Hypokalemia and hyperkalemia in patients on peritoneal dialysis: incidence and associated factors.

BACKGROUND: Hypokalemia is a well-described electrolyte disturbance in patients on peritoneal dialysis (PD). Hyperkalemia, however, is still overlooked, although it also represents a risk factor for mortality. Angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers (ACE/ARB), diuretics, and proton pump inhibitor (PPI) can interfere with potassium levels in these patients. METHODS: This is a retrospective study that evaluated monthly serum potassium in a 5-year period. Serum potassium disturbances were evaluated as time-average and number of hypo- and hyperkalemia episodes per patient. Prescribed medication such as ACE/ARB, diuretics, and omeprazole were recorded. RESULTS: We evaluated 2025 potassium measurements obtained from 146 patients on PD. Serum potassium ranged from 2.5 to 8.3 mEq/L with an average of 4.72 ± 0.74 mEq/L. Hypokalemia was found in 59 measurements (2.9%) obtained from 35 patients (23.9%) whereas hyperkalemia was demonstrated in 269 (13.3%) measurements obtained from 74 patients (50.7%). Hypokalemia was associated with low albumin (p = 0.022), and omeprazole use (p = 0.024). Black race was a protector factor (p = 0.031). Omeprazole-associated hypokalemia was seen only in non-anuric patients and remained an independent risk factor even after adjustments. Patients who had hyperkalemia were more likely to be anuric (p = 0.001) and in use of furosemide (p = 0.0001). CONCLUSION: Hyperkalemia and hypokalemia are very frequent in patients on PD and should be closely monitored. Interventional studies should address the impact of discontinuing omeprazole in the levels of potassium.

Hyperkalemia in chronic kidney disease.

Hyperkalemia is a frequent finding in patients with chronic kidney disease (CKD). This increase in serum potassium levels is associated with decreased renal ion excretion, as well as the use of medications to reduce the progression of CKD or to control associated diseases such as diabetes mellitus and heart failure. Hyperkalemia increases the risk of cardiac arrhythmia episodes and sudden death. Thus, the control of potassium elevation is essential for reducing the mortality rate in this population. Initially, the management of hyperkalemia includes orientation of low potassium diets and monitoring of patients' adherence to this procedure. It is also important to know the medications in use and the presence of comorbidities to guide dose reduction or even temporary withdrawal of any of the potassium retention-related drugs. And finally, the use of potassium binders is indicated in both acute episodes and chronic hyperkalemia.

Hyperkalemia in chronic kidney disease

SUMMARY Hyperkalemia is a frequent finding in patients with chronic kidney disease (CKD). This increase in serum potassium levels is associated with decreased renal ion excretion, as well as the use of medications to reduce the progression of CKD or to control associated diseases such as diabetes mellitus and heart failure. Hyperkalemia increases the risk of cardiac arrhythmia episodes and sudden death. Thus, the control of potassium elevation is essential for reducing the mortality rate in this population. Initially, the management of hyperkalemia includes orientation of low potassium diets and monitoring of patients' adherence to this procedure. It is also important to know the medications in use and the presence of comorbidities to guide dose reduction or even temporary withdrawal of any of the potassium retention-related drugs. And finally, the use of potassium binders is indicated in both acute episodes and chronic hyperkalemia.

RESUMO A hiperpotassemia é um achado frequente em pacientes com doença renal crônica (DRC). Esta elevação do nível sérico de potássio está associada à diminuição da excreção renal do íon, assim como ao uso de medicações para retardar a progressão da DRC ou para controlar doenças associadas, como diabetes mellitus e insuficiência cardíaca. A hiperpotassemia aumenta o risco de episódios de arritmia cardíaca e morte súbita. Assim, o controle da elevação de potássio é essencial para a diminuição da taxa de mortalidade nessa população. O manejo da hiperpotassemia inclui, inicialmente, orientação de dietas com baixo teor de potássio e acompanhamento da aderência dos pacientes a esse procedimento. Também é importante conhecer as medicações em uso e a presença de comorbidades, a fim de orientar a redução de doses ou até mesmo a suspensão temporária de alguma das drogas relacionadas à retenção de potássio. E, finalmente, o uso de quelantes de potássio é indicado tanto em episódios agudos como nos casos de hiperpotassemia crônica.

