Myelotoxicity and kidney dysfunction related to the use of trimethoprim-sulfamethoxazole for the treatment of Pneumocystis jirovecii pneumonia: a case report of severe adverse events with a common drug.

Trimethoprim-sulfamethoxazole (TMP-SMX) is the primary therapeutic option for Pneumocystis jirovecii pneumonia (PCP). Gastrointestinal symptoms and cutaneous rash are common side effects, with hyperkalemia being uncommon in patients without kidney dysfunction, and myelotoxicity being even rarer. We present the case of a male patient with hypertension and a recent diagnosis of non-Hodgkin lymphoma, undergoing rituximab treatment for two months. He was admitted to the intensive care unit due to dyspnea, tachypnea, and pleuritic pain, requiring mechanical ventilation. Chest computed tomography showed bilateral and multilobed ground-glass opacities, compromising more than 80% of the lung parenchyma. Pulmonary tuberculosis and COVID-19 were ruled out. An angiotomography and Doppler ultrasound revealed an extensive pulmonary thrombus and deep venous thrombosis. Empiric treatment with TMP-SMX for PCP was initiated, but within four days, the patient experienced metabolic acidosis and severe hyperkalemia, necessitating hemodialysis. He also presented with progressive pancytopenia and critical levels of leukopenia and thrombocytopenia. The hypothesis of TMP-SMX-induced myelotoxicity was suspected. Considering the unavailability of an alternative treatment, it was opted to continue TMP-SMX and initiate a granulocyte-colony-stimulating factor. However, the patient maintained medullary deterioration, becoming refractory to the transfusion of blood derivates. On the 17th day of treatment, a clinical decision was made to suspend TMP-SMX, leading to improvements within 48 hours in marrow and kidney functions, metabolic acidosis, and hyperkalemia. Despite all efforts, the patient died after 35 days of hospitalization due to hospital-acquired infections. This case highlights the importance of clinicians recognizing potential myelotoxicity with TMP-SMX and promptly discontinuing the drug if necessary.

Potassium levels in women with polycystic ovary syndrome using spironolactone for long-term.

OBJECTIVE: Spironolactone (SPL) has been used to manage hyperandrogenic manifestations in women with polycystic ovary syndrome (PCOS), but data on the risk of hyperkalemia in this population are scarce. The aim of this study was to evaluate the incidence of hyperkalemia in women with PCOS using SPL in the long term. DESIGN: Single-centre retrospective study. PATIENTS: Inclusion and analysis of 98 treatment periods in 78 women with PCOS (20 of whom were duplicates, returning after treatment interruption for a mean of 38 months) who received SPL for a minimum of 12 months and had at least three measurements of potassium levels over time. MEASUREMENTS: Clinical and hormonal profiles before and during SPL treatment. RESULTS: Mean age was 29.1 (SD: 9.6) years, and body mass index was 32.2 (SD: 8.1) kg/m². Nine patients had diabetes, and 22 had prediabetes. SPL was used in combination with combined oral contraceptive pills in 55 participants and progestin-only pills/long-acting reversible contraception in 28; metformin was added in 35, and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers in 15. Median SPL dose was 100 (range: 50-150) mg. A total of 327 serum potassium measurements were obtained (84 pre-exposure and 243 postexposure). Four potassium measurements were above the reference range before exposure and 19 during exposure. All potassium measurements above the reference range during follow-up were classified as mild hyperkalemia (5.1-5.5 mEq/L). CONCLUSIONS: The present findings suggest that women with PCOS, without kidney or heart disease, using SPL combined with hormonal contraception for managing clinical hyperandrogenism have a low incidence of hyperkalemia and well-tolerated minor adverse effects.

Serum Potassium Trajectory during Acute Kidney Injury and Mortality Risk.

