Trimethoprim-sulfamethoxazole therapy in outpatients: is hyperkalemia a significant problem?

A prospective, randomized clinical study was undertaken to determine the effect of standard-dose trimethoprim-sulfamethoxazole combination treatment on serum potassium concentrations in outpatients treated in an ambulatory clinic. Ninety-seven patients were treated with oral antibiotics for a variety of infections. Fifty-one patients treated with trimethoprim-sulfamethoxazole (trimethoprim, 320 mg/day; sulfamethoxazole, 1,600 mg/day) constituted the treatment group, while 46 patients treated with other antibiotics served as controls. Serum potassium, sodium, and chloride concentrations, serum carbon dioxide content, blood urea nitrogen level, serum creatinine level, and serum glucose concentration were measured. The baseline serum potassium concentration in the treatment group was 4.30 +/- (SD) 0.36 mmol/l, and it increased significantly (p < 0.001) to 4.66 +/- 0.45 mmol/l on day 5 of therapy. Subgroup analysis of mean serum potassium concentration on day 5 of therapy failed to detect clinically relevant hyperkalemia. In patients with a serum creatinine level equal to or greater than 1.1 mg/dl (K+, 4.83 +/- 0.48 mmol/l), a nonsignificant difference (p = 0.3) in the potassium concentration was noted on day 5 as compared with patients with a serum creatinine level <1.1 mg/dl (K+, 4.63 +/- 0.44 mmol/l). Although diabetics had a higher serum potassium concentration (K+, 4.91 +/- 0.44 mmol/l) than nondiabetics (K+, 4.61 +/- 0.44 mmol/l), the difference was not statistically significant (p = 0.055). Patients aged >/=50 years (K+, 4.82 +/- 0.59 mmol/l) had a significantly different (p = 0.046) serum potassium concentration on day 5 than patients aged <50 years (K+, 4.55 +/- 0.28 mmol/l). In contrast, the baseline serum potassium concentration in the control group was 4.37 +/- 0.45 mmol/l, and it decreased (p = 0.1) to 4.22 +/- 0.4 mmol/l on 5 days of drug therapy. Trimethoprim-sulfamethoxazole therapy, when used to treat a variety of infections, leads to an increase in serum potassium concentration in most patients. After 5 days of therapy with this drug, the treatment group developed a statistically significant rise in the serum potassium concentration as compared with the control group. However, severe hyperkalemia (K+ >/=5.5 mmol/l) occurred in only 3 patients (6%) treated with trimethoprim-sulfamethoxazole. In addition, none of the subgroups of treated patients developed clinically important hyperkalemia. This suggests that outpatients, in contrast to acquired immunodeficiency syndrome patients and hospitalized patients with mild renal insufficiency, develop severe or life-threatening hyperkalemia less commonly when treated with this antimicrobial regimen. However, outpatients having risk factors which may predispose to the development of hyperkalemia should be carefully monitored when treated with trimethoprim-sulfamethoxazole.     

CELLULAR POTASSIUM DEPLETION PREDISPOSES TO HYPOKALAEMIA AFTER ORAL SODIUM PHOSPHATE

Background : Oral sodium phosphate has become an attractive alternative to polyethylene glycol for colonic cleansing preparatory to elective colorectal surgery. Its use, however, has been associated with hypokalaemia. The authors of the present study tested the hypothesis that patients with cellular depletion of potassium are at significant risk for hypokalaemia with oral sodium phosphate bowel preparation. Methods : In 23 patients, total body potassium was measured by whole-body counting and intracellular water volume was measured by bioimpedance analysis before oral sodium phosphate bowel preparation. Patients were divided into those whose serum potassium fell to 3.5 mmol/L or lower (Group 1) and those whose did not after sodium phosphate treatment (Group 2). Results : The fall in serum potassium concentration over the period of oral sodium phosphate administration was significantly negatively correlated with intracellular potassium concentration measured prior to administration (r=-0.65, P= 0.0009). In Group 1, serum potassium concentration fell from 4.1 ± 0.1 (standard error of the mean (SEM)) mmol/L to 3.2 ± 0.1 mmol/L (P± 0.0001) while in Group 2 there was no significant change in this concentration (4.0 ± 0.1 vs 3.9 ± 0.1 mmol/L) as a result of sodium phosphate treatment. Intracellular potassium concentration prior to administration of sodium phosphate was significantly lower in Group 1 (117 ± 9 mmol/L vs 143 ± 7 mmol/L, P < 0.05). Conclusions : Caution should be exercised when treating patients with oral sodium phosphate who are considered to be cellularly depleted of potassium. These patients are at risk of hypokalaemia after this treatment.     