Prescription of renin-angiotensin-aldosterone system inhibitors (RAASi) and its determinants in patients with advanced CKD under nephrologist care.

Renin-angiotensin-aldosterone system inhibitors (RAASi) are recommended for chronic kidney disease (CKD) patients. In this study, we describe RAASi prescription patterns in the Chronic Kidney Disease Outcomes and Practice Patterns Study (CKDopps) in Brazil, Germany, France, and the United States (US). 5870 patients (mean age 66-72 years; congestive heart failure [CHF] in 11%-19%; diabetes in 43%-54%; serum potassium ≥5 in 20%-35%) were included. RAASi prescription was more common in Germany (80%) and France (77%) than Brazil (66%) and the United States (52%), where the prevalence of prescription decreases particularly in patients with CKD stage 5. In the multivariable regression model, RAASi prescription was least common in the United States and more common in patients who were younger, had diabetes, hypertension, or less advanced CKD. In conclusion, RAASi prescription patterns vary by country, and by demographic and clinical characteristics. RAASi appear to be underused, even among patients with strong class-specific recommendations. Although the reasons for this variation could not be fully identified in this cross-sectional observation, our data indicate that the risk of hyperkalemia may contribute to the underuse of this class of agents in moderate to advanced CKD.

Hyperkalemia in electrical burns: A retrospective study in Colombia.

INTRODUCTION: Classically, hyperkalemia has been regarded as a complication in patients with electrical burns. The etiology of hyperkalemia includes metabolic acidosis, destruction of red blood cells, rhabdomyolysis and the development of renal failure. The purpose of this study was to determine the prevalence of hyperkalemia within the first 24h after electrical burn injury and to evaluate the possible association of serum potassium concentration with cutaneous burn size (%TBSA) and serum creatine phosphokinase (CPK) concentration. METHODS: A retrospective, cross-sectional study was conducted, based on review of medical records of adult patients hospitalized in the first 24h post electrical injury. Serum potassium (K+) levels were divided into low, normal, and high groups, with breakpoints at 3.5mmol/L and 5.0mmol/L and normal 3.6-4.9mmol/L. To assess potential differences according to the time elapsed between the time of the injury and the sampling time, data were grouped as follows: t1: samples obtained in the first 6h post-injury; t2: samples taken at 6-12h; t3: samples taken at 12-24h. RESULTS: 336 patients were studied. The median age was 32 years old (IQR: 25-43). 95.2% of patients were men. Low and normal values of K+ were observed in 13.7% and 85.1%, respectively. The prevalence of hyperkalemia was only 1.2%, and was not related to previously-administered medications or to simple blood gas pH value during admission. CPK>10,000IU/L was observed in 22.6%. No association was found between the serum potassium concentration and either %TBSA burned or the highest CPK value. CONCLUSIONS: First, patients admitted to our burn unit with electrical injury accompanied by significant skin and muscle injury rarely exhibit hyperkalemia. Secondly, the presence of hyperkalemia is independent of the severity of rhabdomyolysis or the extent of the burn.

Water, electrolyte, acid-base, and trace elements alterations in cirrhotic patients.

Chronic hepatic patients, and particularly those suffering from cirrhosis, are predisposed to different sort of water, electrolyte, acid-base, and trace elements disorders due to their altered liver function, and also to their exposition to infectious, inflammatory, oncologic, and pharmacologic variables whose combination undermines their homeostatic capability. Hyponatremia, hypokalemia, hyperkalemia, hypocalcemia, metabolic acidosis, respiratory, and metabolic alkalosis are the main internal milieu alterations in this group.

