Correction Of Hyperkalemia Research Articles

Hypokalemia Induced Partial Nephrogenic Diabetes Insipidus: A Case Report

Diabetes insipidus is a condition characterised by a large volume of diluted urine production andincreased thirst. In this case report, a 49-year-old gentleman presented with 3 months of polyuria andpolydipsia. He had a repeated history of hypokalemia. On the evaluation of polyuria and polydipsia,he was diagnosed with partial nephrogenic diabetes insipidus based on his inability to concentrateurine after a water deprivation test and his less than 50% response to exogenous desmopressin.On the evaluation of recurrent hypokalemia, the investigation reports met biochemical criteria forthe diagnosis of Gitelman syndrome. He was encouraged to increase his fluid intake as required,and potassium chloride supplementation relieved his symptoms. This case report demonstrates thereversibility of nephrogenic diabetes insipidus with a correction of hyperkalemia.

Secondary Hyperkalemic Paralysis: a Case Report and an Update Review of 128 Cases

Introduction: Acute flaccid paralysis (AFP) is characterized by progressive weakness with signs of impairment of the lower motoneuron. Secondary hyperkalemic paralysis is a cause of AFP that must be quickly recognized to prevent cardiac and neurological deterioration.
 Methods: We present a case of secondary hyperkalemic paralysis admitted to the emergency department and then we updated a systematic review of published cases of secondary hyperkalemic paralysis published in 2015, including case reports published from 2014 to 2021.
 Results: We present a 69-years-old man admitted to the emergency department due to acute ascending generalized weakness. The neurological examination showed symmetrical tetraparesis (strength 2/5 in lower limbs and 4/5 in the upper limbs). Sensory and cranial nerves testing were unremarkable. He also had intense fasciculations in the cervical region and in the proximal muscles of the upper limbs. Initial laboratory showed potassium of 9.3 mEq/dL. The correction of hyperkalemia led to a complete reversal of weakness and fasciculations. Our patient was diagnosed with renal impairment secondary to a systemic lupus erythematosus was the cause of the secondary hyperkalemic paralysis.
 Discussion: We found 128 cases of secondary hyperkalemic paralysis in Literature. The most common symptom was flaccid tetraparesis. Sensory and cranial nerves testing are usually unremarkable. Electrocardiogram is abnormal in almost all patients, particularly with a tall peaked T wave or wide QRS complex. Renal failure is the most common cause of secondary hyperkalemic paralysis. Correction of hyperkalemia is associated with excellent motor outcomes.

Junctional Bradikardia pada Pasien Hiperkalemia

Hyperkalemia is a life-threatening electrolyte abnormality resulting in cardiac arrhythmia. Hyperkalemia may also cause bradycardia with junctional rhythm. However, the prevalence of hyperkalemia accompanying symptomatic bradycardia has only been explored in a few case reports. Thus we present a case of hyperkalemia with uncommon ECG findings. It has been reported that a 76 years old woman with type 2 diabetes mellitus, hyperkalemia and suspected coronary artery disease complaining about palpitation. Electrocardiography (ECG) showed junctional bradycardia with tall T wave and laboratory examination showed mild hyperkalemia (5.8 mmol/L). After one day of observation, severe hypotension was detected. Unexpectedly the cardiac rhythm was returned into the sinus after correction of hyperkalemia using calcium gluconate, insulin, dextrose, and salbutamol. As serum potassium level rises, sinoatrial and atrioventricular conduction was blocked, causing escape rhythm (junctional escape rhythm). In hyperkalemia, cardiotoxicity can be caused by an increase in resting membrane potential, decreased depolarization and duration of depolarization. When detected on ECG, hyperkalemia should be treated urgently and important to identify underlying causes or precipitating factors of hyperkalemia. Sinus node dysfunction is not excluded in this case. Hyperkalemia can present a bradycardia junctional rhythm. Although the increasing serum potassium levels were low, hyperkalemia may have affected the conduction system leading to the ECG changes.Keywords: hyperkalemia, junctional bradycardia, symptomatic bradycardia