Is spironolactone safe for dialysis patients?

BACKGROUND: Spironolactone is useful in heart failure, but is not given to dialysis patients for fear of hyperkalaemia. This study evaluated the safety of spironolactone administration in haemodialysis patients. METHODS: Fifteen haemodialysis outpatients with mean serum potassium <5.6 mEq/l over the preceding 4 months were treated with spironolactone 25 mg daily for 28 days. Serum potassium was measured before every haemodialysis during the study. Aldosterone and renin were measured at the beginning and end of the study. Patients were monitored for side effects. Data were examined with a paired t-test, with patients serving as their own controls and P < 0.05 considered significant. A sample size of 14 was required to achieve a power of 0.8 and a P = 0.05 to detect a potassium difference of 0.5 +/- 0.6 mEq/l. All patients were analysed as intention-to-treat. RESULTS: The mean potassium level was 4.6 +/- 0.6 mEq/l at baseline and 4.9 +/- 0.9 mEq/l at study completion (P = 0.14). Thirteen patients completed the trial with no potassium levels >6.0 mEq/l. Four patients had potassium levels between 5.5 and 6.0 mEq/l. One patient was withdrawn at day 20 after developing hyperkalaemia (7.6 mEq/l). Another patient was withdrawn at day 25 after missing a dialysis treatment. There were no differences in either baseline or 28 day aldosterone or renin levels (16.8 +/- 28.8 vs 11.7 +/- 6.1 ng/dl and 3.5 +/- 3.9 vs 3.5 +/- 3.5 ng/ml/h, respectively). Infrequent side effects included dry mouth, nosebleed, pruritis, gynecomastia and diarrhoea. No significant leukopenia or anaemia was noted. CONCLUSIONS: Spironolactone may be considered as a treatment option for selected chronic haemodialysis patients with heart disease.     

Cardiac arrhythmias due to severe hypokalemia in a patient with classic Bartter disease

We report a young girl with classic Bartter disease (type III) with severe hypokalemia (2.0 mmol/l) who developed a prolonged heart rate-corrected QT interval of 510 ms (upper reference 430 ms) and ST segment depression in all leads. Holter electrocardiography was performed (with a plasma potassium level of 2.0 mmol/l) and it disclosed a stable sinus rhythm, a prolonged correct QT interval, more-evident ST segment depression during an increase in heart rate, a few single premature ventricular complexes, and nocturnal conduction abnormalities such as second-degree atrioventricular block 2:1. In the light of these results, the treatment was modified by increasing indomethacin from 1.5 to 3 mg/kg per day and adding spironolactone at a dose of 5 mg/kg per day. After 10 days, plasma potassium levels increased to 2.7 mmol/l and electrocardiographic abnormalities regressed. No other cardiac abnormalities were noted when the serum potassium was maintained >2.5 mmol/l. In conclusion, this case report supports the link between arrhythmic events and chronic renal hypokalemic alkalosis in renal tubular disorders. We highlight the importance of standardizing the use of rest electrocardiography and 24-h Holter monitoring to diagnose arrhythmic events in children with severe hypokalemic renal disorders, especially in those with a plasma potassium <2.5 mmol/l. The importance of beginning early medical treatment, to improve plasma potassium levels and reverse cardiac abnormalities, is emphasized.     

Safety of low-dose spironolactone administration in chronic haemodialysis patients.