BACKGROUND: The association between potassium (sK) level trajectory and mortality or the need for kidney replacement therapy (KRT) during acute kidney injury (AKI) has not been adequately explored. METHODS: In this prospective cohort, AKI patients admitted to the Hospital Civil de Guadalajara were enrolled. Eight groups based on the sK (mEq/L) level trajectories during 10 days of hospitalization were created (1) normokalemia (normoK), defined as sK between 3.5-5.5; (2) hyperkalemia to normoK; (3) hypokalemia to normoK; (4) fluctuating potassium; (5) persistent hypoK; (6) normoK to hypoK; (7) normoK to hyperK; (8) persistent hyperK. We assessed the association of sK trajectories with mortality and the need for KRT. RESULTS: A total of 311 AKI patients were included. The mean age was 52.6 years, and 58.6% were male. AKI stage 3 was present in 63.9%. KRT started in 36% patients, and 21.2% died. After adjusting for confounders, 10-day hospital mortality was significantly higher in groups 7 and 8 (OR, 1.35 and 1.61, p < 0.05, for both, respectively), and KRT initiation was higher only in group 8 (OR 1.38, p < 0.05) compared with group 1. Mortality in different subgroups of patients in group 8 did not change the primary results. CONCLUSION: In our prospective cohort, most patients with AKI had alterations in sK+. NormoK to hyperK and persistent hyperK were associated with death, while only persistent hyperK was correlated with the need for KRT.

Implication of AV node blockers in patients with end-stage renal disease undergoing head and neck surgery; BRASH syndrome: a case report.

BRASH (Bradycardia, Renal failure, Atrioventricular [AV]-node blocker medications, Shock, and Hyperkalemia), a novel syndrome, is a synergistic interaction between AV node blockers and hyperkalemia, resulting in bradycardia. We report a case of BRASH syndrome with marked bradycardia in a patient with End-Stage Renal Disease (ESRD) associated with synergistic interaction between mild hyperkalemia and AV node blockers. Anesthesiologists should be aware of these clinical features, in which ESRD patients with baseline mild hyperkalemia are particularly susceptible to bradycardia. This report will help in its early recognition as well as enable comprehensive and appropriate treatment strategies without further invasive therapy.

Non-lupus full house nephropathy in pediatrics: Case reports / Nefropatía full house no lúpica en pediatría: reporte de dos casos.

Full house nephropathy is defined as the simultaneous detection of IgA, IgG, IgM, C3, and C1q deposits by immunofluorescence, usually indicating lupus nephritis. There are patients with this immunofluorescence pattern, but with negative autoantibody serology, which means they cannot be diagnosed with systemic lupus erythematosus. Patients presenting with full house nephropathy but no other criteria for lupus are diagnosed as having nonlupus full house nephropathy. Here, we describe two cases: A male patient who debuted with rapidly progressive glomerulonephritis and a female patient with nephrotic syndrome. Both had negative autoantibody serology, findings in the renal biopsy of class IV lupus nephritis and afull house immunofluorescence pattern. Histological findings in non-lupus full house nephropathy are similar to those in lupus nephritis and, probably, similar physiopathological bases. However, prospective studies are needed to determine risk factors and the renal prognosis and to make suggestions for specific treatments.

La nefropatía full house se refiere a la detección simultánea de depósitos de IgA, IgG, IgM, C3 y C1q en la inmunofluorescencia, lo que generalmente indica la presencia de nefritis lúpica. Hay pacientes con este patrón de inmunofluorescencia, pero con serología negativa para autoanticuerpos, por lo que no se les puede diagnosticar un lupus eritematoso sistémico. Este tipo de nefropatía, en la que no se presentan otros criterios para lupus, se denomina nefropatía full house no lúpica. En esta presentación, se describen dos casos: un paciente que ingresó con una glomerulonefritis rápidamente progresiva y una paciente con síndrome nefrótico, ambos con serología negativa para autoanticuerpos, hallazgos en la biopsia renal indicativos de nefritis lúpica de clase IV y un patrón full house en la inmunofluorescencia. La nefropatía full house no lúpica tiene rasgos histológicos similares a los de la nefritis lúpica y, probablemente, sus bases fisiopatológicas son parecidas. Sin embargo, se necesitan estudios prospectivos para conocer los factores de riesgo y el pronóstico renal, y poder hacer sugerencias sobre tratamientos específicos.

Hipodermóclise para correção de desidratação hiperosmolar e distúrbios eletrolíticos graves: relato de caso / Hypodermoclysis for correction of hyperosmolar dehydration and severe electrolyte disturbances: a case report

O tratamento de desidratação e distúrbios eletrolíticos graves é contraindicado por meio de hipodermóclise, mas o nível de evidência da recomendação se baseia na opinião de especialistas. Descreve-se caso clínico de paciente com idade avançada, com indicação de cuidados paliativos, que evoluiu com desidratação hiperosmolar com hipernatremia grave, injúria renal aguda e hipercalemia. Tratou-se a paciente com solução hipotônica por meio da técnica de hipodermóclise, com resolução completa do quadro. Conclui-se que há necessidade de mais estudos sobre o uso da hipodermóclise para o tratamento de distúrbios hidroeletrolíticos graves.

