Hypokalemia: a potent risk for QTc prolongation in clarithromycin treated rats.

Clarithromycin belongs to macrolide group of antibiotics commonly known for their proarrhythmic potency. Besides agents interfering with CYP 3A, electrolyte imbalance might influence repolarization problems of clarithromycin. The proarrhythmic tendency of clarithromycin particularly in association with hypokalemia manifested a change in QT interval in rat electrocardiogram (ECG). Varying degree of hypokalemia was induced by intraperitoneal injection of furosemide (50, 30, and 10 mg/kg, for seven days). The serum electrolyte levels confirmed that hypokalemia was established in the groups receiving furosemide. Simultaneously, clarithromycin was orally administered in the doses of 100 and 80 mg/kg for seven days. ECG was measured for 5 min in anaesthetised rat before and after 2 h of treatment. The QT interval was corrected for heart rate and reported as corrected QT (QTc). Distinct QTc interval prolongation was observed in groups receiving furosemide (50 and 30 mg/kg) alone and in all the groups receiving clarithromycin alongside furosemide. Neither, clarithromycin (80 mg/kg) nor furosemide (10 mg/kg) exhibited any significant change in the QTc interval but in combination these drugs led to a significant increase in the QTc interval. Most interestingly, potassium supplementation was found to reduce QTc interval in the group presenting with maximum QTc prolongation. These results suggest that hypokalemic condition potentiates the clarithromycin induced QTc prolongation, thereby indicating the importance of monitoring serum electrolyte during clarithromycin therapy. Although, selection of rat for examination of proarrhythmic liability is controversial, this report may be considered as an evidence of hypokalemia potentiating clarithromycin induced QTc prolongation.

Enhanced feeding in very-low-birth-weight infants may cause electrolyte disturbances and septicemia--a randomized, controlled trial.

BACKGROUND & AIMS: High supply of protein and energy has been introduced to very-low-birth-weight infants to improve growth and cognitive development. The aim of this study was to compare two different feeding strategies on postnatal growth and clinical outcome during neonatal hospitalization. METHODS: Fifty very-low-birth-weight infants were randomized to either an enhanced or a standard feeding protocol within 24 h after birth. Chi-square and T-tests were applied. RESULTS: First week protein, fat and energy supply was significantly higher in the intervention group compared to the control group (all P < 0.001). After inclusion of 50 patients we observed a higher occurrence of septicemia in the intervention group, 63% vs. 29% (P = 0.02), and no more patients were included. The infants in the intervention group demonstrated improved postnatal growth, but they also disclosed significant electrolyte deviations during the first week of life with hypophosphatemia, hypokalemia and hypercalcemia. First week phosphate nadir was lower in the infants experiencing septicemia (1.23 (0.50) mmol/L) as compared to the infants without (1.61 (0.61) mmol/L) (P = 0.03). CONCLUSION: Our study implies that enhanced feeding may induce electrolyte imbalances in VLBW infants, and that deleterious side effects similar to those seen in refeeding syndrome may occur. ClinicalTrials.gov, number NCT01103219 and the EudraCT number is 2010-020464-38.

Síndrome de Gitelman: confusión diagnóstica en una paciente con antecedentes de Trastorno de la conducta alimentaria / Gitelman's Syndrome: diagnosis in a female patient with a history of eating disorders

Introducción. El síndrome de Gitelman es una tubulopatía distal, generalmente de herencia autosómica recesiva, que cursa como una alcalosis metabólica con hipomagnesemia e hipocalciuria. Mientras que la causa de la hipomagnesemia se desconoce, la hipocalciuria se explica por la disminución de la entrada de cloruro de sodio en el túbulo distal. Estos pacientes pueden presentar debilidad muscular, fatiga, hipotensión y condrocalcinosis secundaria a la hipomagnesemia crónica. Su tratamiento consiste en potasio, magnesio oral y diuréticos ahorradores de potasio. El diagnóstico puede retrasarse durante años, ya que los pacientes pueden mantenerse asintomáticos durante largos períodos de tiempo. Las alteraciones bioquímicas con las que cursa pueden orientar hacia otros diagnósticos. Métodos. Se describe el caso de una mujer afecta de este síndrome. Resultados. El diagnóstico clínico se confirmó por el estudio de las mutaciones del gen SLC12A3. Conclusiones. pesar de los antecedentes psicopatológicos de los pacientes, es preciso y necesario descartar siempre una enfermedad orgánica, que puede confundir el diagnóstico al tener en común las mismas alteraciones clínicas, bioquímicas y del medio interno (AU)