BACKGROUND: Prevention of cardiovascular diseases is essential in chronic haemodialysis patients. Recently, low-dose spironolactone has been shown to decrease cardiovascular mortality in patients with severe heart failure. However, since haemodialysis patients are prone to hyperkalaemia, a known side effect of spironolactone, this treatment is not used in this population. We performed a study to assess whether low-dose spironolactone (3 x 25 mg/week) could be administered without inducing hyperkalaemia in haemodialysis patients. METHODS: The study design included a 2-week baseline period, followed by a 4-week treatment period in which doses of spironolactone were started at 12.5 mg three times/week for 2 weeks, then increased to 25 mg three times/week, and followed by a 2-week wash-out period. Fourteen patients receiving low-dose spironolactone after each dialysis were compared with 21 haemodialysis patients (control group). RESULTS: Low-dose spironolactone did not change mean serum potassium (4.9 +/- 0.7 vs 4.9 +/- 0.3 mmol/l: control). The mean plasma canrenone level induced by administration of spironolactone 25 mg three times/week in the 14 treated patients was 13 +/- 5.3 ng/ml. Serum aldosterone was not significantly modified by the administration of spironolactone in these patients [before, median 0.35; interquartile range (IQR) 0.11-2.83 nmol/l vs after, median 0.22; IQR 0.12-0.60 nmol/l, NS]. Dietary potassium intake and the use of ion-exchange resin, angiotensin-converting enzyme inhibitors and beta-blockers were similar for the two groups throughout the study. CONCLUSION: This non-randomized and non-blinded study shows that administration of 25 mg spironolactone thrice weekly is not associated with an increased frequency of hyperkalaemia in haemodialysis patients when they are carefully monitored. More studies are required, however, before concluding that spironolactone administration is safe in the chronic haemodialysis population.     

Mutation profile and treatment of Gitelman syndrome in Chinese patients

Background

Gitelman syndrome (GS) is a rare autosomal recessive disease caused by loss-of-function mutations in the SLC12A3 gene, and is characterized by hypokalemia and metabolic alkalosis. In this study, we aimed to study the genotype, phenotype, and treatment in 42 GS patients, the largest sample size so far in mainland China.

Method

We retrospectively studied the clinical data and genetic characteristics of 42 patients diagnosed with GS in Peking Union Medical College Hospital from 2012 to 2015. Therapeutic efficacy of spironolactone and potassium supplements was also studied retrospectively.

Results

Eighty-one mutation alleles were found in 42 patients, and total of 52 distinctly different mutation alleles were identified, of which 15 were new mutation alleles. p.Asp486Asn was a hotspot in our series, with the allele frequency being 19.7 % (16/81), and was found in 13 patients (31.0 %). Treatment with spironolactone or potassium supplements alone significantly increased serum potassium concentration by 0.36 ± 0.37 and 0.45 ± 0.35 mmol/l, respectively (both P < 0.05), and combined therapy with spironolactone and potassium increased serum potassium concentration by 0.69 ± 0.64 mmol/l (P < 0.05).

Conclusions

18.5 % (15/81) mutation sites identified in 42 Chinese GS patients are novel. p.Asp486Asn mutation is a hotspot, which is different from the reports from other countries. Spironolactone could moderately elevate serum potassium level, and spironolactone in combination with potassium supplements tended to be more effective.

     

Measurement of electrolyte concentrations in expressed prostatic secretion and urine from patients with chronic prostatitis and its implications

This study was aimed at measuring concentration of electrolytes, especially K+ in expressed prostatic secretion (EPS) and urine from patients with chronic prostatitis. The concentration of potassium, sodium, chloride, calcium in EPS and urine of 31 controls and 79 patients with prostatitis were measured and analyzed. There was no significant difference in the concentrations of potassium, sodium, chloride and calcium between the patients and the controls. Among the patients treated effectively, potassium concentration was 40.66 +/- 17.10 mmol/l before treatment and 33.42 +/- 17.27 mmol/l after treatment. While among the patients treated ineffectively, potassium concentration was measured as 37.57 +/- 16.93 mmol/l and 50.66 +/- 18.77 mmol/l before and after treatment respectively. The concentrations of electrolytes in prostatic fluid varied greatly between individuals. Potassium concentration in EPS decreased significantly after treatment among the patients with obvious treatment effectiveness, while increased among those who failed the treatment. EPS potassium concentration was also found to be lower in patients with pain than those without pain. No significant difference was found between the normal group and the no-pain patients.     

Treatment of pediatric hyperkalemia with sodium polystyrene sulfonate

Objective

To describe the safety and efficacy of sodium polystyrene sulfonate (SPS) in pediatric patients with acute hyperkalemia.

Methods

A retrospective chart review of all patients less than 18 years of age administered SPS for acute hyperkalemia at Texas Children’s Hospital between 2011 and 2014.