Менеджмент гиперкалиемии у детей с хронической болезнью почек

Актуальность. Гиперкалиемия является наиболее распространенным электролитным нарушением, наблюдаемым у пациентов с заболеваниями почек, особенно с хронической болезнью почек (ХБП), сахарным диабетом, сердечной недостаточностью или тех, кто находится на лечении антагонистами ренин-ангиотензин-альдостероновой системы. Цель исследования: изучение распространенности гиперкалиемии у детей с ХБП 1–5-й ст. и внедрение поэтапного подхода с использованием калиевого биндера полистиренсульфоната натрия (ПСН) для лечения гиперкалиемии. Материалы и методы. В 300 образцах крови детей с ХБП 1–5-й ст. определяли уровень сывороточного калия (СК). У 23 пациентов с ХБП 1–5-й ст. изучали эффективность и переносимость ПСН для коррекции гиперкалиемии. ПСН назначали перорально из расчета 1 г/кг массы тела в сутки, разделяя рассчитанную дозу на 3 приема. Курс лечения длился 4 недели с последующим переходом на поддерживающую терапию в дозе 0,5 г/кг массы тела. Результаты. Полученные результаты продемонстрировали, что нормокалиемия (уровень СК 3,5–5,4 ммоль/л) имела место у 73,3 % детей с ХБП 1–5-й ст. Диапазон значений СК 5,0–5,4 ммоль/л определен у 60 пациентов (20,0 %) с ХБП 1–5-й ст. Легкая степень гиперкалиемии (5,5–5,9 ммоль/л) регистрировалась у 13,7 % детей с ХБП 1–5-й ст., средняя степень гиперкалиемии (6,0–6,4 ммоль/л) — у 7 %, и тяжелая степень гиперкалиемии (≥ 6,5 ммоль/л) — у 6 % соответственно. Через 4 недели лечения ПСН уровень СК снизился с 5,9 ± 0,4 ммоль/л до 4,7 ± 0,3 ммоль/л (р < 0,05). Использование ПСН сопровождалось незначительным повышением в сыворотке крови уровня натрия (с 138,3 ± 2,4 ммоль/л до 140,7 ± 2,2 ммоль/л), не выходящего за границы нормального диапазона. Терапия ПСН хорошо переносилась, только 1 из 23 пациентов прекратил прием ПСН из-за желудочно-кишечной непереносимости. Выводы. Дисбаланс уровня СК у детей с ХБП 1–5-й ст. начинается с пороговых значений 5,0–5,4 ммоль/л, что требует тщательного контроля и свое­временного поэтапного подхода с целью устранения прогрессирования гиперкалиемии и минимизации возможности возникновения нежелательных последствий. ПСН — калиевый биндер — эффективное медикаментозное средство, которое можно использовать для последовательного и безопасного снижения уровня СК у детей с ХБП с гиперкалиемией в составе комплексной терапии.

Serum potassium and heart failure: association, causation, and clinical implications

Dyskalemia (hypo- and hyperkalemia) is a common clinical encounter in patients with heart failure (HF), linked to underlying pathophysiologic alterations, pharmacological treatments, and concomitant comorbidities. Both hypo- and hyperkalemia have been associated with a poor outcome in HF. However, it is not known if this association is causal. In order to investigate this relation, we implemented the Bradford Hill criteria for causation examining the available literature. Of note, hypokalemia and low-normal potassium levels (serum potassium <4.0mmol/L) appear to be associated with adverse clinical outcomes in HF in a cause-and-effect manner. Conversely, a cause-and-effect relationship between hyperkalemia (serum potassium >5.0mmol/L) and adverse clinical outcomes in HF appears unlikely. We also examined the benefits of renin-angiotensin-aldosterone system inhibitors (RAASi) therapy uptitration in patients with HF and reduced ejection fraction. In fact, hyperkalemia often limits RAASi use, thereby negating or mitigating their clinical benefits. Finally, serum potassium levels in HF should be maintained within the range of 4.0-5.0mmol/L, and although the correction of hyperkalemia does not appear to improve clinical outcomes per se, it may enable the optimal titration of RAASi, offering indirect clinical benefit.