Gitelman Syndrome is a pathology in the distal tubule, generally of autosomal recessive inheritance, presenting as a metabolic alkalosis with hypomagnesemia and hypocalciuria. While the cause of hypomagnesemia is unknown, hypocalciuria is explained by the reduction of sodium chloride entrance in the distal tubule. Patients suffering from Gitelman Syndrome may present muscular weakness, fatigue, hypotension and chondrocalcinosis secondary to chronic hypomagnesemia. The treatment consists on potassium, oral magnesium and potasium-sparing diuretics. Diagnosis may be delayed for years, given that patients can remain asymptomatic for long periods of time. Biochemical alterations can lead to other diagnosis (AU)

Implementing continuous quality improvement process in potassium management in peritoneal dialysis patients.

BACKGROUND: Abnormal plasma potassium levels are not uncommon in peritoneal dialysis (PD) patients. Here, we implemented a continuous quality improvement (CQI) approach that mainly focused on dietary management to improve potassium control in PD patients. METHODS: All clinically stable patients who visited the PD clinic monthly were included in this study. A CQI team that included nephrologists, primary nurses, dietician, patients, and their family members was organized, and it monitored patients for 6 months. Patients were asked to provide their dialysis records and 3-day dietary records at each visit. Dialysis adequacy, including potassium and phosphorus removals, was checked before and after the implementation of CQI. Changes in dietary prescription, without altering dialysis prescriptions and potassium supplementation, were made monthly, according to patients' dietary information and blood potassium levels. RESULTS: In total, 84 patients (28 male and 56 female) were included in this study. At baseline, the prevalence of hyperkalemia and hypokalemia was 14.3% each. After the intervention, the prevalence of hyperkalemia dropped to 10.7% and 6% at 3 months and 6 months, respectively. The prevalence of hypokalemia dropped to 8.3% and 7.1% at 3 months and 6 months, respectively. CONCLUSIONS: Our data suggest that implementing CQI, with a focus on dietary intervention, could significantly reduce the prevalence of potassium abnormality in PD patients.

Síndrome de realimentación / Refeeding syndrome

El síndrome de realimentación (SR) es un cuadro clínico complejo que ocurre como consecuencia de la reintroducción de la nutrición (oral, enteral o parenteral) en pacientes malnutridos. Los pacientes presentan trastornos en el balance de fl uidos, anomalías electrolíticas —como hipofosfatemia, hipopotasemia e hipomagnesemia— alteraciones en el metabolismo hidrocarbonado y déficits vitamínicos. Esto se traduce en la aparición de complicaciones neurológicas, respiratorias, cardíacas, neuromusculares y hematológicas. En este artículo se han revisado la patogenia y las características clínicas del SR, haciendo alguna sugerencia para su prevención y tratamiento. Lo más importante en la prevención del SR es identificar a los pacientes en riesgo, instaurar el soporte nutricional de forma prudente y realizar una corrección adecuada de los déficits de electrolitos y vitaminas (AU)

Refeeding syndrome is a complex syndrome that occurs as a result of reintroducing nutrition (oral, enteral or parenteral) to patients who are starved or malnourished. Patients can develop fluid-balance abnormalities, electrolyte disorders (hypophosphataemia, hypokalaemia and hypomagnesaemia), abnormal glucose metabolism and certain vitamin defi ciencies. Refeeding syndrome encompasses abnormalities affecting multiple organ systems, including neurological, pulmonary, cardiac, neuromuscular and haematological functions. Pathogenic mechanisms involved in the refeeding syndrome and clinical manifestations have been reviewed. We provide suggestions for the prevention and treatment of refeeding syndrome. The most important steps are to identify patients at risk, reintroduce nutrition cautiously and correct electrolyte and vitamin defi ciencies properly (AU)

[Celiac crisis with quadriplegia due to potassium depletion as presenting feature of celiac disease]. / Crise coeliaque associée à une tétraplégie par hypokaliémie de déplétion révélatrice d'une maladie coeliaque.

