High-Dose Insulin for Hyperkalemic Cardiac Arrest.

ABSTRACT: Hyperkalemic cardiac arrest diagnosis can be elusive and management difficult as the cardiac rhythm restoration is often not achieved until the potassium level decreases to a relatively normal level for the patient who suffers the arrest. Current treatment modalities can take hours to achieve this goal. We describe two patients who survived a witnessed hyperkalemic cardiac arrest after being managed with conventional advanced cardiac life support and unconventionally high doses of intravenous insulin.

Nitrogen-Phosphorus-Potassium containing liquid fertilizer intoxication presenting with extreme hyperkalemia, metabolic acidosis and ECG changes.

Liquid fertilizers are widely used for fertilizing in- and outdoor vegetation. Despite the easy accessibility and widespread use, serious intoxications are rare. This case report describes a 61-year-old woman who was treated for life-threatening hyperkalemia, metabolic acidosis and ECG changes after intentional ingestion of liquid fertilizer. Our case shows that intake of liquid fertilizer, though infrequent, can cause serious, life threatening complications.

Implications of differences between point-of-care blood gas analyser and laboratory analyser potassium results on hyperkalaemia diagnosis & treatment.

BACKGROUND: Hyperkalaemia is managed in the emergency department (ED) following measurement of potassium results by blood gas analysers (BGA) or laboratory analysers (LAB). AIMS: To determine the prevalence of clinically significant differences between BGA and LAB potassium results and the impact on ED hyperkalaemia management. METHODS: Retrospective analysis of time-matched ED BGA and LAB potassium samples from 2019 to 2020 (taken within 15 min, one or both results ≥6.0 mmol/L). Mean differences and 95% limits of agreement (LoA) were determined for pairs with one or both results ≥6.0 mmol/L and a separate 500 consecutive sample pairs. RESULTS: Four hundred eighty-eight matched BGA and LAB samples met the inclusion criteria. Of these, 201 (41.2%) differed by ≤0.5 mmol/L, 169 (34.6%) included a haemolysed LAB sample, and 12 (2.5%) had an unreportable BGA sample. One hundred six (21.7%) pairs differed by >0.5 mmol/L, and 60/106 (57%) had normal LAB potassium results, but BGA indicated moderate/severe hyperkalaemia (two of these pairs received hyperkalaemia treatment). Of patients with a haemolysed LAB sample, or where pairs differed by >0.5 mmol, 48 were treated with insulin and five (10.4%) experienced hypoglycaemia. Mean differences and LoA for pairs with LAB results <6.0 mmol/L but BGA ≥6.0 mmol/L demonstrated unacceptable agreement, with 18 (25.7%) BGA results exceeding 8.0 mmol/L. CONCLUSIONS: Potentially significant discordance may occur between BGA and LAB potassium results. Clinicians need to be aware of factors impacting both analytical methods' accuracy (such as poor venepuncture or sample handling, (K) EDTA interference) and undetectable haemolysis with BGA measurements. We recommend BGA hyperkalaemia be confirmed with LAB results using a non-haemolysed sample where time permits.

Salt-Losing Syndrome in a Girl with Type I and II Pseudohypoaldosteronism.