Impact of Renin-Angiotensin Aldosterone System Inhibition on Serum Potassium Levels among Peritoneal Dialysis Patients.

BACKGROUND: The chronic use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blocker has been associated with hyperkalemia in patients with reduced renal function even after the initiation of hemodialysis. Whether such medications may cause a similar effect in peritoneal dialysis patients is not well established. So, the aim of our study was to analyze the impact of renin-angiotensin-aldosterone inhibitors on the serum levels of potassium in a national cohort of peritoneal dialysis patients. METHOD: A prospective, observational, nationwide cohort study was conducted. We identified all incident patients on peritoneal dialysis that had angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB) prescribed for at least 3 months and a similar period of time without these medications. Patients were divided into 4 groups: Groups I and III correspond to patients using, respectively, an ACEi or ARB and then got the drug suspended; Groups II and IV started peritoneal dialysis without the use of any renin-angiotensin aldosterone system inhibitor and then got, respectively, an ACEi or ARB introduced. Changes in potassium serum levels were compared using 2 statistical approaches: (1) the non-parametric Wilcoxon test for repeated measures and (2) a crossover analysis. RESULTS: Mean potassium serum levels at the first phase of the study for Groups I, II, III, and IV were, respectively, 4.46 ± 0.79, 4.33 ± 0.78, 4.41 ± 0.63, and 4.44 ± 0.56. Changes in mean potassium serum levels for Groups I, II, III, and IV were -0.10 ± 0.60, 0.02 ± 0.56, -0.06 ± 0.46, and 0.03 ± 0.50, respectively. CONCLUSION: The use of ACEi and ARB was not associated with a greater risk for hyperkalemia in stable peritoneal dialysis patients independently of residual renal function.

Pseudohipoaldosteronismo y aparente exceso de mineralocorticoides: cara y ceca en dos pacientes pediátricos / Pseudohypoaldosteronism and apparent mineralocorticoid excess: two faces, two pediatric patients

Los síndromes endocrinológicos con hipofunción o hiperfunción con niveles paradójicos de dosajes hormonales han sido bien caracterizados en los últimos años del siglo XX, a partir del desarrollo de técnicas genéticas y moleculares. Presentamos dos pacientes con pseudohipoaldosteronismo y aparente exceso de mineralocorticoides como síndromes en espejo, con la intención de alertar al médico clínico respecto de su consideración como entidad diagnóstica en niños con alteraciones hidroelectrolíticas. (AU)

Endocrinological syndromes with underactive or overactive hormonal levels with paradoxical dosages have been well characterized over the years of the twentieth century, from the development of genetic and molecular techniques. We present two patients with pseudohypoaldosteronism and apparent mineralocorticoid excess as mirror syndromes, with the aim to alert the clinician regarding their consideration as a diagnostic entity in children with fluid and electrolyte disturbances. (AU)

Pseudohiperkalemia por trombocitosis esencial: una entidad pobremente reconocida / Pseudohyperkalaemia in essential thrombocytosis: a poorly recognized