INTRODUCTION: Adult coeliac disease revealed by coeliac crisis and quadriplegia due to potassium depletion is an extremely rare situation. CASE REPORT: A 26-year-old woman presented with a suddenly developed weakness of all four limbs and a severe diarrhea. Authors emphasize coeliac crisis, which is a presenting feature of coeliac disease, characterized by acute diarrhea with life-threatening acid base and electrolyte abnormalities. The patient improved with correction of hypokalemia and gluten-free diet. CONCLUSION: A severe acute diarrhea with metabolic and systemic complications, the so-called coeliac crisis, is a possible presenting clinical feature of a previously undiagnosed adult celiac disease.

Safety and effectiveness of a modification of diet in renal disease equation-based potassium replacement protocol.

BACKGROUND: No data exist regarding the safety and effectiveness of a potassium replacement protocol for hospitalized patients when potassium replacement dosing regimens (KRDRs) are adjusted to Modification of Diet in Renal Disease estimation of glomerular filtration rate (MDRD GFR). OBJECTIVE: To evaluate the effectiveness and safety of a potassium replacement protocol in which KRDRs are prescribed based on MDRD GFR and serum potassium deficiency (Kdef). METHODS: Patients prescribed the potassium replacement order set were identified in a retrospective fashion. Serum potassium, prescriber-defined goal serum potassium, and MDRD GFR data were collected for patients who received protocol KRDRs. The KRDR to be administered is selected based on Kdef (goal serum potassium minus measured serum potassium) of 0.1-0.2, 0.3-0.5, or more than 0.5 mEq/L and the patients' MDRD GFR of greater than 70, 40-70, or less than 40 mL/min/1.73 m(2) (any patient undergoing dialysis is included in the <40 mL/min/1.73 m(2) group). Efficacy was evaluated by determining the change in serum potassium level (Delta K) following potassium replacement, the number of KRDRs needed to achieve goal serum potassium, and the milliequivalents of potassium needed to achieve goal serum potassium levels. Safety was assessed by the incidence of serum potassium values greater than 5.0 mEq/L following replacement. RESULTS: One hundred forty-nine patients were evaluated. There were 184 protocol initiations and 257 KRDRs administered to achieve goal serum potassium levels. The DeltaK was 0.50 +/- 0.40 mEq/L (mean +/- SD) following KRDR. The Delta K was similar between MDRD GFR groups. One hundred thirty six (73.9%) protocol initiations required 1 KRDR, and 168 (91.3%) protocol initiations required 1 or 2 KRDRs to achieve goal serum potassium. Patients whose MDRD GFR was 40-70 mL/min/1.73 m(2) were less likely to achieve goal serum potassium value after 1 KRDR (58.2% vs 79.6% >70 group and 84.6% <40 group). This was true regardless of the patient's goal serum potassium. One (0.54%) serum potassium greater than 5.0 mEq/L occurred following a KRDR. CONCLUSIONS: Our potassium replacement protocol based on MDRD GFR and Kdef effectively corrects hypokalemia. Fewer protocol initiations achieved goal serum potassium levels in the group with MDRD GFR 40-70 mL/min/1.73 m(2). Hyperkalemia rarely occurred following KRDR.

A different hypothesis on hyponatremia in psychiatric patients: treatment implications and experiences.

Polydipsia, chronic or intermittent, with or without hyponatremia, frequently occurs among chronic patients with schizophrenia. The pathogenesis of polydipsia remains poorly understood. The key assumption of our hypothesis is that in some of these patients, polydipsia and hyponatremia are consequences of patients' adjustment to a prolonged intake of an insufficient diet, dominantly poor in potassium. Deficits of potassium, without significant hypokalemia, may cause impairment of the urine-concentrating ability with polyuria-polydipsia. A fall of intracellular tonicity, dominantly due to a decreased amount of K(+) and attendant anions in cells, should be accompanied with a fall of extracellular osmolality. Because of the diminished content of ions that may diffuse out of cells and because osmotic equilibrium between the ECF and ICF compartments cannot be established in a short period of time, these patients have a diminished ability to adapt to an excessive intake of fluids. These mechanisms might be related to the development of polydipsia and water intoxication in patients with different mental and somatic disorders. The experiences with the therapeutic effects of diets containing an sufficient amount of potassium in two patients with schizophrenia are described. Further investigations are needed, and we suggest a possible approach to test our hypotheses.