P0198SODIUM ZIRCONIUM CYCLOSILICATE INCREASES SERUM BICARBONATE CONCENTRATIONS AMONG PATIENTS WITH HYPERKALAEMIA: RESULTS FROM THREE RANDOMIZED, MULTI-DOSE, PLACEBO CONTROLLED TRIALS

Abstract Background and Aims Sodium zirconium cyclosilicate (SZC; formerly ZS-9) is an orally-administered, non-absorbable, inorganic, selective potassium (K+) binder for the treatment of adults with hyperkalaemia. SZC entraps K+ throughout the gastrointestinal tract in exchange for hydrogen and sodium ions. In addition to serum K+ reduction, phase 2 clinical trial data have shown an increase in serum bicarbonate and a decrease in serum urea. This may be due to SZC trapping of ammonium ions (which are of a similar size to K+ ions) in the gastrointestinal tract. Maintaining serum bicarbonate ≥22 mmol/L preserves kidney function and reduces metabolic bone disease. Thus, SZC-induced increase in serum bicarbonate may represent an effect of clinical significance. We present a post hoc analysis of central laboratory-measured serum bicarbonate, urea, and urine pH data from three randomized, placebo-controlled, phase 3 studies of SZC among patients with hyperkalaemia (ZS-003, HARMONIZE, and HARMONIZE-Global). Method In all studies, patients initially received up to 10 g SZC three times a day (TID) for 48 hours for correction of hyperkalaemia (randomized placebo-controlled in ZS-003, open-label in HARMONIZE and HARMONIZE-Global), followed by randomization to maintenance therapy with SZC up to 15 g once a day (QD) versus placebo for up to 29 days among those who achieved normokalaemia during the correction phase. Results The analysis included 753 patients from the initial 48-hour correction phase of ZS-003, and 208 and 214 patients who completed the 29-day maintenance phase of HARMONIZE and HARMONIZE-Global, respectively. Significant dose-dependent increases from baseline in serum bicarbonate of 0.3–1.5 mmol/L occurred within 48 hours of SZC TID in ZS-003 (Figure A), which occurred regardless of chronic kidney disease (CKD) stage (Figure B). Similar acute increases in HARMONIZE and HARMONIZE-Global were maintained over 29 days with SZC ≥10 g (Figure C) and ≥5 g QD (Figure D), respectively. Mixed-model least-squares mean serum bicarbonate increases from baseline versus placebo over 15–29 weeks with SZC were 2.2 mmol/L (p &amp;lt;0.001) and 2.8 mmol/L (p &amp;lt;0.001) in HARMONIZE (SZC 15 g QD) and HARMONIZE-Global (SZC 10 g QD), respectively. In ZS-003, the proportion of patients with serum bicarbonate &amp;lt;22 mmol/L at correction phase baseline, 27.3%, fell to 16.5% (p = 0.025) at 48 hours among patients receiving SZC 10 g TID. In HARMONIZE and HARMONIZE-Global, the proportion of patients with serum bicarbonate &amp;lt;22 mmol/L at correction phase baseline, 39.4% and 87.9%, respectively, fell to 4.9% (p = 0.005) and 70.1% (p = 0.006) at 29 days, respectively, among patients receiving the highest SZC maintenance dose (15 g and 10 g, respectively). Parallel decreases in serum urea and increases in urine pH were also observed with SZC in all three studies. Mixed-model least-squares mean serum urea decreases from baseline versus placebo over 15–29 weeks with SZC were −1.0 mmol/L (p = 0.029) and −2.9 mmol/L (p &amp;lt;0.001) in HARMONIZE (SZC 15 g QD) and HARMONIZE-Global (SZC 10 g QD), respectively. Corresponding increases in urine pH were 0.23 (p = 0.001) and 0.35 (p &amp;lt;0.001), respectively. Path analysis demonstrated that changes in serum urea (but not changes in serum potassium or urine pH) were associated with the SZC effect on serum bicarbonate. Conclusion SZC consistently and dose-dependently increases serum bicarbonate concentrations, reduces the proportions of patients with serum bicarbonate &amp;lt;22 mmol/L, decreases serum urea, and increases urine pH during treatment of hyperkalaemia. These changes in serum bicarbonate occur regardless of CKD stage and are sustained during ongoing maintenance therapy. The increase in serum bicarbonate is associated with change in serum urea rather than with changes in serum K+ or urine pH, supporting the hypothesis that SZC traps ammonia in the gastrointestinal tract independently to its effect on K+ binding.

Hyperkalemia in heart failure: current treatment and new therapeutic perspectives.