The treatment of dehydration and severe electrolyte disturbances using hypodermoclysis is usually contraindicated, but the level of evidence for its recommendation is based on expert opinion. This case report describes an older patient receiving palliative care who developed hyperosmolar dehydration with severe hypernatremia, acute kidney injury, and hyperkalemia. She was treated with hypodermoclysis using a hypotonic solution, which led to complete resolution of the condition. In conclusion, further studies on the use of hypodermoclysis for the treatment of severe hydroelectrolytic disorders are needed.

Successful medical management of perinephric abscess and urosepsis following urethral obstruction in a cat.

OBJECTIVE: To describe the clinical presentation and medical management of a cat with perinephric abscessation and urosepsis following urethral obstruction and catheterization. CASE SUMMARY: A 2-year-old intact male domestic shorthaired cat presented to an emergency and referral center for lethargy, vomiting, and hematuria. Severe azotemia and hyperkalemia were observed on a serum biochemistry panel. The patient was diagnosed with urethral obstruction and was treated with urethral catheterization, calcium gluconate, IV fluid therapy, buprenorphine, and prazosin. The patient's azotemia improved, and the hyperkalemia resolved. Urinary catheterization was discontinued. The patient developed pyrexia, worsening azotemia, hypoalbuminemia, hyperbilirubinemia, and dysuria. Urethral catheterization was repeated. Abdominal radiographs showed left renomegaly, and abdominal ultrasound revealed left perinephric fluid. Ultrasound-guided centesis of the perinephric fluid revealed septic inflammation, and the sample was consistent with urine based upon sample creatinine. Fluid from the perinephric abscess and urine from the bladder both grew Pasturella spp. The patient was treated with perinephric catheterization, saline lavage, and a continuous infusion of cefotaxime for 72 h. The patient's azotemia quickly resolved, and the patient was discharged after 6 days of hospitalization. The patient was reported to have made a full recovery. NEW OR UNIQUE INFORMATION PROVIDED: This is the first described case of perinephric abscess and urosepsis following urethral obstruction in a cat and its successful medical management. Perinephric abscess not associated with intrarenal abscess has not previously been identified. Additionally, continuous antimicrobial infusion to treat overwhelming infection and the use of the RapidBac Vet immunoassay for point-of-care detection of urinary tract infection has not been described in cats.

A physiology-based approach to a patient with hyperkalemic renal tubular acidosis / Abordagem diagnóstica de um paciente com acidose tubular renal hipercalêmica

ABSTRACT Hyperkalemic renal tubular acidosis is a non-anion gap metabolic acidosis that invariably indicates an abnormality in potassium, ammonium, and hydrogen ion secretion. In clinical practice, it is usually attributed to real or apparent hypoaldosteronism caused by diseases or drug toxicity. We describe a 54-year-old liver transplant patient that was admitted with flaccid muscle weakness associated with plasma potassium level of 9.25 mEq/L. Additional investigation revealed type 4 renal tubular acidosis and marked hypomagnesemia with high fractional excretion of magnesium. Relevant past medical history included a recent diagnosis of Paracoccidioidomycosis, a systemic fungal infection that is endemic in some parts of South America, and his outpatient medications contained trimethoprim-sulfamethoxazole, tacrolimus, and propranolol. In the present acid-base and electrolyte case study, we discuss a clinical approach for the diagnosis of hyperkalemic renal tubular acidosis and review the pathophysiology of this disorder.

RESUMO A acidose tubular renal hipercalêmica é uma acidose metabólica de ânion gap normal que invariavelmente indica anormalidade na secreção de íons potássio, amônio e hidrogênio. Na prática clínica, está geralmente atribuída a um estado de hipoaldosteronismo real ou aparente, causado por doenças ou toxicidade por drogas. Descrevemos um paciente de 54 anos, transplantado hepático, que foi admitido com fraqueza muscular associada à hipercalemia, potássio plasmático de 9,25 mEq/L. A investigação adicional revelou acidose tubular renal tipo 4 e importante hipomagnesemia com elevada fração de excreção de magnésio. A história patológica pregressa incluía um diagnóstico recente de Paracoccidioidomicose - uma infecção sistêmica fúngica endêmica que ocorre em algumas partes da América do Sul -, e as medicações de uso habitual continham sulfametoxazol-trimetoprim, tacrolimus e propranolol. No presente relato de caso, discutiremos uma abordagem clínico-laboratorial para o diagnóstico da acidose tubular renal hipercalêmica, assim como da hipomagnesemia, revisando a fisiopatologia desses transtornos.