BACKGROUND Pseudohypoaldosteronism (PHA) is characterized by renal tubular resistance to aldosterone and leads to hyponatremia, hyperkalemia, and metabolic acidosis. PHA is divided into 2 types: PHAI and PHAII. PHAI can be dominant (systemic disease) or recessive (renal form). PHAII causes hypertension with hyperkalemia and is recognized mostly in adults. PHA can be a life-threatening disease due to salt-wasting syndrome and severe hypovolemia. CASE REPORT We describe the case of a 2-month-old girl who was admitted to our hospital with hypovolemic shock due to salt-wasting syndrome. Laboratory tests revealed severe electrolyte abnormalities: hyponatremia (Na-116 mmol/L), hyperkalemia (K-10 mmol/L) and metabolic acidosis (pH-7.27; HCO3-12 mmol/L). Serum aldosterone was >100 ng/dL. Genetic analysis confirmed mutations in SCNN1A and CUL3 gene responsible for PHAI and PHAII. Supplementation with NaCl, pharmacological treatment of hyperkalemia, and restriction of potassium in the diet resulted in the normalization of serum electrolytes and proper future development. CONCLUSIONS Pseudohypoaldosteronism should always be considered in the differential diagnosis of hyponatremia and hyperkalemia in children. Salt loss syndrome can lead to hypovolemic shock and, when unrecognized and untreated, to death of a child due to arrythmias and brain edema. The presence of 2 types of PHA in the same patient increases the risk of salt loss and at the same time significantly increases the risk of hypertension because of genetic predisposition and regular diet. Increased salt concentration in sweat and saliva may suggest pseudohypoaldosteronism.

[Hypercalcemia after hyperkalemia]. / Hypercalciëmie na een hyperkaliëmie.

BACKGROUND: Hyperkalemia is a common yet dangerous phenomenon in patients with chronic kidney disease (CKD). Patients suffering from CKD are therefore often treated with potassium-binding supplements such as calcium polystyrene sulfonate (CPS). Hypercalcemia is a known side effect of CPS. However, the increase in serum calcium is usually small. CASE DESCRIPTION: A 68 year old male patient suffering from CKD was treated with a daily administration of 80mg CPS. He presented with complaints of a dry mouth, thirst and malaise. Blood tests showed an elevated serum calcium of 3,25 mmol/L (2,15- 2,55 mmol/L). Additional diagnostics revealed no abnormalities. The hypercalcemia was attributed to the use of CPS only after the exclusion of a wide differential diagnosis. CONCLUSION: Although CPS induced hypercalcemia is usually mild, a more severe course is possible. Knowledge about the composition of medication is paramount to prevent such side effects.

Dyskalemia risk associated with fixed-dose anti-hypertensive medication combinations.

A model-based meta-analysis quantified comparative dyskalemia risk (hyper- or hypo-kalemia) in hypertensive patients treated with angiotensin receptor blockers (ARBs), a calcium channel blocker (CCB) and/or a thiazide diuretic (hydrochlorothiazide; HCTZ) as monotherapy or as fixed-dose combinations. Among 15 randomized controlled trials in a US Food and Drug Administration regulatory review database, dyskalemia events were reported by five trials (24 treatment arms, 11,030 subjects, 8-week median follow up time). The five trials evaluated monotherapy (ARB or HCTZ) alongside dual (ARB + HCTZ, ARB + CCB, or HCTZ + CCB) or triple fixed-dose combinations (ARB + CCB + HCTZ). Hypo- and hyper-kalemia rates were analyzed jointly to account for correlation. Significant drug class, drug, or dose effects were included in the final model. Effect on various drug- and dose combinations on dyskalemia risk were simulated and compared with model-estimated placebo arm dyskalemia risk. After a typical follow-up of 8 weeks, fixed-dose combinations of ARB with a high dose (25 mg) of HCTZ were associated with a higher hypokalemia risk difference (RD) from placebo (e.g.,Valsartan + HCTZ: 2.52%[95%CIs:1.17, 4.38%]). However, when ARB was combined with a lower, 12.5 mg dose of HCTZ, hypokalemia RD from placebo was not significant (Valsartan + HCTZ: -0.03%[-0.80, 0.71%]). ARB monotherapy raised hyperkalemia RD from placebo (1.3%[0.3, 3.6%]). Hyperkalemia risk was not appreciably higher than placebo for any FDC that combined ARB with HCTZ (Valsartan + HCTZ: 0.06%[-1.48, 1.64%]). In uncomplicated hypertensive patients, ARB + 12.5 mg HCTZ fixed-dose combinations are safer with respect to dyskalemia than either ARB or HCTZ monotherapy for initial antihypertensive treatment.