INTRODUCCIÓN: La hiperkalemia representa una emergencia médica frecuentemente manejada en servicios de urgencia. Identificar una pseudohiperkalemia en pacientes que presentan recuentos plaquetarios elevados permite evitar terapias innecesarias e iatrogenia que pueden tener consecuencias potencialmente fatales. PRESENTACIÓN DEL CASO: Mujer de 73 años, con enfermedad renal crónica (ERC) etapa-3a (etiología no precisada). En consulta neurológica por crisis isquémica transitoria (abril 2011), se demostró hiperkalemia de 6,0 mEq/L (suero), tasa de filtración glomerular(TFG) de 51 mL/min y trombocitosis de 1.113.000 plaquetas/mm3. Se trata la hiperkalemia con furosemida y dieta pobre en potasio. Inició hidroxiurea indicada por hematología. En control nefrológico (diciembre 2012) presenta hiperkalemia de 7,5 mEq/L (suero), TFG de 37 ml/min y trombocitosis de 1.052.000 plaquetas/mm3. Electrocardiograma (ECG), sin signos de cardiotoxicidad acordes al nivel de kalemia. Se sospechó pseudohiperkalemia secundaria a trombocitosis esencial (PSTE), se suspendió atenolol, furosemida y se continuó hidroxiurea. En febrero de 2013 presentó kalemia de 6,1 mEq/L (suero), trombocitosis de 713.000 plaquetas/mm3 y TFG de 31 mL/min. En mayo de 2014 la kalemia en suero fue de 5,5 mEq/L y en plasma de 5,2 mEq/L; trombocitosis de 503.000plaquetas/mm3 y TFG de 23 ml/min, confirmándose la PSTE. DISCUSIÓN: Hiperkalemia asociada a trombocitosis exige descartar PSTE. La regresión de la kalemia junto con la trombocitosis y ECG sin alteraciones en hiperkalemia, apoyan este diagnóstico. Su confirmación exige demostrar una hiperpotasemia mayor en suero que en plasma (0,36 +/-0,18 meq/L). Tratar una pseudohiperkalemia, puede generar iatrogenia (hipokalemia y/o hemoconcentración que aumenta riesgo de trombosis). Se descarta hiperkalemia secundaria a ERC con TFG>15ml/min

INTRODUCTION: Hyperkalemia is a medical emergency often managed in emergency services. Identifying a pseudohiperkalemia in patients with high platelet counts will avoid unnecessary iatrogenic therapies, which can have potentially fatal consequences. CASE REPORT: 73 year old woman, with chronic kidney disease (CKD) stage-3a (unknown etiology). In neurological consultation by transient ischemic attack (april 2011) it was evidenced a hyperkalemia of 6.0 mEq/L (serum), glomerular filtration rate (GFR) of 51 mL/min and thrombocytosis of 1,113,000 platelets/mm3. Hyperkalemia is treated with furosemide and potassium poor diet. Started on hydroxyurea indicated by hematology. Nephrology consultant (december 2012) realized hyperkalemia of 7.5 mEq/L (serum), GFR of 37mL/min and thrombocytosis of 1,052,000 platelets/mm3. EKG with no sign of cardiotoxicity was found in relation to potassium serum level. A pseudohyperkalemia secondary to essential thrombocytosis (PSET) was suspected. Atenolol and furosemide were discontinued and hidroxiurea was continued. In February 2013 potassium serum level was 6.1 mEq/L, platelet count: 713,000/ mm3 and GFR: 31 mL/min. In may 2014 serum potassium was 5.5 mEq/L and plasma potassium was 5.2 mEq/L; platelet count: 503,000//mm3 and GFR: 23 mL/min, confirming PSET. DISCUSSION: Hiperkalemia associated with thrombocytosis requires to rule out PSET. Regression of serum potassium with platelet count and the abscense of EKG changes with simultaneous hyperkalemia, support this diagnosis. Confirmation of PSTE diagnosis needs to demonstrate a potassium serum level greater than in plasma (0.36 +/- 0.18 mEq/L). Treating a pseudohiperkalemia can generate iatrogenia (hypokalemia and/or hemoconcentration, increasing the risk of thrombosis). A hyperkalemia secondary to CKD is ruled out with GFR >15mL/min

Acute kidney injury after massive attack of Africanised bees.

Acute kidney injury (AKI) is a well-documented complication of massive attack by Africanised bees and can be observed 48-72 h after the accident. We report a case of Africanised bees attack followed by severe and lethal AKI. A 56-year-old man was admitted to emergency department after a massive attack of Africanised bees (>1000 bee stings). He was unconscious, presenting with hypotension and tachycardia. Mechanical ventilation, volume expansion and care for anaphylaxis were instituted. The patient was transferred to the intensive care unit (ICU) and after 48 h he developed rhabdomyolysis, oliguria, increased creatinine levels, hyperkalaemia and refractory acidosis. A diagnosis of AKI secondary to rhabdomyolysis and shock was made. The patient was treated with a prolonged course of haemodialysis. However, he progressed to refractory shock and died 5 days after admission.