A physiology-based approach to a patient with hyperkalemic renal tubular acidosis.

Hyperkalemic renal tubular acidosis is a non-anion gap metabolic acidosis that invariably indicates an abnormality in potassium, ammonium, and hydrogen ion secretion. In clinical practice, it is usually attributed to real or apparent hypoaldosteronism caused by diseases or drug toxicity. We describe a 54-year-old liver transplant patient that was admitted with flaccid muscle weakness associated with plasma potassium level of 9.25 mEq/L. Additional investigation revealed type 4 renal tubular acidosis and marked hypomagnesemia with high fractional excretion of magnesium. Relevant past medical history included a recent diagnosis of Paracoccidioidomycosis, a systemic fungal infection that is endemic in some parts of South America, and his outpatient medications contained trimethoprim-sulfamethoxazole, tacrolimus, and propranolol. In the present acid-base and electrolyte case study, we discuss a clinical approach for the diagnosis of hyperkalemic renal tubular acidosis and review the pathophysiology of this disorder.

Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review / Diabetes mellitus e acidose tubular renal hipercalêmica: relatos de caso e revisão da literatura

ABSTRACT Hyporeninemic hypoaldosteronism, despite being common, remains an underdiagnosed entity that is more prevalent in patients with diabetes mellitus. It presents with asymptomatic hyperkalemia along with hyperchloraemic metabolic acidosis without significant renal function impairment. The underlying pathophysiological mechanism is not fully understood, but it is postulated that either aldosterone deficiency (hyporeninemic hypoaldosteronism) and/or target organ aldosterone resistance (pseudohypoaldosteronism) may be responsible. Diagnosis is based on laboratory parameters. Treatment strategy varies according to the underlying pathophysiological mechanism and etiology and aims to normalize serum potassium. Two clínical cases are reported and the relevant literature is revisited.

RESUMO Apesar de comum, o hipoaldosteronismo hiporeninêmico continua a ser uma entidade sub-diagnosticada, com maior prevalência em pacientes com diabetes mellitus. A doença cursa com hipercalemia assintomática acompanhada de acidose metabólica hiperclorêmica sem disfunção renal significativa. O mecanismo fisiopatológico subjacente não é entendido em sua totalidade, mas postula-se que a deficiência de aldosterona (hipoaldosteronismo hiporeninêmico) e/ou a resistência à aldosterona no órgão-alvo (pseudo-hipoaldosteronismo) possam ser responsáveis. O diagnóstico é fundamentado em parâmetros laboratoriais. A estratégia terapêutica varia de acordo com o mecanismo fisiopatológico subjacente e a etiologia, mas seu objetivo é normalizar o potássio sérico. O presente artigo relata dois casos e analisa a literatura relevante sobre o assunto.

Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review.

Hyporeninemic hypoaldosteronism, despite being common, remains an underdiagnosed entity that is more prevalent in patients with diabetes mellitus. It presents with asymptomatic hyperkalemia along with hyperchloraemic metabolic acidosis without significant renal function impairment. The underlying pathophysiological mechanism is not fully understood, but it is postulated that either aldosterone deficiency (hyporeninemic hypoaldosteronism) and/or target organ aldosterone resistance (pseudohypoaldosteronism) may be responsible. Diagnosis is based on laboratory parameters. Treatment strategy varies according to the underlying pathophysiological mechanism and etiology and aims to normalize serum potassium. Two clínical cases are reported and the relevant literature is revisited.

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

In silico ischaemia-induced reentry at the Purkinje-ventricle interface.