Metabolic Acidosis, Hyperkalemia, and Renal Unresponsiveness to Aldosterone Syndrome: Response to Treatment with Low-Potassium Diet.

Gordon syndrome involves hyperkalemia, acidosis, and severe hypertension (HTN) with hypercalciuria, low renin and aldosterone levels. It is commonly observed in children and adolescents. Such patients respond successfully to sodium restriction and thiazide diuretics. In this article, we present three cases of metabolic acidosis, hyperkalemia, and renal unresponsiveness to aldosterone (MeHandRU Syndrome). All three patients did not have HTN or hypercalciuria and demonstrated normal renin and aldosterone levels. These patients did not respond to thiazide-type diuretic therapy and salt restriction. Two males (aged 55- and 62-year) and a female patient (aged 68-year) presented to the clinic with unexplained hyperkalemia (5.9 mEq/L, 5.9 mEq/L and 6.2 mEq/L, respectively). On physical examination, blood pressure (BP) was found to be normal (<140/90 mm Hg). Over the counter potassium supplement, nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, potassium sparing diuretic use, as well as hyporeninemic hypoaldosteronism states such as diabetes mellitus were excluded. Plasma renin and aldosterone levels were normal. All three patients had low transtubular potassium gradient, despite high serum potassium levels. None of the patients reported a family history of hyperkalemia or kidney failure. All failed to demonstrate a response to hydrochlorothiazide and salt restriction. After careful consideration, strict low potassium diet (<2 g/day) was initiated in consultation with the dietician. Diuretic therapy was discontinued while BP remained within normal range (<140/90 mm Hg). At eight weeks, all three patients demonstrated normalization of potassium and correction of acidosis. At follow-up of six months, all patients are maintaining a normal potassium level. We suggest that potassium restriction can be successful in patients presenting with MeHandRU syndrome.

Hyperkalaemia and hypokalaemia outpatient management: a survey of 500 French general practitioners.

AIMS: How general practitioners (GPs) manage dyskalaemia is currently unknown. This study aimed at describing GP practices regarding hypokalaemia or hyperkalaemia diagnosis and management in their outpatients. METHODS AND RESULTS: A telephone survey was conducted among French GPs with a 20-item questionnaire (16 closed-ended questions and 12 open-ended questions) regarding their usual management of hypokalaemia or hyperkalaemia patients, both broadly and more specifically in patients with heart failure and/or chronic kidney disease and/or in patients treated with angiotensin-converting enzyme/angiotensin receptor blockers or mineralocorticoid receptor antagonists. We aimed to interview 500 GPs spread geographically throughout France. This descriptive survey results are presented as mean ± standard deviation (if normally distributed or as median and inter-quartile range if the distribution was skewed). Categorical variables are expressed as frequencies and proportions (%). A total of 500 GPs participated in the study. Dyskalaemia thresholds (for diagnosis and intervention) and management patterns were highly heterogeneous. The mean ± SD (range) potassium level leading to 'intervene' was 5.32 ± 0.34 mmol/L (4.5-6.5) for hyperkalaemia and 3.23 ± 0.34 mmol/L (2.0-6.5) for hypokalaemia. Potassium levels leading to refer the patient to the emergency department (ED) were 6.14 ± 0.55 (4.5-10) and 2.69 ± 0.42 mmol/L (1-4), respectively. Potassium binders (51-65%) or potassium supplements (67-74%) were frequently used to manage hyperkalaemia or hypokalaemia. GPs uncommonly referred their dyskalaemic patients to cardiologists or nephrologists (or to the emergency department, if the latter was deemed necessary owing to the severity of the dyskalaemia). We identified an association between the close vicinity of GP office from an ED and 'referring a heart failure patient' (19.2% with ED vs. 8.6% without ED) and referring a heart failure and chronic kidney disease patient on mineralocorticoid receptor antagonist (16.7% with ED vs. 9.3% without ED). Although the majority (67%) of GPs had an electrocardiogram on hand, it was rarely used (14%) in dyskalaemic patients. Subgroup analyses considering gender, age of the participating GPs, and high-income/low-income regions did not identify specific patterns regarding the multidimensional aspect of dyskalaemia management. CONCLUSIONS: Owing to the considerable heterogeneity of French GP practices toward dyskalaemia diagnosis and management approaches, there is a likely need to standardize (potentially enabled by therapeutic algorithms) practices.