Clinicopathologic and electrocardiographic features of Akita dogs with high and low erythrocyte potassium phenotypes.

BACKGROUND: Canine RBCs are expected to have high sodium and low potassium (LK) concentrations. However, some dogs have a low sodium and high potassium (HK) phenotype due to a Na-K pump in the mature RBC membrane. Awareness of this particularity avoids misinterpretation of hyperkalemia in affected dogs. OBJECTIVE: The purpose of this study was to compare the CBCs, serum biochemistry profiles, urinalysis data, and electrocardiography data in HK and LK Akita dogs. METHODS: In this study, the intra-RBC potassium (KRBC) was measured in 48 healthy adult Akita dogs. The HK group included dogs with KRBC concentration at least 5-fold that of plasma, while the LK dogs served as controls. RESULTS: The HK phenotype was determined in 10 dogs (21%). With the exception of higher plasma potassium concentrations in the HK group compared with LK controls (6.6 mmol/L vs 4.4 mmol/L, P < .001), there were no other differences in serum biochemistry variables. In hematology, mean HGB concentration (13.5 vs 15.9, P < .001), PCV (42.9 vs 46.7, P = .009), RBC (6.1 vs 7.4, P < .001), and MCHC (31.3 vs 34.0, P < .001) were significantly lower in the HK group, while MCV (70.0 vs 63.4, P < .001) was higher compared with the LK controls. There were no significant differences in urinalysis or electrocardiography data between groups. CONCLUSIONS: HK Akita dogs showed significant differences in several hematologic variables, as well as higher plasma potassium concentration. Therefore, the HK phenotype should be considered in the interpretation of these variables in this breed.

The dysfunction of ammonia in heart failure increases with an increase in the intensity of resistance exercise, even with the use of appropriate drug therapy.

BACKGROUND: Hyperammonemia during rest periods is a dysfunction in heart failure (HF). The low formation of ammonia during exercise reflects an inefficiency of purine metabolism. Hyperkalemia in response to physical exercise is common in HF and may contribute to a contractile inefficiency in type II fibers, leading to early fatigue. We tested the hypothesis that during resistance exercise of high intensity and low volume, this disorder of ammonia metabolism would be more intense, due to the hyperkalemia present in HF. METHODS: Alternating resistance exercise (RE) of low intensity and high volume, and high intensity and low volume, were applied to 18 patients with an interval of 7 days between them (functional class II-III New York Heart Association, FE = 33.5 ± 4%) and compared with 22 healthy controls matched for age and gender. Ammonia, potassium and lactate levels were assessed before and immediately after the RE. RESULTS: Significant differences: Deltas (control vs. HF) in 40% RE: lactate (mg/dl) 26.3 ± 10 vs. 37.7 ± 7; p < 0,001, ammonia (ug/dl) 92.5 ± 18 vs. 48.9 ± 9; p < 0.001. Deltas (control vs. HF) in 80%RE: lactate(mg/dl) 45.0 ± 12 vs. 54.1 ± 11; p < 0.05, ammonia(ug/dl) 133.5 ± 22 vs. 32.2 ± 7; p < 0.001, potassium (mEq/L) 1.6 ± 0.4 vs. 2.0 ± 0.8; p < 0.05. A negative correlation was found between the deltas of ammonia and potassium (r = -0.74, p < 0.001) in the HF group. CONCLUSIONS: We conclude that in HF, there is an inefficiency of purine metabolism that increases with increasing exercise intensity, but not with an increase of total volume. These findings suggest that hyperkalemia may play an important role in the disorders of purine metabolism.