Results

Our cohort consisted of 156 patients (mean age 6.8?±?6.1 years). The peak mean potassium concentration observed was 6.5?±?0.77 mmol/l prior to administration of SPS. The mean SPS dose was 0.64?±?0.32 g/kg. The majority (91 %) of the SPS doses were given orally. The nadir mean potassium concentration in the 48 h post-SPS was 4.7?±?1.2 mEq/l, which occurred at 16.7?±?14.7 h post-dose. In the 48 h following SPS administration, 68 (43 %) patients required at least one additional intervention after SPS dose. Patients who required an additional intervention after initial SPS dose differed significantly in weight, baseline serum potassium, and were more likely to have received SPS treatment via the rectal route. A gastrointestinal adverse event was documented in 24 (15 %) patients.

Conclusions

SPS was used effectively and safely in the majority of patients in this report. However, it may not be appropriate as a first single-line agent in patients with severe acute hyperkalemia who require a greater than 25 % reduction in serum potassium levels or those at a high risk for cardiac arrhythmias.

     

Transient type 1 pseudo-hypoaldosteronism: report on an eight-patient series and literature review

Eight boys aged 2–12 weeks with urinary tract malformations (UTMs) exhibited features of transient type 1 pseudo-hypoaldosteronism (TPHA1) in the course of urinary tract infection (UTI). Hyponatremia (120.9 ± 5.8 mmol/l), hyperkalemia (6.9 ± 0.9 mmol/l), metabolic acidosis (plasma bicarbonate 11 ± 1.4 mmol/l), and a rise in serum creatinine levels (145 ± 101 μmol/l) were associated with high urinary sodium (Na) and low potassium (K) excretion. Tubular resistance to aldosterone was indicated by high plasma aldosterone concentrations (170.4 ± 100.5 ng/dl), high levels of the plasma aldosterone to potassium ratio (25.2 ± 15.6), and diminished urinary K/Na values (0.31 ± 0.19). With appropriate therapy, serum electrolytes, creatinine, and acid–base balance normalized within 2 weeks. A Medline search revealed another 85 cases of TPHA1 reported to date. All of the 93 patients were less than 7 months of age and 90% were less than 3 months of age, 90.3% suffered from UTM, with associated UTI in 89% of them, 11% had UTM in the absence of UTI, and 9.7% showed isolated UTI. These findings indicate that early infancy is the main contributing factor for TPHA1 to occur and that UTI and UTM are additional factors, with at least one being required for its development.     

Bartter's syndrome: clinical study of its treatment with salt loading and propranolol.

The clinical course of a 9 year old black male with Bartter's syndrome who has been followed since age 1 1/2 years is presented. He had been unable to conserve sodium on a low salt diet and has failed to show improvement in serum electrolytes while on a sodium loading regimen. He is now refractory to spironolactone and KCI therapy, even in conjunction with supplemental sodium. On two separate trials his electrolytes have approached normal with the combination of propranolol and spironolactone along with KCI and NaCl supplementation. However, his response to this regimen has been a temporary one with relapse to the pretreatment chemical status despite increasing doses of propranolol and potassium chloride.     

Urinary electrolytes and hypertension in elderly Kazakhs

Background. Deficiency of potassium (K) intake is associated with hypertension, and high dietary K intake may have a preventive effect. The prevalence of hypertension and incidence of stroke are higher in Kazakhs than in other ethnic groups in the People's Republic of China (PRC). The Barkol area in the Xinjiang region in PRC is an area with a high population of Kazakhs. We carried out a study in this region that involved blood pressure monitoring and the examination of serum and urinary electrolytes in the Kazakh and Han populations of the area. Methods. Twenty-four-hour ambulatory blood pressure monitoring and urine collections were performed for each study subject. In each subject, urine was collected simultaneously for 24 h during the blood pressure monitoring. Serum and urinary electrolytes were measured. Results. The prevalence of hypertension was higher in the Kazakh population than in the Han (men, 53%; women, 43% in the Kazakhs; men, 40%; women, 30% in the Han; P < 0.001). Urinary excretion of potassium was lower in Kazakhs than in Han (Kazakh, 18.9 ± 8.7 mmol/day; Han, 36.5 ± 11.3 mmol/day; P < 0.001). Urinary excretion of sodium was lower in Kazakhs than in Han (Kazakhs, 181.4 ± 77.6 mmol/day; Han, 194.1 ± 75.9 mmol/day; P < 0.001). Mean 24-h blood pressure was higher in Kazaks than in Han, and this value correlated positively with the urinary sodium/potassium ratio (r = 0.39; P < 0.001). Conclusions. The prevalence of hypertension was higher in Kazakhs than in Han in the Barkol area in the Xinjiang region. Kazakhs had a low intake of potassium. The sodium/potassium ratio was higher in Kazakhs than in Han. A high Na/K ratio, together with low intake of potassium, may be a factor in Kazakh hypertension. Received: February 8, 2001 / Accepted: July 5, 2001     