Predictors of Hyperkalemia and Hypokalemia in Individuals with Diabetes: a Classification and Regression Tree Analysis.

BACKGROUND: Both hyperkalemia and hypokalemia can lead to cardiac arrhythmias and are associated with increased mortality. Information on the predictors of potassium in individuals with diabetes in routine clinical practice is lacking. OBJECTIVE: To identify predictors of hyperkalemia and hypokalemia in adults with diabetes. DESIGN: Retrospective cohort study, with classification and regression tree (CART) analysis. PARTICIPANTS: 321,856 individuals with diabetes enrolled in four large integrated health care systems from 2012 to 2013. MAIN MEASURES: We used a single serum potassium result collected in 2012 or 2013. Hyperkalemia was defined as a serum potassium ≥ 5.5 mEq/L and hypokalemia as < 3.5 mEq/L. Predictors included demographic factors, laboratory measurements, comorbidities, medication use, and health care utilization. KEY RESULTS: There were 2556 hypokalemia events (0.8%) and 1517 hyperkalemia events (0.5%). In univariate analyses, we identified concordant predictors (associated with increased probability of both hyperkalemia and hypokalemia), discordant predictors, and predictors of only hyperkalemia or hypokalemia. In CART models, the hyperkalemia "tree" had 5 nodes and a c-statistic of 0.76. The nodes were defined by prior potassium results and eGFRs, and the 5 terminal "leaves" had hyperkalemia probabilities of 0.2 to 7.2%. The hypokalemia tree had 4 nodes and a c-statistic of 0.76. The hypokalemia tree included nodes defined by prior potassium results, and the 4 terminal leaves had hypokalemia probabilities of 0.3 to 17.6%. Individuals with a recent potassium between 4.0 and 5.0 mEq/L, eGFR ≥ 45 mL/min/1.73m2, and no hypokalemia in the previous year had a < 1% rate of either hypokalemia or hyperkalemia. CONCLUSIONS: The yield of routine serum potassium testing may be low in individuals with a recent serum potassium between 4.0 and 5.0 mEq/L, eGFR ≥ 45 mL/min/1.73m2, and no recent history of hypokalemia. We did not examine the effect of recent changes in clinical condition or medications on acute potassium changes.

kEDTA Sample Contamination: A Reappraisal.

BACKGROUND: Potassium EDTA (kEDTA) contamination of serum samples is common, causing spurious hyperkalemia, hypozincemia, and hypocalcemia that if unrecognized may adversely affect patient care. Gross kEDTA contamination is easy to detect, but identification of spurious electrolytes due to small amounts of contamination requires measurement of serum EDTA. We validated an EDTA assay on the Abbott Architect and reassessed its value in identifying kEDTA contamination and in studying mechanisms for contamination. METHODS: Within- and between-batch imprecision, linearity, recovery, interference, and carryover were assessed. Serum supplemented with k2EDTA plasma, to mimic sample contamination, was used to study its effect on potassium, calcium, zinc, magnesium, and alkaline phosphatase. Our current laboratory protocol for identification of kEDTA contamination, based on measurement of serum calcium, was compared to that of EDTA measurement. RESULTS: The EDTA assay displayed acceptable performance characteristics. Hemoglobin was a positive interferent. EDTA was detectable in serum contaminated with 1% (v:v) k2EDTA plasma. An increase in serum potassium of 0.54 mmol/L (11.9%) was observed at a measured EDTA concentration of 0.19 mmol/L, equivalent to 3.2% (v:v) contamination. At this EDTA concentration reductions were also observed in zinc (71%), calcium (1%), alkaline phosphatase (ALP) (4%), and magnesium (2.4%). The serum EDTA assay detected contamination in 31/106 patient samples with hyperkalemia (potassium ≥6.0mmol/L), 20 of which were undetected by the current laboratory protocol. CONCLUSIONS: The EDTA assay displayed acceptable performance, with the ability to reliably measure EDTA at low concentrations. Only a small amount of kEDTA causes significant spurious hyperkalemia and is only reliably detected with EDTA measurement.

