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Hyperkalemia is an electrolyte disorder defined as a plasma potassium concentration greater than 5 mmol/L. Plasma potassium represents approximately 2 % of the total body potassium, and its regulation depends mainly on renal excretion and transcellular shifts. Various pathologies can alter potassium homeostasis and lead to acute or chronic hyperkalemia. The rate of change in plasma potassium concentration is critical because the faster it occurs, the faster life-threatening symptoms develop. Therefore, acute hyperkalemia should be urgently treated. There is no «threshold» value defining the severity of the situation, but the electrocardiographic changes appear to be valuable indicators of severity. Several medical associations have issued recommendations regarding the emergency management of hyperkalemia, but there is no scientific consensus. In this article, we summarize the current knowledge and propose a practical management algorithm for the management of acute hyperkalemia.

Hyperkalemia is common in everyday clinical practice, and is a major risk factor for mortality. It mainly affects patients with chronic renal failure (CKD), diabetes or receiving treatment with inhibitors of the renin-angiotensin-aldosterone system (iRAAS). Therapeutic management aims not only to avoid the complications of hyperkalemia, but also to avoid discontinuation of cardio- and nephroprotective treatments such as iRAAS. The use of polystyrene sulfonate, widely prescribed, is often limited by patient acceptability. Recent data have cast doubt on its safety, particularly in terms of digestive tolerance. Two new potassium exchange molecules have appeared on the market: patiromer and zirconium sulfonate. Their value in clinical practice, and their acceptability in the event of prolonged prescription, remain to be demonstrated. The combination of a thiazide diuretic or an inhibitor of the sodium-glucose cotransporter type 2 (iSGLT2) with iRAAS therapy in CKD, may also improve control of kalemia. At present, there are no recommendations for the positioning of the various hypokalemic treatments. The choice of these treatments must be adapted to the patient's pathologies and consider the other expected effects of these molecules., (Copyright © 2024 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.)

Introduction: In France, no consensus document on the management of persistent hyperkalaemia is currently available. Variability in clinical practices has been observed., Methods: A consensus statement on the definition and the management of persistent hyperkalaemia was developed by a Delphi panel of French nephrologists between December 2019 (26 voting participants among 40 invited panellists in first round) and June 2020 (20 voting participants among 26 panellists in second round)., Results: Persisting hyperkalaemia not controlled with current treatment strategies may be defined as the occurrence of two or more hyperkalaemia episodes within a year despite the administration of cation-exchange resins or loop diuretics during the same year. Some patient characteristics (diabetes, chronic kidney disease from stage 3B to stage 5 without dialysis, chronic heart failure) are associated with an increased risk of developing persistent hyperkalaemia. There is a medical need for the management of persistent hyperkalaemia in patients treated with renin-angiotensin-aldosterone system inhibitors that is not met by current treatment strategies (including available cation-exchange resins)., Conclusions: The panel expressed a need for new treatment strategies validated by clinical trials., (Copyright © 2021 Société francophone de néphrologie, dialyse et transplantation. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Hyperkalemia is common in medicine and requires rapid management. Besides the easily evoked causes such as renal failure, adrenal insufficiency, cell lysis or iatrogenic causes, false or pseudo-hyperkalemia should not be forgotten., Observations: Three patients (1 man, 2 women, aged 78, 84, 88) were managed for thrombocytosis (between 1306 and 2404 G/L) and non-symptomatic hyperkalemia (between 6.1 and 7.7mmol/L) are reported. Kalemia on blood collected in heparin tube was normal (4.4-4.6mmol/L). Therefore, no specific treatment for this pseudohyperkalemia was required., Conclusion: The combination of thrombocytosis and non-symptomatic hyperkalemia should suggest the diagnosis of pseudohyperkalemia and should prompt for a control of kalemia on blood collected in heparin tube. The recognition of this diagnosis is important in order to avoid unnecessary and potentially deleterious treatment of hyperkalemia., (Copyright © 2021 Société Nationale Française de Médecine Interne (SNFMI). Published by Elsevier Masson SAS. All rights reserved.)

Potassium is involved in the voltage and excitability of the myocytes. Its homeostasis is dependent on dietary intake and its predominant renal elimination. The renin-angiotensin-aldosterone system regulates its elimination. Acute and chronic hyperkalemia is a risk factor for cardiac mortality. Chronic renal failure and heart failure are the major comorbidities. RAAS inhibitor therapies are the major iatrogenic factors in hyperkalemia. Approximately 90% of patients with hyperkalemia are over 50 years of age and 43% are over 75 years of age. Only 4.9% of hyperkalemias are managed with resin therapy. One-third of patients have 3 comorbidities, and 14% have 5 or more comorbidities. The main comorbidities are hypertension (74.0%), dyslipidemia (56.3%), renal failure (55.2%), diabetes (44.7%), coronary artery disease such as angina and myocardial infarction (23.3%) and heart failure (12%). It should be noted that 2/3 of the patients receiving resins were also receiving ARBSIs and tended to have more co-morbidities. Hyperkalemia is underestimated and requires strict monitoring in patients with renal failure or heart failure. Resins are not suitable for long-term adherence and new therapies such as patiromer would reduce the risk of hyperkalemia.