AIMS: This computational modelling work illustrates the influence of hyperkalaemia and electrical uncoupling induced by defined ischaemia on action potential (AP) propagation and the incidence of reentry at the Purkinje-ventricle interface in mammalian hearts. METHODS AND RESULTS: Unidimensional and bidimensional models of the Purkinje-ventricle subsystem, including ischaemic conditions (defined as phase 1B) in the ventricle and an ischaemic border zone, were developed by altering several important electrophysiological parameters of the Luo-Rudy AP model of the ventricular myocyte. Purkinje electrical activity was modelled using the equations of DiFrancesco and Noble. Our study suggests that an extracellular potassium concentration [K(+)]o >14 mM and a slight decrease in intercellular coupling induced by ischaemia in ventricle can cause conduction block from Purkinje to ventricle. Under these conditions, propagation from ventricle to Purkinje is possible. Thus, unidirectional block (UDB) and reentry can result. When conditions of UDB are met, retrograde propagation with a long delay (320 ms) may re-excite Purkinje cells, and give rise to a reentrant pathway. This induced reentry may be the origin of arrhythmias observed in phase 1B ischaemia. CONCLUSION: In a defined setting of ischaemia (phase 1B), a small amount of uncoupling between ventricular cells, as well as between Purkinje and ventricular tissue, may induce UDBs and reentry. Hyperkalaemia is also confirmed to be an important factor in the genesis of reentrant rhythms, since it regulates the range of coupling in which UDBs may be induced.

Hiperpotassemia: conduta sinoventricular em paciente idoso, em insuficiência renal e cetoacidose diabética / Hyperpotassemia and sinoventricular conduction in elderly patient with renal insufficiency and diabetic ketoacidosis

Paciente idoso, portador de cardiomiopatia isquêmica, hipertenso, com leve disfunção renal e diabético insulinodependente, por suspensão do uso da insulina desenvolveu cetoacidose com grave desidratação e severa hiperpotassemia, que reverteu com o uso de medicações. Analisam-se interessantes aspectos eletrocardiográficos inerentes ao caso.

An elderly patient with ischemic cardiomyopathy, hypertension, slight renal dysfunction and insulindependentdiabetes developed ketoacidosis aftersuspending insulin use, with severe dehydration and severe hyperpotassemia, both reverted throughmedications. This paper analyzes interesting eletrocardiographic aspects of this case.

Bloqueo AV completo, reversible, en relación a hiperkalemia grave por enalapril y espironolactona: caso clínico / Complete atrioventricular block, reversible, related to serious hyperkalemia due to enalapril and spironolactone: case report

La hiperkalemia es una de las principales complicaciones potenciales del uso de drogas del tipo IECA, bloqueadores ARAII y antagonistas del receptor de aldosterona, en relación a su dosis, su eventual uso combinado y la función renal del paciente. A continuación se reporta el caso de un paciente de 71 años de edad, hipertenso y diabético que se encontraba en tratamiento con Enalapril 10 mg c/12 h y Furosemida 40 mg a/ 12 h, que sufre una bloqueo aurículo ventricular de 3º grado, secundario a una hiperkalemia de 8.53 mEq/l.

Hyperkalaemia in congestive heart failure patients using ACE inhibitors and spironolactone.

BACKGROUND: Recent studies have shown a fall in global mortality with minimal side effects in severe congestive heart failure (CHF) patients receiving angiotensin-converting enzyme inhibitors (ACEI) plus spironolactone (SLN). However, the risk of hyperkalaemia due to ACEI may be increased by the concomitant use of SLN. METHODS: We conducted a retrospective cohort study by examining consecutive cases of severe decompensated CHF admitted to a university hospital in Brazil from March 1999 to March 2000, which had used ACEI with or without SLN. We reviewed charts for the 30 days following admission and assessed various therapeutic regimens used for heart failure as well as serum potassium and creatinine, before and after drug exposure. The primary end-point was the development of hyperkalaemia (K > or = 5.5 mEq/l). For analysis, the subjects were split into patients treated with ACEI/SLN (n = 49) and patients treated with ACEI (n = 51) by itself. RESULTS: Although demographical and clinical features were comparable between the two groups, ACEI/SLN patients had a higher proportion of class IV CHF. We found 16 cases of hyperkalaemia in ACE/SLN patients, but only one case in ACEI subjects. The odds ratio for developing hyperkalaemia in ACEI/SLN patients was 24. When class III CHF subjects were excluded, the odds ratio was 14.6 (95% confidence interval: 1.8-119.6). The best predictors of hyperkalaemia were class IV CHF, increases in creatinine following treatment and diabetes. CONCLUSIONS: Patients with severe decompensated CHF using ACEI with SLN are at major risk for developing hyperkalaemia.

Transient neonatal hyperkalemia in the antenatal (ROMK defective) Bartter syndrome.