Potassium in hemorrhagic shock: a potential marker of tissue hypoxia.

BACKGROUND: This study was designed to evaluate serum potassium level variation in a porcine model of hemorrhagic shock (HS). METHODS: Eight pigs were studied in a controlled hemorrhage model of HS. Blood withdrawal began at a 50 mL/min to 70 mL/min rate, adjusted to reach a mean arterial pressure (MAP) level of 60 mm Hg in 10 minutes. When MAP reached 60 mm Hg, the blood withdrawal rate was adjusted to maintain a MAP decrease rate of 10 mm Hg every 2 minutes to 4 minutes. Arterial and mixed venous blood samples were collected at MAP levels of 60 mm Hg, 50 mm Hg, 40 mm Hg, 30 mm Hg, 20 mm Hg, and 10 mm Hg and analyzed for oxygen saturation, Po2, Pco2, potassium, lactate, bicarbonate, hemoglobin, pH, and standard base excess. RESULTS: Significant increase in serum potassium occurred early in all animals. The rate of rise in serum potassium and its levels accompanied the hemodynamic deterioration. Hyperkalemia (K >5 mmol/L) incidence was 12.5% at 60 mm Hg and 50 mm Hg, 62.5% at 40 mm Hg, 87.5% at 30 mm Hg, and 100% at 20 mm Hg. Strong correlations were found between potassium levels and lactate (R = 0.82), SvO2 (R = 0.87), DeltapH (R = 0.83), and DeltaPco2 (R = 0.82). CONCLUSIONS: Serum potassium increase accompanies the onset of HS. The rise in serum potassium was directly related to the hemodynamic deterioration of HS and strongly correlated with markers of tissue hypoxia.

Hyperkalemia during spironolactone use in patients with decompensated heart failure.

BACKGROUND: The incidence of hyperkalemia related to spironolactone use is low in stable heart failure; however, it has not been studied during decompensation. OBJECTIVE: To evaluate the influence of spironolactone on serum potassium in decompensated heart failure (HF). METHODS: In a cohort study, patients that had been hospitalized due to decompensated HF, with left ventricular ejection fraction (LVEF) < 0.45 and serum potassium between 3.5 and 5.5 mEq/l were selected. The patients were divided according to spironolactone use (Group S) or no use (Group C). The outcome was potassium increase (> 6.0 mEq/l) and the use of calcium polystyrene. A multivariate analysis through logistic regression was carried out and values of p < 0.05 were considered significant. RESULTS: A total of 186 patients (group S: 56; group C: 130) were studied; LVEF of 0.25, aged 55.5 years and 65.2% of them males. The incidence of hyperkalemia was 10.7% in group S and 5.4% in group C (p = 0.862). The multivariate analysis showed that serum urea > 60.5 mg/dl during the hospitalization presents a relative risk of 9.6 (95%CI 8.03 - 11.20; p = 0.005) for the occurrence of hyperkalemia. CONCLUSION: The incidence of hyperkalemia was two-fold higher with spironolactone use, but it was not statistically significant. The increase in urea levels was associated to the hyperkalemia. Randomized studies are necessary to clarify this issue.

Hiperpotassemia na vigência de espironolactona em pacientes com insuficiência cardíaca descompensada / Hyperkalemia during spironolactone use in patients with decompensated heart failure