Metabolic complications of chronic kidney disease (CKD) are frequent; the aims of this review are to present a 2018 update for hyperkalemia, hyperphosphatemia and anemia. Hyperkalemia is defined by a plasma level above 5.0 mmol/L, after ruling out pre-analytical problems such as hemolysis. It is frequent in CKD, most often due to drugs and notably renin/ angiotensin blockers. Chronic hyperkalemia is deleterious, with an increased risk of mortality. Therapeutic strategies to decrease the incidence and severity of hyperkalemia are therefore crucial in nephrology: experts recommend to maintain the renin/angiotensin blockers as long as possible, whilst associating diuretics and potassium binders. There are apparent discrepancies between optimal protein intake and decreased phosphate intake in CKD; this is even more important in dialysis since protein decrease is associated with denutrition and subsequent increased risk of mortality. Nutritional phosphate intake from vegetables are less absorbed; in contrast, phosphate additives are almost completely absorbed in the gastro-intestinal tract. These "hidden" intake may increase the total daily phosphate intake by 1 000 mg. As such in addition to optimized dialysis, phosphate binders should be used but compliance may be challenging on the long-term. Educational programs focused on phosphate are also mandatory in CKD patients. "Absolute" iron deficiency is less frequent than "functional" iron deficiency in CKD patients: both require the use of iron supplementation, and the latter may benefit from additional erythropoietin stimulating agents (ESA) when hemoglobin is below 10 g/dL. Intravenous iron is more efficient to correct iron deficiency both in pre-dialysis and dialysis especially in patients with chronic deficiency. Last generation intravenous preparations have largely demonstrated their safety. One indication of iron supplementation one should not forget in nephrology is the patient with moderate CKD and heart failure since the expected benefits are multiple, notably in terms of quality of life, renal function and functional capacity. Cet article fait partie du numéro supplément Innovations en Néphrologie réalisé avec le soutien institutionnel de Vifor Fresenius Medical Care Renal Pharma., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Hyperkaliaemia is a serious electrolyte disorder that is favored by many comorbidities, such as chronic renal failure or some treatments such as renin-angiotensin-aldosterone system blockers. The new oral treatments by chelation of intestinal potassium have demonstrated : 1) their effectiveness in the management of serum potassium by maintaining the treatments at optimal dosages ; 2) their safety of use by the absence of serious side effect and 3) the ease of use with a daily intake., Competing Interests: Le Pr Pierre-Yves Martin a participé à des comités consultatifs pour Vifor et Astra Zeneca. Le Dr Caroline Blanc n’a déclaré aucun conflit d’intérêts en relation avec cet article.

Nephrology emergencies are not the most frequent in the emergency room but they often generate some diagnostic and therapeutic problems. Most common renal emergencies are due most often to acute renal failure whatever the cause, electrolytes disturbances, hypertensive crisis and less frequently intoxications or acute decompensation of chronic kidney diseases. The goal of this paper is to review some of these clinical situations both in the diagnostic and therapeutic perspective but essentially to discuss when the nephrologist should be called in the emergency room so that the coordination of care is optimal for the patients.

A 79-year-old man with atherosclerosis presented blue toes and livedo reticularis. The patient had eroded aortic atheromatous plaques, and cholesterol embolization syndrome was suspected. An endovascular technique to exclude sources of cholesterol emboli was however performed. The patient immediately presented with severe muscle pain and total functional disability of lower limbs, new ischemic lesions of toes, anal and genital necrosis, and a livedo extended up to the abdomen. A massive rhabdomyolysis occurred associated with acute kidney injury and hyperkaliemia treated by continuous renal replacement therapy with regional citrate anticoagulation. Steroids have been introduced and renal function improved. Cholesterol crystals were also found on a skin biopsy, performed before endovascular procedure., (Copyright © 2013 Société française d’anesthésie et de réanimation (Sfar). Published by Elsevier SAS. All rights reserved.)