Hyperkalemia in heart failure is a condition that can occur with relative frequency because it is related to pathophysiological aspects of the disease, and favored by drugs that form the basis of chronic cardiac failure therapy. Often, associated comorbidities, such as kidney failure or diabetes mellitus can further adversely affect potassium levels. Hyperkalemia can result in acute and even severe clinical manifestations that put patients at risk. On the other hand, the finding of hyperkalemia in a chronic context can lead to a reduction in dosages or to suspension of drugs such as angiotensin-converting enzymes inhibitor, angiotensin receptor blocker, angiotensin receptor neprilysin inhibitor, and mineralcorticoid receptor antagonist, first line in the treatment of the disease, with negative effects in prognostic terms. Therapies for the correction of hyperkalemia have so far mainly concerned the treatment of acute clinical pictures. Newly developed molecules, such as patiromer or sodium zirconium cyclosilicate, now open new prospectives in the long-term management of hyperkalemia, and allow us to glimpse the possibility of a better titration of the cardinal drugs for heart failure, with consequent positive effects on patient prognosis. The aim of this review is to focus on the problem of hyperkalemia in the setting of heart failure, with particular regard to its incidence, its prognostic role, and the underlining pathophysiological mechanisms. The review also provides an overview of therapeutic strategies for correcting hyperkalemia in acute and chronic conditions, with a focus on the new potassium binders that promise to improve management of heart failure.

New frontiers for management of hyperkalaemia: the emergence of novel agents.

Hyperkalaemia is a common electrolyte abnormality, associated with higher risk of morbid events, and increasing in prevalence—in part, due to increasing rates of comorbidities such as heart failure, chronic kidney disease, diabetes mellitus, and the use of renin-angiotensin-aldosterone system inhibitors (RAASi). In spite of this growing problem, the existing treatments for chronic hyperkalaemia have been limited, and are typically confined to dietary potassium restrictions and cessation or modification of RAASi, with latter option being potentially problematic given the known morbidity and mortality benefit of RAASi therapy in certain disease states, such as heart failure. The use of sodium polystyrene sulfonate (SPS/Kayexelate) for chronic hyperkalaemia has been low, due to poor tolerability, potential gastrointestinal safety concerns, and remaining uncertainty in regards to its efficacy. Given the shortcomings of existing therapies, novel treatments are clearly needed. There are now two novel treatment options, patiromer and sodium zirconium cyclosilicate (SZC), both approved by the FDA and EMA for treatment of chronic hyperkalaemia. These novel compounds have been demonstrated in multiple studies to be efficacious in achieving and maintaining normal serum potassium levels, over an extended time period, in patients with hyperkalaemia; and appear to be relatively safe and well-tolerated. Whether the correction of hyperkalaemia with these agents will allow optimization of RAASi, which could theoretically lead to improvement in clinical outcomes, especially in patients with heart failure, remains to be determined. Several clinical trials are ongoing to address these important knowledge gaps.

Pathology of Resin-Induced Gastrointestinal Damage: Report of 15 Cases and Review of Literature.

< strong > Objective: < /strong > Medication resins such as Kayexalate and Sevelamer used in the setting of chronic kidney disease for the correction of hyperkalemia and hyperphosphatemia are associated with gastrointestinal mucosal injury. In this study we describe the clinico-pathological features of Resin-induced gastrointestinal mucosal injury highlighting the histo-morphological appearances and differential diagnoses. The aim of this study is to increase the awareness of pathologists and clinicians alike to an under-reported etiology and pattern of intestinal mucosal injury related to medical resin therapy which may at times pose a clinical emergency. < strong > Material and Method: < /strong > The archives of the Department of Histopathology, Mubarak Al Kabir hospital were analyzed for cases of resin-induced gastrointestinal mucosal injury between 2013 and 2018. < strong > Results: < /strong > Of the 15 cases, Kayexalate crystals were identified in 7 cases, Sevelamer in 5 cases and both together were seen in 3 cases. Resin crystals were identified in the gastric antrum&duodenum (3 cases), colon (9 cases in the left colon, 2 cases in the right colon) and anal canal (1 case). The histological tissue reactions included mucosal necrosis (1 case), inflammatory polyps (2 cases), mucosal ulcerations with granulation tissue formation (10 cases), perforation (1 case) , and luminal crystals (1 case). < strong > Conclusion: < /strong > Accurate and timely recognition of the resin crystals in biopsy samples with clinical correlation is mandatory to avoid serious complications.