Bartter syndrome presenting as poor weight gain and abdominal mass in an infant.

Bartter syndrome, a group of disorders that encompasses multiple genetic defects with similar clinical presentation, has been divided into six different genotypes, according to different genetic defects, and into three main clinical variants (or phenotypes). Classic laboratory findings in all variants include hypochloremia, hypokalemia, and metabolic alkalosis with excessive excretion of chloride and potassium. Classic Bartter syndrome, neonatal Bartter syndrome, and Gitelman syndrome are the three main clinical variants. Classic Bartter syndrome and neonatal Bartter syndrome have defects in genes that affect transport channels in the ascending loop of Henle, where as in Gitleman syndrome the defect occurs in the transport channels of the distal convoluted tubule. Classic Bartter syndrome and neonatal Bartter syndrome have similar presenting symptoms, potential outcomes, and treatment, but different ages at presentation. Gitelman syndrome, a more benign condition than the other clinical variants, has the classic hallmark finding of hypomagnesemia and low to normal excretion of calcium. This differentiates it from the classic and neonatal variants of the disease. With early diagnosis and proper treatment, Bartter syndrome has a good prognosis. But failure to identify it can lead to tubulointerstitial nephritis and renal failure. We present a case of a 6-month-old boy with Bartter syndrome who presented with poor weight gain and an abdominal mass.

Pacientes con riesgo de desnutrición: valoración de 11 casos gravemente desnutridos con nutrición parenteral total individualizada / No disponible

nutricional individualizado durante la primera semana con nutriciónparenteral total en pacientes con desnutrición moderada-gravesusceptibles de desarrollar un síndrome de renutrición.Método: Estudio retrospectivo observacional desde enero2003 a junio 2006 incluyendo todos los pacientes adultos condesnutrición moderada-grave que recibieron >= 5 días de nutriciónparenteral total. Se describió el soporte nutricional y se evaluó laaparición de alteraciones hidroelectrolíticas y metabólicas gravesdurante la primera semana de nutrición.Resultados: Se incluyeron 11 pacientes con índice de masacorporal medio de 15,4 kg/m2 que recibieron una media de 23kcal/kg/día. No aparecieron alteraciones hidroelectrolíticas ometabólicas graves. Tres pacientes presentaron hipofosfatemia, 5hipopotasemia y 4 hipomagnesemia, todas leves-moderadas ycorregidas, excepto en dos casos, a la semana de nutrición.Conclusiones: El soporte nutricional individualizado en pacientescon desnutrición moderada-grave no produjo ningún síndromede renutrición. La indivualización de la nutrición es una estrategiaesencial para evitar las complicaciones de una sobrealimentación

Objective: To describe and assess the efficacy and safety ofindividualised nutritional support during the first week of total parenteralnutrition in moderately to severely malnutritioned patientswho are susceptible to the refeeding syndrome.Method: Retrospective observational study carried outbetween January 2003 and June 2006, including adult patientswith moderate to severe malnutrition who received >= 5 days totalparenteral nutrition. The nutritional support was described andthe appearance of severe hydroelectrolytic and metabolic disturbanceswere assessed during the first week of nutrition.Results: The study included 11 patients with a mean bodymass index of 15.4 kg/m2. These patients received an average of23 Kcal/kg/day. They did not show any signs of severe hydroelectrolyticor metabolic disturbances. Three patients presentedwith hypophosphataemia, five with hypokalaemia and four withhypomagnesaemia, all of which were mild to moderate and withthe exception of two cases, all were corrected within one week offeeding.Conclusions: Individualised nutritional support in moderatelyto severely malnourished patients does not produce refeeding syndrome.Individualised nutrition is an essential strategy for avoidingcomplications associated with overfeeding

Central pontine myelinolysis associated with hypokalaemia in anorexia nervosa.