FUNDAMENTO: A incidência de hiperpotassemia relacionada à espironolactona é baixa na insuficiência cardíaca estável, entretanto não foi estudada durante a descompensação. OBJETIVO: Avaliar a influência da espironolactona na insuficiência cardíaca descompensada sobre o potássio sérico. MÉTODOS: Em um estudo de coorte, selecionamos pacientes hospitalizados por descompensação da insuficiência cardíaca, FEVE < 0,45 e potássio sérico entre 3,5 e 5,5 mEq/l. Os pacientes foram divididos segundo o uso da espironolactona (grupo E) ou não (grupo C). O desfecho foi aumento do potássio (> 6,0 mEq/l) e uso de poliestireno de cálcio. Realizou-se a análise multivariada pela regressão logística, e p < 0,05 foi considerado significante. RESULTADOS: Foram estudados 186 pacientes (grupo E: 56; grupo C: 130), FEVE 0,25, idade 55,5 anos e 65,2 por cento de homens. A incidência de hiperpotassemia foi de 10,7 por cento no grupo E e de 5,4 por cento no grupo C (p = 0,862). A análise multivariada mostrou que a uréia sérica > 60,5 mg/dl, durante a internação, apresenta risco relativo de 9,6 (IC 95 por cento 8,03 - 11,20; p = 0,005) para a ocorrência de hiperpotassemia. CONCLUSÃO: A incidência de hiperpotassemia foi duas vezes maior com espironolactona, mas não estatisticamente significante. Elevação da uréia foi associada à hiperpotassemia. Estudos randomizados são necessários para esclarecer o assunto.

BACKGROUND: The incidence of hyperkalemia related to spironolactone use is low in stable heart failure; however, it has not been studied during decompensation. OBJECTIVE: To evaluate the influence of spironolactone on serum potassium in decompensated heart failure (HF). METHODS: In a cohort study, patients that had been hospitalized due to decompensated HF, with left ventricular ejection fraction (LVEF) < 0.45 and serum potassium between 3.5 and 5.5 mEq/l were selected. The patients were divided according to spironolactone use (Group S) or no use (Group C). The outcome was potassium increase (> 6.0 mEq/l) and the use of calcium polystyrene. A multivariate analysis through logistic regression was carried out and values of p < 0.05 were considered significant. RESULTS: A total of 186 patients (group S: 56; group C: 130) were studied; LVEF of 0.25, aged 55.5 years and 65.2 percent of them males. The incidence of hyperkalemia was 10.7 percent in group S and 5.4 percent in group C (p = 0.862). The multivariate analysis showed that serum urea > 60.5 mg/dl during the hospitalization presents a relative risk of 9.6 (95 percentCI 8.03 - 11.20; p = 0.005) for the occurrence of hyperkalemia. CONCLUSION: The incidence of hyperkalemia was two-fold higher with spironolactone use, but it was not statistically significant. The increase in urea levels was associated to the hyperkalemia. Randomized studies are necessary to clarify this issue.

Hyperkalemia, renal failure, and converting-enzyme inhibition: an overrated connection.

Hyperkalemia is widely viewed as a common complication of ACE inhibition in azotemic patients. These renal failure patients are the patients who benefit most from ACE inhibition. Because we could not confirm this notion after a retrospective evaluation of 236 azotemic patients, we studied 2 models of renal mass reduction. In the first, we did a 5/6 nephrectomy (Nx) on rats and studied them 2 weeks after surgery (before chronic renal changes had developed). A second group was studied 16 weeks after Nx, once chronic renal failure was established. Rats in both models were treated with quinapril in drinking water. After baseline evaluation, we challenged them either by a high-K(+) diet or by blocking aldosterone receptors. We found that although quinapril blocked the K(+)-induced increase in aldosterone, serum K(+) levels and K(+) balance were maintained before and during high K(+) intake or during simultaneous spironolactone administration. We conclude that in hemodynamically stable rats with reduced renal mass and renal dysfunction, the administration of an ACE inhibitor does not cause severe hyperkalemia.

Potassium metabolism in extremely low birth weight infants in the first week of life.