Potassium metabolism in continuous ambulatory peritoneal dialysis patients

Background: Hypokalemia is common and may have contributed to the poor clinical outcome in peritoneal dialysis (PD) patients. In this study, we made a detailed investigation on the potassium metabolism in continuous ambulatory peritoneal dialysis (CAPD) patients and tried to find out the possible factors associated with the high prevalence of hypokalemia in PD patients. Methods: A cross-sectional survey in 243 clinically stable CAPD patients was made in our PD center in 2010. Patients were divided into four groups according to whether they were anuric or not and different dialysis regimens. Patients’ demographic data and data on potassium metabolism including dietary potassium intakes, residual renal potassium, and peritoneal dialysis potassium removal were collected. Results: The average potassium intake in our 243 PD patients was 32.1?±?11.1?mmol/day. The total potassium removal was significantly higher in non-anuric patients as compared to anuric patients (33.2?±?9.1 vs. 23.0?±?4.7?mmol/day for 3 exchanges per day and 35.2?±?8.9 vs. 28.6?±?6.3?mmol/day for 4 exchanges per day, respectively, p?p?p?p?R² linear?=?0.645, p?Conclusions: Our study suggested that if potassium intake was limited in PD patients, we should be aware of the risk of hypokalemia with high doses of PD when patients have good RRF. Our study also suggested that potassium removal in PD patients may not necessarily reflect potassium intake even if serum potassium is normal, the effect of ICW should be considered when evaluating potassium homeostasis.     

Urinary nitrite excretion and urinary variables in patients with primary nocturnal frequency of micturition: effects of indomethacin suppositories

Urinary nitrite excretion was measured in patients with primary nocturnal frequency of micturition (PNFM) and in normal individuals. Effects of indomethacin suppository on urine volume and other urinary variables were evaluated. The study comprised seven patients with PNFM and seven healthy control (age range 30–45 years). Nitrite was assayed in spot morning urine samples; urine volume, urine osmolality and electrolytes, serum osmolality and electrolytes and functional bladder capacity (FBC) were assayed. Both groups were then given 100 mg of indomethacin suppository daily for a maximum of 10 days and urinary variables were re-evaluated during day 10. Results showed that urinary nitrite excretion of patients with PNFM was greater than that of the normal subjects (230±62 umol/l vs. 42±30 umol/l, P<0.05). The mean (SD) 24 h urine volume and osmolality, the night urine volume and osmolality, serum osmolality, FBC, creatinine clearance, fractional excretion of sodium (FENa), fractional excretion of potassium (FEK), and urinary excretion of glucose and potassium were lower in patients with PNFM as compared with normal individuals, although not statistically significantly so, except for FBC that was significantly lower in the patients. Urinary excretion of sodium, calcium, chloride, phosphorus, magnesium, day-night urinary volume ratio, spot morning osmolality, nocturnal index, and nocturnal polyuria index were higher in patients with PNFM. Indomethacin decreased the 24 h urinary volume by 21%, creatinine clearance by 12%, osmolar clearance by 14% and urinary protein excretion by 38% in the patients. These variables decreased by 26, 45, 17 and 12% respectively in the healthy subjects, whereas 24 h urinary protein excretion increased mildly by 9%. Indomethacin increased day-night urinary volume ratio by 73% in the healthy subjects. It might be concluded that urinary nitrite excretion, urinary excretion of sodium, chloride, phosphorus, calcium, and magnesium increased and FBC decreased in patients with PNFM; Indomethacin decreased urinary volume, FENa, FEK, osmolar clearance, and free water clearance in the healthy subjects and the patients. These might explain the mechanism of action of indomethacin to reduce frequency of voiding. The possible interaction of prostaglandin and NO in the pathogenesis of PNFM is discussed.     