The objectives are to slow the progression of chronic kidney disease (CKD), to take all the cardiovascular risk factors into account, to screen for and treat specific complications and to prepare, if necessary, for renal replacement treatment (transplantation or dialysis). The principal treatment targets are: blood pressure less than 130/80 mmHg and proteinuria less than 0.5 g/day (ratio of proteinuria/creatinuria <50mg/mmol). The first-line treatment to reach these goals is angiotensin conversion enzyme inhibitors (ACE inhibitors), combined with diet and other life style changes. The periodicity of clinical and laboratory assessments depends on the CKD stage, the speed of disease progression and the need to reassess the impact of therapeutic interventions. Comprehensive multidisciplinary management can slow or even stop the progression of CKD and reduce its cardiovascular complications, which are the leading cause of death in these patients., (Copyright © 2012. Published by Elsevier Masson SAS.)

Potassium (K+) is a key component of the resting membrane potential of all cells that influences many important biologic events. The clinical importance of K+ is that surpluses or deficits in K+ in the extracellular fluid may predispose the patient to cardiac arrhythmias. The kidneys adjust overall K+ homeostasis by increasing or decreasing the rate of excretion of K+. Urinary excretion of K+ has 2 components: (i) the concentration of K+ in the tubular fluid that depends on the capacity of the cortical collecting duct to secrete K+. The capacity is determined by the lumen-negative transepithelial potential difference generated by the electrogenic reabsorption of Na+. Aldosterone and to a lesser degree HCO3- and Na+ in the tubular fluid are implicated in the generation of the potential difference. This component is evaluated by the transtubular K+ gradient (TTKG). (ii) The volume of fluid delivered to the cortical collecting duct that depends on the osmolar rate of excretion. These 2 components can be calculated if blood osmolality is higher than urine osmolality. Thus, investigating K+ abnormalities is based on the determination of TTKG and osmolar rate of excretion in the cortical collecting duct, on other clinical (extracellular fluid, blood pressure...) and biological data (24-hour K+ excretion, renin, aldosterone...) easily available. First treatment of K+ abnormality is the treatment of its cause. Insulin and glucose supply and dialysis are the best symptomatic treatments of hyperkalaemia., (Copyright 2010 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.)

Hyperkalemia is a frequently met electrolytic disorder in clinical practice. Blood potassium concentration is primarily under the control of cellular transfer, driven either by the acid basic equilibrium, the action of catecholamines and insulin, and secondarily by the kidney. In the majority of cases, hyperkaliemia is due to renal failure, together with the effect of drugs. The clinical symptoms, particularly cardiac manifestations, of hyperkaliemia can be serious, and this is why the identification of its cause and its treatment are of the utmost importance. The diagnostic strategy rests on a detailed history taking, centered on the drug therapies. The transtubular gradient of potassium can be useful, when there is a suspicion of hypoaldosteronism.

Introduction: The classical cause of hyperkalemic paralysis is the hereditary hyperkalemic paralysis. Very rarely, secondary forms of hyperkalemic paralysis have been reported., Exegesis: Four cases of acute paralysis mimicking Guillain-Barre syndrome in three cases and revealing severe hyperkalemia are presented. All the four patients had moderate chronic renal insufficiency. In two cases, the patients received spironolactone. One case was associated with lysis syndrome. All the 4 cases dramatically improved with the treatment of hyperkalemia., Conclusion: These cases pointed out the possibility for acute peripheral paralysis to reveal severe hyperkalemia.

The treatment of dyskalemia must be primarily etiological and later symptomatic. When moderate but significant hypokaliemia exists (K < 3 mmol/l or 3.5 mmol/l with cardiac disease), oral K supplements must be/given. The intravenous route must be reserved for emergency or impossible oral administration. Acute and severe hyperkalemia (K > 7 mmol/l) must be first corrected by different intravenous measures with secondary oral intervention. In chronic and/or moderate hyperkaliemia (K > 5.5 mmol/l), the oral route for treatment is preferred. In any case, the research of the cause (mainly drug induced) is fundamental.

Potassium is the most important intracellular cation, playing a role in neuromuscular excitability. Dyskalemia is common. The consequence of this ionic perturbation could be serious related to its magnitude. Thus a quick etiological approach and a medical intervention are needed to rapidly correct this potentially lethal ionic disturbance and prevent its recurrence.

The objective of this study was to analyse the clinical and therapeutic aspects of stone-induced anuria based on the analysis of 25 cases. The mean age of the patients was 51 years. The stones were bilateral in 54% of cases, and consisted of uric acid stones in 52% of cases. The diagnosis was based on laboratory and radiological findings. Dialysis was indicated in eight patients because of major metabolic disorders. Urinary diversion was performed by insertion of a ureteric catheter or percutaneous nephrostomy. The medium- to long-term prognosis was favourable in two-thirds of cases, but 3 immediate deaths were observed due to delayed diagnosis.