Severe Hyperkalemia Immediately After Birth.

BACKGROUND Hyperkalemia is an important cause of arrhythmias and a medical emergency that requires urgent treatment. The etiology is usually multifactorial. It is most frequently caused by impaired potassium secretion, followed by transcellular potassium shifts and an increased potassium load. CASE REPORT A male newborn developed monomorphic ventricular tachycardia 2 hours after birth. He was born in the 35th week of gestation by urgent C-section following placental abruption. Laboratory results showed hemolytic anemia (Hb 99 g/L, Hct 0.31) with increased bilirubin levels and reticulocytosis, thrombocytopenia (39×109/L), hypoglycemia (0.8 mmol/L), and severe hyperkalemia (9.8 mmol/L). Umbilical artery blood gas analysis showed hypoxemia with acidosis (pO2 3.8 kPa, pH 7.21, pCO2 7.84 kPa, HCO3 23.3 mmol/L, BE -5 mmol/L). Creatinine (102 µmol/L) and urea (9.8 mmol/L) were mildly elevated. Inflammatory markers were also increased (CRP 26 mg/L, blood leukocyte count 24×109/L). Early-onset sepsis, caused by Candida albicans, was confirmed approximately 24 hours after birth. Non-invasive ventilation with 35-40% O2 was necessary due to transient tachypnea. The neonate received a transfusion of packed red blood cells, a 10% glucose infusion, and empirical antibiotic therapy. Hyperkalemia accompanied by arrhythmias was treated with calcium gluconate, insulin, Sorbisterit enema, and, finally, by exchange transfusion. CONCLUSIONS We report a case of severe hyperkalemia in a newborn immediately after birth. Making a decision as early as possible regarding exchange transfusion is essential in patients with hyperkalemia with electrocardiogram changes and hemodynamic instability.

Hyperkalaemia in people with diabetes: occurrence, risk factors and outcomes in a Danish population-based cohort study.

AIMS: To examine the incidence, risk factors and clinical outcomes of hyperkalaemia in people with diabetes in a real-world setting. METHODS: Using Danish health registries, we identified a population-based cohort of people with first-time drug-treated diabetes, in the period 2000-2012. First, the cumulative incidence of hyperkalaemia, defined as first blood test with potassium level >5.0 mmol/l after diabetes treatment initiation, was ascertained. Second, in a case-control analysis, risk factors were compared in people with vs without hyperkalaemia. Third, clinical outcomes were assessed among individuals with hyperkalaemia in a before-after analysis, and among people with and without hyperkalaemia in a matched cohort analysis. RESULTS: Of 68 601 individuals with diabetes (median age 62 years, 47% women), 16% experienced hyperkalaemia (incidence rate 40 per 1000 person-years) during a mean follow-up of 4.1 years. People who developed hyperkalaemia had a higher prevalence of chronic kidney disease [prevalence ratio 1.74 (95% CI 1.68-1.81)], heart failure [prevalence ratio 2.35 (95% CI 2.18-2.54)], use of angiotensin-converting enzyme inhibitors [prevalence ratio 1.24 (95% CI 1.20-1.28)], use of spironolactone [prevalence ratio 2.68 (95% CI 2.48-2.88)] and potassium supplements [prevalence ratio 1.59 (95% CI 1.52-1.67)]. In people with diabetes who developed hyperkalaemia, 31% were acutely hospitalized within 6 months before hyperkalaemia, increasing to 50% 6 months after hyperkalaemia [before-after risk ratio 1.67 (95% CI 1.61-1.72)]. The 6-month mortality rate after hyperkalaemia was 20%. Compared with matched individuals without hyperkalaemia, the hazard ratio for death was 6.47 (95% CI 5.81-7.21). CONCLUSIONS: One in six newly diagnosed people with diabetes experienced a hyperkalaemic event, which was associated with severe clinical outcomes and death.