OBJECTIVE: Nonoliguric hyperkalemia has been reported to occur in the first week of life in as many as 50% of extremely low birth weight (ELBW) infants. We studied potassium balance and renal function in the first 5 days of life to characterize potassium metabolism during the three phases of fluid and electrolyte homeostasis that we have described in ELBW infants and to elucidate the factors that contribute to the development of nonoliguric hyperkalemia. STUDY DESIGN: Plasma potassium concentration (PK), potassium intake and output, and renal clearances were obtained for the first 6 days of life in 31 infants with a birth weight of 1000 gm or less. Collection periods in which urine flow rate was greater than or equal to 3 ml/kg per hour and weight loss was greater than or equal to 0.8 gm/kg per hour were denoted to be diuretic. Prediuresis includes all collection periods before the first diuretic period; diuresis includes all collection periods between the first and last diuretic periods; postdiuresis includes all collection periods after the last diuretic period. Infants with a PK greater than 6.7 mmol/L on at least one measurement were denoted to have hyperkalemia. RESULTS: PK increased initially after birth--despite the absence of potassium intake- and then decreased and stabilized by the fourth day of life. Diuresis occurred in 27 of 31 infants. The age at which PK peaked was closely related to the onset of diuresis. PK decreased significantly during diuresis as the result of a more negative potassium balance, despite a significant increase in potassium intake. In fact, PK fell to less than 4 mmol/L in 13 of 27 infants during diuresis. After the cessation of diuresis, potassium excretion decreased even though there was a significant increase in potassium intake, potassium balance was zero, and PK stabilized. Hyperkalemia developed in 11 of 31 infants. The pattern of change in PK with age was similar in infants with normokalemia and hyperkalemia: PK initially increased (essentially in the absence of potassium intake) and then decreased and stabilized by the fourth day of life. However, the rise in PK after birth was greater in infants with hyperkalemia than in those with normokalemia: 0.7 +/- 0.2 versus 1.8 +/- 0.2 mmol/L (p < 0.001). No differences in fluid and electrolyte homeostasis or renal function were identified as associated with hyperkalemia. CONCLUSIONS: PK increases in most ELBW infants in the first few days after birth as a result of a shift of potassium from the intracellular to the extracellular compartment. The increase in the glomerular filtration rate and in the fractional excretion of sodium, with the onset of diuresis, facilitates potassium excretion, and PK almost invariably decreases. Hyperkalemia seems to be principally the result of a greater intracellular to extracellular potassium shift immediately after birth in some ELBW infants.

Neonatal presentation of Gordon syndrome.

Gordon syndrome, the association of hypertension with hyperkalemic acidosis, has been described in older children and adults. We report an affected family in which two of the members had exhibited the metabolic manifestations of the disease since infancy. Both patients responded well to thiazides. To our knowledge, these are the youngest patients with documented cases of Gordon syndrome.

Internal potassium shift in premature infants: cause of nonoliguric hyperkalemia.

To study the pathophysiology of nonoliguric hyperkalemia, we measured serum potassium concentration and external K balance (intake and excretion), and estimated internal K balance (a shift from intracellular space to extracellular space) in 24 nonoliguric premature infants during the first 72 hours after birth. Data were analyzed from two aspects: gestational age (group 1, 24 to 28 weeks, n = 9; group 2, 29 to 32 weeks, n = 9; group 3, 33 to 36 weeks, n = 6) and postnatal age (0 to 72 hours). Serum K concentration rose from baseline (0 hour) to 24 hours in groups 1 and 2 (p < 0.01) but did not rise in group 3. The external K balance was negative in all groups during the study period, and was more negative in the more premature infants (group 1 > group 2 > group 3) during the second 24 hours. There was a significant difference (p < 0.01) between the internal K balance of the three groups during the first 24 hours (group 1 > group 2 > group 3), and the K shift decreased significantly (p < 0.05) during the study period in groups 1 and 2. The more premature the infants, the larger the K shift and the larger the rise in serum K concentration during the first 24 hours, and the more negative the external K balance after 24 hours. These data indicate that K loading caused by the K shift associated with prematurity produces a rapid rise in serum K concentration, resulting in an increase in urinary K excretion. We conclude that an internal K shift inversely proportional to gestational and postnatal age is the primary cause of nonoliguric hyperkalemia in very premature infants.