Brugada-Like Electrocardiographic Patterns Induced by Hyperkalemia

Brugada syndrome was described in 1992 as a new clinical and electrocardiographic syndrome involving susceptibility to ventricular arrhythmias and sudden cardiac death in patients with no obvious structural heart disease. Brugada syndrome is characterized by a hereditary anomaly in the sodium ion channel (mutation of the SCN5A gene) identified by a wide QRS associated with the ST-segment elevation and the T‑wave inversion in the right precordial leads. The Brugada-like electrocardiographic pattern can be caused by sodium channel-blocking drugs and electrolyte disorders. Hyperkalemia may produce multiple ECG abnormalities, including the ST-segment elevation and pseudomyocardial infarction with a resolution of these abnormalities after the correction of hyperkalemia. This article describes 8 cases of pseudoanteroseptal myocardial infarction in acute renal insufficiency with hyperkalemia. The ST-segment elevation related to hyperkalemia is resolved by the reduced serum potassium level. Clinicians should recognize that hyperkalemia is one of the etiologies of the Brugada-like electrocardiographic pattern.

開心術体外循環中の高カリウム血症に対する落差灌流式血液透析濾過法の考案とその性能評価

開心術体外循環中に生じた高カリウム血症（K＝5.5mmol/L以上）を補正する手段として、体外循環中でも簡便に施行できる落差灌流式血液透析濾過法を考案した。体外循環中に高カリウム血症を呈し本法を施行した連続11症例（男：女＝2：9、平均年齢63.6&pm;12.9歳）を対象とした。本法では輸血セット（内径3.0mm）を用い、血液濾過用補充液（サブラッド®BSG）を落差により血液と向流になるように血液濃縮器（MAQUET BC140plus®）ホローファイバー外側を灌流させた。総落差は150cm、血液流量は400mL/minとした。体外循環中の心筋保護液注入によるカリウム負荷量は69.0&pm;33.1mmolで、照射赤血球濃厚液輸血量は5.5&pm;3.6単位であった。血中カリウム濃度の最高値は6.41&pm;0.76mmol/Lであったが、本法の施行により体外循環離脱までに4.82&pm;0.22mmol/Lと有意に（p＜0.0001）低下した。また体外循環開始直後と離脱直前ではナトリウム、カリウム、水素イオン濃度指数、重炭酸イオン濃度に有意差を認めなかった。本法は体外循環中に生じた高カリウム血症の補正に有用であった。

Management of patients with chronic kidney disease

Chronic kidney disease (CKD) is a silent disease which worsens gradually to end-stage kidney disease (ESKD). US kidney disease outcomes quality initiative (KDOQI) guidelines indicate five stages of CKD based on the severity of kidney function which is assessed by estimating the glomerular filtration rate (GFR) by the modification of diet in renal disease (MDRD) formula. The management of CKD patients with mild renal damage (stage 1-2 KDOQI) is articulated on the reduction of proteinuria (<500mg/day), reduction of sitting systolic and diastolic blood pressure (<130/80mmHg), salt restriction diet, diuretics (furosemide, spironolactone), antihypertensive agents (ACE inhibitors or ARBs (angiotensin II receptor blockers) or both as first-line therapy), additional other antihypertensives (aliskiren, non-dihydropyridine calcium channel blockers, beta blockers), body weight reduction, cigarette smoking stopping, allopurinol therapy and non-use of some drugs (non-steroidal anti-inflammatory agents, acetaminophen, bisphosphonates, oral estrogens) and herbals. The management of CKD patients with moderate-severe renal damage (stage 3-5 KDOQI) is based on the above recommendations plus low protein diet, correction of hyperkalaemia, metabolic acidosis, and administration of vitamin D derivates and erythropoietin for the correction of mineral metabolism disorders and anemia, respectively. In conclusion, patients with CKD (stage 1-2 KDOQI) may be correctly managed by primary care physicians, individuals in stage 3-5 KDOQI need the supervision of nephrologists to assess those patients who progress to ESKD and require renal replacement therapy.