OBJECTIVE: Identification of neonatal hyperkalemia as a complication of Bartter syndrome (BS), a disorder usually characterized by hypokalemic metabolic alkalosis. Study design Case-series description of a group of 12 infants with mutations in the renal potassium channel ROMK, causing one of the antenatal variants of BS. RESULTS: Prematurity, postnatal polyuria, and dehydration were seen in all cases. Plasma potassium was as high as 9.0 +/- 1.2 mmol/L and sodium as low as 124 +/- 3.5 mmol/L, appearing usually at day 3 of life and normalizing by the end of the first postnatal week. No hyperkalemia was found in 12 neonates with the variant of BS and deafness. The mean plasma potassium level during the first week of life among a group of very low-birth-weight infants with similar relative azotemia was 4.9 +/- 1 mmol/L (P <.001). The postneonatal period in the ROMK-defective children with BS was characterized by failure to thrive, hypercalciuria, nephrocalcinosis, and minimal-to-no hypokalemia. CONCLUSIONS: Early postnatal hyperkalemia, sometimes severe, may complicate antenatal BS associated with ROMK mutations. Its association with hyponatremia and hyperreninemic hyperaldosteronism may erroneously suggest the diagnosis of pseudohypoaldosteronism type 1. The expression of ROMK in both the thick ascending limb and cortical collecting duct may explain this apparently tubular maturation phenomenon.

Hyperkalemic periodic paralysis M1592V mutation modifies activation in human skeletal muscle Na+ channel.

Mutations in the human skeletal muscle Na+ channel underlie the autosomal dominant disease hyperkalemic periodic paralysis (HPP). Muscle fibers from affected individuals exhibit sustained Na+ currents thought to depolarize the sarcolemma and thus inactivate normal Na+ channels. We expressed human wild-type or M1592V mutant alpha-subunits with the beta1-subunit in Xenopus laevis oocytes and recorded Na+ currents using two-electrode and cut-open oocyte voltage-clamp techniques. The most prominent functional difference between M1592V mutant and wild-type channels is a 5- to 10-mV shift in the hyperpolarized direction of the steady-state activation curve. The shift in the activation curve for the mutant results in a larger overlap with the inactivation curve than that observed for wild-type channels. Accordingly, the current through M1592V channels displays a larger noninactivating component than does that through wild-type channels at membrane potentials near -40 mV. The functional properties of the M1592V mutant resemble those of the previously characterized HPP T704M mutant. Both clinically similar phenotypes arise from mutations located at a distance from the putative voltage sensor of the channel.

Un caso atípico de abdomen agudo / Atipical case of acute abdomen

Introducción: El potasio es el ión más importante en el funcionamiento de las células excitables, la hiperkalemia se relaciona con efectos peligrosos sobre miocardio, músculo liso y nervios periféricos. A pesar de la clara asociación fisiopatológica entre el aumento del potasio y el íleo paralítico, no se han hallado casos que mencionen al abdomen agudo como forma de presentación en la búsqueda bibliográfica por Medline de los últimos diez años. Se presenta por tanto un caso en el cual el motivo de consulta fue dolor abdominal. Presentación: Paciente de sexo femenino, 83 años, consulta por dolor abdominal muy intenso asociado a náuseas y oliguria de 24 hs de evolución. Antecedentes: tromboembolismo de pulmón a repetición a pesar de estar anticoagulada de forma suficiente, hipertensión pulmonar, fibrilación auricular, medicada con furosemida, espironolactoma, digoxina, acenocumarol. Examen físico: desasosegada, taquipneica, soplo de regurgitación tricúspidea, abdomen doloroso, sin ruidos hidroaéreos. Urea: 108 mg por ciento, creatinina: 1,91 mg/dl, K: 6,8 meq, Ph: 7,52, Po2: 142, PCo2 35, COH3 29,9. ECG: ritmo nodal. Colon por enema: dolicocolon. Ecografía abdominal y endoscopía esófago-gástrica normales. Se trata con soluciones polarizantes, cediendo el dolor abdominal y retornando el ritmo cardíaco a fibrilación auricular, recupera el ritmo diurético y normaliza urea y creatinina. Conclusiones: 1) Esta hiperkalemia sin fallo renal crónico previo fue multifactorial. a- Uso prolongado de espironolactona en paciente deshidratada con escaso aporte de Na. b- Seudohipoaldosteronismo. c- Alcalosis mixta. 2) Debido a la acción del potasio sobre las células excitables, la hiperkalemia puede provocar íleo paralítico y presentarse como abdomen agudo sobre todo en pacientes polimedicados