Gamstorp's disease or hyperkaliemic periodic paralysis is a rare pathology leading to spells of generalized hypotonia due to hyperkaliema. It is hard to say how far pregnancy affects the course of the disease and what is the impact of the disease on pregnancy. We report a case of Gamstorp's disease during pregnancy and we insist on the fact that because it can be crippling during its acute phases, close surveillance is needed during pregnancy. Screening for malignant hyperthermia should be carried out. During labour, kaliemia level should be monitored repeatedly and the expulsion phase kept as short as possible if necessary by forceps delivery.

Malignant hyperthermia (MH), triggered by anaesthesia, is a rare and potentially fatal condition. It requires immediate and specific treatment. This review focuses on anticipation and organisation of treatment. Anticipation means that dantrolene should be available, that an anaesthetic machine should be kept free from all vapours of halogenated anaesthetics, and methods of cooling should be planned. A prompt availability in all operating theatres of dantrolene and the required machines is emphasized. Treatment of a MH episode includes stopping the administration of triggering agents, administering dantrolene, correcting metabolic and respiratory acidosis, and cooling. Different aspects of the cardiovascular pharmacology of dantrolene are discussed. Other drugs are seldom required if proper treatment is started soon enough after the crisis. Complications may arise during a fulminant episode. They are difficult to treat, and may lead to sequelae. A rational approach to the treatment of hyperkalaemia, circulatory and renal failure is discussed. After the crisis, dantrolene should be continued for a short time. Finally, the nonspecific signs which can give the earliest diagnosis possible of MH are discussed: an early diagnosis and early treatment with dantrolene are essential in reducing the mortality of malignant hyperthermia.

Hyperkalaemia with severe myocardial consequence may complicate the treatment of heart failure. In five patients who developed kalaemia ranging from 6.5. to 8.6. mEq/l, the ECG showed altered auriculogram and/or widened QRS, the latter change being associated with ST segment elevation and very large T wave in one case. Such hyperkalaemia cannot be termed iatrogenic, although it is promoted by diuretic-induced hyponatraemia and dehydration. The essential part is played by an aggravation of the haemodynamic status, responsible for acute renal insufficiency with oligoanuria, and by the attendant metabolic acidosis. The correction of this metabolic acidosis promotes diuresis, causing potassium depletion and the rapid regression of electrocardiographic abnormalities. Parenteral alkalinization with sodium bicarbonate, associated with furosemid to prevent sodium overload, instituted in emergency, is the only way to prevent asystole or ventricular fibrillation when kalaemia exceeds 8 mEq/l.

Hyperkalaemia is a common and serious clinical condition in medical and surgical intensive care units. It is mainly encountered in patients with overt or latent cardiac and/or renal failure, and often aggravated by dietetic and therapeutic mismanagement. Hyperkalaemia depresses cardiac contractility, automaticity, conductivity and excitability, leading to ECG changes which must be recognized before clinical cardiovascular deterioration occurs if treatment is to be given to reverse an irremediably fatal evolution: ST-T changes and widening of the QRS with axial deviation shortly precede sinoatrial, intraatrial and atrioventricular block, the characteristic appearances of atrial standstill and ventricular and junctional hyperexcitability. The ECG changes faithfully follow the rise in serum potassium with few exceptions, such as associated electrolytic and acid-base disturbances (usually acidosis). Treatment must be administered as soon as a rise in potassium is observed. It may be administered intravenously (hypertonic glucose and insulin, calcium gluconate, furosemide, buffer solution and, above all, sodium bicarbonate or hypertonic saline) or orally (cation exchange resin). Renal dialysis may be required secondarily.

Auricular asystoly (A.A.) was the electrocardiographic pattern of 6 patients admitted for electrolytic disorders secondary to either renal failure or inadequate treatment. A rapid increase of blood potassium was the unique commun abnormality found to explain the dysrhytmia. Bradycardia (between 25 and 55 beats/mn) was present in each case with or without clinical symptoms. Temporary prophylactic pace maker insertion was performed in 4/7 patients. Recovery appeared after dialysis treatment in 6 cases, medical treatment in one, sinus rhythm being present in 6 and chronic atrial fibrillation in one. Prognosis of A.A. due to hyperkaliemia is good when hydroelectrolytic disorders are rapidly corrected. Follow up of blood electrolytes and electrocardiogram must be regular to prevent reccurencies.

In a patient with shock and hyperkalemia , a peritoneal dialysis, started to treat an hyperkalemia , showed the presence of chocolate-like pus in the peritoneal cavity, and confirmed the intraperitoneal rupture of an amoebic liver abscess . Peritoneal dialysis led to the correction of the metabolic disorders and of the shock and restored the diuresis, ensuring favourable conditions to surgical intervention. Surgical drainage of the abscesses and ornidazole treatment led to complete recovery.