Comparing Continuous Venovenous Hemodiafiltration and Peritoneal Dialysis in Critically Ill Patients with Acute Kidney Injury: A Pilot Study

There are few reports on the role of peritoneal dialysis in critically ill patients requiring continuous renal replacement therapies. Patients with acute kidney injury and multi-organ involvement were randomly allotted to continuous venovenous hemodiafiltration(CVVHDF, group A) or to continuous peritoneal dialysis (CPD, group B). Cause and severity of renal failure were assessed at the time of initiating dialysis. Primary outcome was the composite correction of uremia, acidosis, fluid overload, and hyperkalemia. Secondary outcomes were improvement of sensorium and hemodynamic instability, survival, and cost. Groups A and B comprised 25 patients each with mean ages of 45.32 ± 17.53 and 48.44 ± 17.64 respectively. They received 21.68 ± 13.46 hours and 66.02 ± 69.77 hours of dialysis respectively (p = 0.01). Composite correction was achieved in 12 patients of group A (48%) and in 14 patients of group B (56%). Urea and creatinine clearances were significantly higher in group A (21.72 ± 10.41 mL/min and 9.36 ± 4.93 mL/min respectively vs. 22.13 ± 9.61 mL/min and 10.5 ± 6.07 mL/min, p < 0.001). Acidosis was present in 21 patients of group A (84%) and in 16 of group B (64%); correction was better in group B (p < 0.001). Correction of fluid overload was faster and the amount of ultrafiltrate was significantly higher in group A (20.31 ± 21.86 L vs. 5.31 ± 5.75 L, p<0.001). No significant differences were seen in correction of hyperkalemia, altered sensorium, or hemodynamic disturbance. Mortality was 84% in group A and 72% in group B. Factors that influenced outcome were the APACHE (Acute Physiology and Chronic Health Evaluation) II score (p=0.02) and need for ventilatory support (p < 0.01). Cost of disposables was higher in group A than in group B [INR 7184 ± 1436 vs. INR 3009 ± 1643, p < 0.001 (US$1=INR 47)]. Based on this pilot study, CPD may be a cost-conscious alternative to CVVHDF; differences in metabolic and clinical outcomes are minimal.

Mild hyperkalemia and low eGFR a tedious recipe for cardiac disaster in the elderly: an unusual reversible cause of syncope and heart block

Hyperkalemia affects the myocardial tissue producing electrocardiographic abnormalities, such as prolongation of the P-R interval, tall peaked T waves, a reduction in the amplitude and an increase in the duration of P wave, and atrial and ventricular arrhythmias, including variable degree heart blocks. Elderly patients are particularly predisposed to developing hyperkalemia and the associated abnormalities due to an age-related reduction in glomerular filtration rate and pre-existing medical problems. Therefore, the impact of aging on potassium homeostasis must be taken into consideration, and preventive measures, such as early recognition of possible hyperkalemia in the geriatric population treated with certain medications or supplements must be investigated. The threshold for cardiac arrhythmias in the elderly can be lower than the general population. We report 3 unusual cases of mild hyperkalemia in elderly patients presenting with hypotension, syncope and variable degree heart blocks which resolved spontaneously with the correction of hyperkalemia.

Mesenchymal Stem Cells Therapy in Acute Renal Failure: Possible Role of Hepatocyte Growth Factor

Management of acute renal failure depends first on correction of the metabolic abnormalities like the correction of hyperkalemia and correction of metabolic acidosis then treatment of the cause as correction of the hypovolemic state during shock or immunosuppressive therapy for glomerulonephritis [3]. Although a number of agents and growth factors have been proven effective in the amelioration of ARF in otherwise healthy animals, no significantly effective new therapy has been introduced into clinical practice in decades. It is for these reasons that fundamentally new strategies for the treatment of ARF are needed.

Correction of Hyperkalemia in Dogs with Chronic Kidney Disease Consuming Commercial Renal Therapeutic Diets by a Potassium-Reduced Home-Prepared Diet