A 31-year-old man was admitted to hospital with of anorexia, binge eating, and self induced vomiting. On admission, he showed a pronounced low weight and disturbance of the body image and was diagnosed as having anorexia nervosa. In addition, electrolyte abnormalities, mainly hypokalaemia, and increased serum renin and aldosterone concentrations were recorded, suggesting pseudo-Bartter syndrome as a complication. Under frequent monitoring of the serum potassium and sodium concentrations, serum electrolytes were gradually corrected, but brain magnetic resonance imaging revealed reversible central pontine myelinolysis (CPM). Although attention has been mainly paid to the association of CPM with rapid correction of hyponatraemia and abnormal osmolality, this case report strongly suggested the involvement of hypokalaemia in the pathogenesis of CPM.

Severe hypokalemia as a cause of acute transient paraplegia following electrical shock.

Transient lower extremity paralysis has been previously reported following high voltage electrical injury. The following case report describes an unusual presentation of transient acute flaccid lower extremity paralysis following a high voltage electrical injury associated with profound hypokalemia and acid/base abnormalities similar to the periodic paralysis syndrome. The patient's symptoms resolved with correction of severe hypokalemia. Potential mechanisms for a metabolic neuromuscular disorder induced by electrical injury are proposed.

Recovery of heart tissue following focal injury induced by dietary restriction of potassium.

Sixty-four Sprague-Dawley rats (initially weighing 200-225 grams) were divided into three groups. Group 1, the experimental group, was fed a potassium depleted diet for 42 days, followed by a potassium repleted diet for up to an additional 14 days. Group 2, the dietary control group, received a potassium deficient diet, but was continuously supplemented by drinking water containing potassium chloride 150 meq/L. Group 3, the control group remained on normal rat chow and tap water during the entire investigation. Quantitative morphometric analysis was used to assess the percent of myocardium occupied by lesion. These data were analyzed by an analysis of variance (ANOVA) for repeated measures, comparing the three groups with one another; a second analysis compared the myocardial lesions of the dietary experimental group during the potassium depletion and repletion periods. At the end of the dietary depletion period (day 42) focal areas of cardiac myocyte necrosis and mononuclear infiltrate were found in the experimental group. Morphometric assessment on day 42 revealed a volume fraction (Vv) of 8.61 (+/- 4.41)%, which was significantly greater (p = 0.0018), as compared with both control groups. Lesion area significantly regressed in two and one half days after potassium was supplemented in the dietary experimental group to 0.58 (+/- 0.34)% Vv (p = 0.0005). Six days after potassium was replaced in the diet, there was no significant difference between the experimental and control groups, and only a limited connective tissue scar was noted in the experimental group. The mechanism of the rapid regression of lesions and the production of only limited connective tissue scar is suggested but requires further elucidation.

The dietary chloride deficiency syndrome.

Chronic depletion of body chloride developed in a group of infants ingesting a diet consisting almost exclusively of chloride deficient Neo-Mull-Soy. Ten of the 12 infants were on this diet three to five months before loss of appetite, failure to thrive, muscle weakness, and lethargy led to a diagnostic evaluation. The outstanding laboratory features were severe hypokalemic metabolic alkalosis, low urinary chloride concentrations (< 10 mEq/liter), and erythrocyturia. There was marked decrease in weight for age in all 12 infants. Head circumference for age had decreased in five of six and length for age in five of ten infants for whom earlier measurements were available. The biochemical abnormalities reverted to normal following dietary supplementation with either sodium or potassium chloride. Appetite, affect, and muscle strength improved, and weight gain resumed. Head circumference for age has moved toward the percentile level present prior to starting Neo-Mull-Soy in all instances. With one exception, length measurements show a similar pattern. The erythrocyturia has decreased or vanished. Chloride deficiency led to contraction of the extracellular volume and the substitution of poorly reabsorbable anions for readily reabsorbable chloride. These alterations caused development of the negative hydrogen ion and potassium balances which led to the hypokalemic metabolic alkalosis.