Hypokalemic rhabdomyolysis in a child with Gitelman’s syndrome

We report here the first published case of a pediatric patient with Gitelman’s syndrome (GS) in whom hypokalemia-associated rhabdomyolysis developed. A 13-year-old girl was admitted with weakness of the extremities, walking difficulty and calf pain. Laboratory data showed a serum potassium level of 2.1 mmol/l and a serum creatinine phosphokinase level of 1,248 IU/l plus myoglobinemia. The presence of normomagnesemia was the basis for a genetic analysis of the thiazide-sensitive sodium chloride cotransporter gene, which revealed compound heterozygous mutations in this gene. Prompt fluid expansion and potassium supplementation led to regression of the muscle symptoms. Hypokalemia can be a rare cause of rhabdomyolysis in patients with GS, even in childhood. We emphasize that genetic analysis is advisable to determine whether the suspicion of GS is warranted.     

High-dose oral vitamin D3 supplementation in rheumatology patients with severe vitamin D3 deficiency

ObjectivesRecent large trials indicate that adherence associated with a daily regimen of vitamin D is low and limits anti-fracture efficacy with vitamin D supplementation. The aim of this report is to describe changes of 25-hydroxyvitamin D (25(OH)D) serum concentrations achieved with a single oral dose of 300 000 IU vitamin D3.MethodsOver a course of 4 months, we identified 33 elderly with severe vitamin D deficiency (25(OH)D < 25 nmol/l) on admission to acute care. Patients were admitted for musculoskeletal pain, bone disease, or gait abnormalities. The mean age was 80.5 years (SD ± 6.1). All patients were treated with a single oral dose of 300 000 IU D3 in combination with 500–1000 mg calcium supplements per day depending on their dietary calcium intake.ResultsBaseline mean 25(OH)D serum concentrations were 15 nmol/l (SD ± 5.5). Mean 25(OH)D serum concentrations increased to 81.4 nmol/l (SD ± 29.7) at 3 months (29 patients) and were still 69.0 nmol/l (SD ± 17.9) at 6 months (26 patients). Mean serum calcium levels were 2.24 mmol/l (SD ± 0.11) at baseline, 2.28 mmol/l (SD ± 0.18) at 3 months, and 2.28 mmol/l (SD ± 0.13) at 6 months. Two patients with mild hypercalcemia (2.69 mmol/l) at 3 months had normal values at 6 months.ConclusionBased on our observations, a single oral dose of 300 000 IU vitamin D3 raises mean 25(OH)D serum concentrations to the target mean of above 75 nmol/l at 3 months and a mean level of 69 nmol/l at 6 months. As calcium absorption is enhanced with higher 25(OH)D serum concentrations, calcium supplementation may need downward adjustment with this regimen to avoid mild hypercalcemia.     

A prospective double-blind randomized placebo-controlled clinical trial to evaluate the safety and efficacy of spironolactone in patients with advanced congestive heart failure on continuous ambulatory peritoneal dialysis

Congestive heart failure (CHF) is frequent in patients with chronic renal failure, and may contribute to high cardiovascular morbidity and mortality. There is little data in the literature about the safety and efficacy of use of spironolactone in patients with end-stage renal disease with heart failure. In this study, we evaluated the safety and efficacy of spironolactone in patients on continuous ambulatory peritoneal dialysis (CAPD) with CHF. This randomized prospective double-blind placebo-controlled clinical trial was performed at the St. Al-Zahra peritoneal dialysis center. Eighteen CAPD patients with New York Heart Association (NYHA) class III or IV heart failure, ejection fraction (EF) ≤45%, serum potassium level ≤5.5 mEq/L and who were eligible, were randomly assigned to taking either spironolactone (25 mg every other day) or placebo for six months. The serum potassium was measured monthly and echocardiography was repeated at the end of the study period. The serum potassium levels rose in both groups, and there was no statistically significant difference intragroup and between the groups during the study period. Only in one patient in the spironolactone group did the serum potassium level reach above the critical level (5.70 mEq/L) at the end of the second month of study, necessitating patient exclusion. The EF did not change significantly in the placebo group (33.3 ± 11.7 vs. 34.2 ± 11.6, F = 1, P = 0.363), but in the spironolactone group the EF rose significantly (25.7 ± 7.3 vs. 33.3 ± 7.8, F = 27.45, P = 0.002). Our study suggests that spironolactone could be used in CHF patients on CAPD to improve their cardiac function, but close monitoring of their serum potassium level is required.     

Hypophosphatemia following open heart surgery: incidence and consequences.