Hyperkalemia occurs in dogs with chronic kidney disease (CKD). (1) To determine the incidence of hyperkalemia in dogs with CKD, (2) to determine the proportion of hyperkalemic dogs that required modification of dietary potassium intake, (3) to evaluate the response to dietary modification. The hospital database was reviewed retrospectively to identify dogs with CKD and persistent (>5.3 mmol/L on at least 3 occasions) or severe (K > or = 6.5 mmol/L) hyperkalemia while consuming a therapeutic renal diet. Records of dogs with hyperkalemia that were prescribed a home-prepared, potassium-reduced diet were evaluated further. Response was evaluated by changes in body weight, BCS, and serum potassium concentration. One hundred and fifty-two dogs were diagnosed with CKD, of which 47% had > or =1 documented episode of hyperkalemia, 25% had > or = 3 episodes of hyperkalemia, and 16% had > or =1 episodes of severe hyperkalemia (K > 6.5 mmol/L). Twenty-six dogs (17.2%) with CKD and hyperkalemia were prescribed a potassium-reduced, home-prepared diet. The potassium concentration of all hyperkalemic dogs on therapeutic diets (potassium content, 1.6 +/- 0.23 g/1,000 kcal of metabolizable energy [ME]) was 6.5 +/- 0.5 mmol/L but decreased significantly to 5.1 +/- 0.5 mmol/L in 18 dogs available for follow-up in response to the dietary modification (0.91 +/- 0.14 g/1,000 kcal of ME, P < .001). Potassium concentration normalized in all but 1 dog. Hyperkalemia is a potential complication of CKD. In a subset of CKD dogs, hyperkalemia can be associated with commercial renal diets and could restrict use of these diets. Appropriately formulated, potassium-reduced, diets are an effective alternative to correct hyperkalemia.

Infarto agudo de miocardio en el seno de una hiperpotasemia: hallazgos electrocardiográficos

Graded hyperkalemia and acute myocardial ischemia are remarkably reflected (and can even be predicted) in the surface ECG when they occur alone. If, however, acute ischemia supervenes in the setting of previous hyperkalemia, the ECG changes are less known. We describe a patient who suffered an acute septal myocardial infarction while his extracellular potassium was high. Changes in the ECG waveform brought about by both acute ischemia and hyperkalemia are emphasized. The origin of a sine-wave ventricular activation pattern, the supraventricular origin and likely sinoventricular conduction, versus ventricular tachycardia is, as well, discussed. Correction of hyperkalemia and other metabolic disturbances, as the first and most important therapeutic target, is critical when the origin and nature of the rhythm are controversial.

Clinical events in association with timing of intraventricular hemorrhage in preterm infants

To ascertain whether any routine practices or clinical manipulations in a neonatal intensive care unit could induce intraventricular hemorrhage (IVH) in preterm infants, we performed ultrasonic monitoring of the germinal layer continuously for 48 hours in 33 extremely premature infants with respiratory distress. Intraventricular hemorrhage developed in 16 of these infants. In four infants the timing of the germinal layer hemorrhage was confirmed with ultrasonic monitoring. Three of the four cases were apparently associated with clinical events occurring at the moment of IVH: manual ventilation for improvement of hypercapnia associated with primary pulmonary hypertension of the newborn; correction of hyperkalemia, which was causing an arrhythmia, with administration of calcium gluconate and sodium bicarbonate; and administration of surfactant-TA to improve respiratory failure caused by pulmonary hemorrhage. In these three infants it appeared that one of the basic factors inducing IVH might be an increase in blood pressure with or without hypercapnia, causing cerebral reperfusion after ischemic damage of the germinal layer.

Cardiac Arrest After Isoflurane Anaesthesia in a Patient with Duchenne??s Muscular Dystrophy

An 8-year-old boy known to have Duchenne's muscular dystrophy suffered a cardiac arrest 10 minutes after he regained consciousness after isoflurane anaesthesia for an orchidopexy procedure. Resuscitation was successful 2 hours after the start of external cardiac compression and after correction of hyperkalaemia and the administration of dantrolene. He later developed myoglobinuria elevated creatine kinase and a metabolic and respiratory acidosis. He demonstrated a delayed increase in rectal temperature.

Cardiac arrest after isoflurane anaesthesia in a patient with Duchenne's muscular dystrophy

An 8-year-old boy known to have Duchenne's muscular dystrophy suffered a cardiac arrest 10 minutes after he regained consciousness after isoflurane anaesthesia for an orchidopexy procedure. Resuscitation was successful 2 hours after the start of external cardiac compression and after correction of hyperkalaemia and the administration of dantrolene. He later developed myoglobinuria elevated creatine kinase and a metabolic and respiratory acidosis. He demonstrated a delayed increase in rectal temperature.