times; the Half-Dose SPS Group received SPS (2.5 g/kg/dose) at the same times; and the Elimination Group received water at 0 and 30 min. after LiCl and SPS at 90, 180 and 360 min. after LiCl. Subgroups of each group were sacrificed at 1, 2, 4 and 8 hr post-treatment and serum analyzed for lithium concentrations. Statistical analyses revealed that, when compared to Controls: 1) SPS significantly lowered serum lithium concentrations; 2) this effect was dose-related; 3) repetitive dosing of SPS appears to enhance the elimination of lithium.

Primary acquired hypoaldosteronism

Primary acquired hypoaldosteronism