OBJECTIVE: Significant hypophosphatemia (SH) is common after major surgery and may be associated with considerable morbidity, including respiratory and cardiac failure. The contribution of SH to these complications after cardiac surgery is not well defined. METHODS: In this prospective study, levels of serum phosphorus and other electrolytes (potassium, magnesium and calcium) were measured in 566 consecutive patients (395 men, 182 women; mean age 65.5+/-11.1 years) undergoing elective cardiac surgery at three time points: prior to surgery, immediately on admission to the ICU, and on the first postoperative day. Preoperative (type of surgery, Bernstein-Parsonnet risk estimate), intraoperative (duration of bypass and cross-clamp, intraoperative fluid and blood product use) and postoperative data (duration of ventilation, duration of ICU and hospital stay, requirement for cardioactive drug support, development of atrial fibrillation, and mortality) were collected. Patients were divided into two groups according to the immediate postoperative phosphate level: SH, phosphate <0.48 mmol/l (mean phosphate 0.28+/-0.13 mmol/l, n = 194), and a control group (mean phosphate value 0.84+/-0.08 mmol/l, n = 372). Patients with SH received treatment with sodium or potassium phosphate (0.8 mmol/kg body weight over 6-12 h). RESULTS: SH was present in 34.3% of patients. There were no differences in the baseline characteristics between the two groups. Patients with SH received more intraoperative blood product transfusions. The postoperative course of patients with SH was characterized by prolonged ventilation (2.1+/-1.7 versus 1.1+/-0.9 days, P = 0.05), more patients requiring cardioactive drugs (12-24 h 16 versus 10.9%, P = 0.05 and >24 h 23.5 versus 13.8%, P = 0.05); and a prolonged hospital stay (7.8+/-3.4 versus 5.6+/-2.5 days, P = 0.05). CONCLUSIONS: SH was common after open-heart surgery and was associated with an increased incidence of important complications. We suggest that phosphate levels be routinely measured immediately after surgery and appropriate therapy instituted.     

The Use of Calcium Carbonate to Treat the Hyperphosphataemia of Chronic Renal Failure

This study evaluates the use of calcium carbonate in chronicrenal failure. Forty-eight patients (25 male, 23 female, meanage 54.3 years, six pre-dialysis, 12 CAPD, 30 haemodialysis)on phosphate restriction and requiring aluminium hydroxide (mean2.4±0.8 g/ day) to control serum phosphate, were convertedto an equivalent dose of calcium carbonate (2.5±0.6 g/day).None received vitamin D analogues. Three months post-conversionthere was a significant decrease in mean (±SEM) serumphosphate (1.86±0.08 versus 1.66±0.05 mmol/l,P<0.01) and serum aluminium (28.3±5.4 versus 13.2±3.0µg/l,P<0.0001); calcium/phosphate product was unchanged. Post-conversionthere was an increase in serum bicarbonate, (20.6±0.5versus 22.1±0.6 mmol/l, P<0.01) and serum calcium(2.32±0.02 versus 2.45±0.03 mmol/l, P<0.0001).No change in serum creatinine, alkaline phosphatase or parathormoneoccurred. No adverse effects were reported but nine (18%) patientsbecame hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom respondedto dose reduction. Hypercalcaemia did not correlate with pre-conversionserum calcium, parathyroid hormone, alkaline phosphatase oraluminium. Calcium carbonate is an effective alternative toaluminium-based phosphate binders. It produces a beneficialincrease in serum calcium and bicarbonate and a significantdecrease in serum aluminium. Hypercalcaemia is unpredictablebut is easily reversible in the majority of patients.     

Severity of postoperative hypophosphatemia in relation to glucose administration and renal handling of phosphate

Major surgery is associated with fall in the concentration of inorganic phosphate in serum, as is intravenous infusion of glucose. Hypophosphatemia during different forms of postoperative dextrose administration was evaluated in patients who had undergone colorectal surgery. They were randomized to two groups. All patients received standardized intravenous fluids on the first 3 postoperative days, but one group had constant infusion of a solution containing glucose (4%), sodium (40 mmol/l) and potassium (20 mmol/l) throughout the observation period, while the other group had a 5-hour infusion of 10% glucose daily, with potassium and sodium solution in between. The amounts of administered glucose and electrolytes were the same in both groups. The serum phosphate levels were significantly lower in the group with constant glucose infusion, due to intergroup difference in renal handling of phosphate. Significantly less phosphate was reabsorbed in the proximal tubules when glucose was given as 24-hour infusion than in the group with 5-hour infusion.