Efficacy and Safety of Patiromer in Hyperkalemia: A Systematic Review and Meta-Analysis.

BACKGROUND: Patients at the highest risk of hyperkalemia are those with chronic kidney disease (CKD) stages 3 and 4. OBJECTIVE: To evaluate the efficacy and safety of patiromer in hyperkalemia in patients with heart failure or CKD. METHODS: The Cochrane Renal Group's Specialized Register was searched through contact with the Trials' Search Coordinator. We aimed at including randomized controlled trials with patiromer in patients with developed or risks of developing hyperkalemia, comparing against an active comparator or placebo. Three studies matched our inclusion and exclusion criteria, which we included in the meta-analysis. All-cause mortality, reduction in hospitalization, episodes of hypokalemia or hyperkalemia, and cardiovascular and gastrointestinal adverse events during the treatment period were our primary outcomes. Serial change in serum potassium (K+) until end of treatment or follow-up during the trial period and all other reported adverse reactions during the treatment period were our secondary outcomes. Meta-analysis (RevMan version 5.3.5) and descriptive statistics were used. RESULTS: There was a non-significant improvement in all-cause mortality and serious cardiovascular events with patiromer than placebo. Hospitalization data were unavailable. Although serious gastrointestinal events were more common with placebo, there was a significant reduction ( P = .02) in the risk of non-serious gastrointestinal events with placebo. Patiromer lowered serum K+ more than placebo, and there were more patients developing hyperkalemia with placebo. High-dose patiromer was associated with better efficacy in some parameters but with more adverse events. CONCLUSION: Although patiromer seems promising, more trials with active comparator are essential to finalize its indication and use in hyperkalemia.

[The most frequent electrolyte disorders in the emergency department : what must be done immediately?]. / Die häufigsten Elektrolytstörungen in der Notaufnahme : Was ist sofort zu tun?

Hyponatremia is the most common form of electrolyte disorder in the emergency room. The symptoms are unspecific and include nausea, dizziness and often falls. Typical symptoms of severe hypernatremia are vomiting, cerebral seizures, somnolence and even coma. The specific initial laboratory diagnostics include measurement of serum electrolytes, serum glucose, serum and urine osmolarity and sodium in urine. The main aim of the clinical examination is to estimate the volume status. If a patient has hypovolemia an infusion of isotonic sodium chloride solution (0.9 %) is the method of choice. If the patient is euvolemic the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or (neurotropic) drugs might be the cause. In these cases the primary measure is restriction of fluid intake. As a rapid correction of sodium levels can lead to pontine myelinolysis, the increase in sodium concentration must not be less than 10 mmol/l within the first 24 h and 18 mmol/l within the first 48 h. Clinical symptoms of hyperkalemia include neurological (e.g. muscle weakness, paresis, hyperreflexia, cramps and dysesthesia), gastrointestinal (e.g. nausea, vomiting and diarrhea) and cardiac symptoms (e.g. dysrhythmia and conductance disorders). Calcium injection stabilizes cardiac rhythm disorders immediately. For a rapid drop in potassium by shifting the potassium to the intracellular space, administration of glucose with insulin and high-dose inhalative administration of betamimetics can be used. Potassium elimination is achieved by infusion of isotonic sodium choride (0.9 %) with i.v. administration of furosemide, ion exchange resins and hemodialysis.

Ileum and colon perforation following peritoneal dialysis-related peritonitis and high-dose calcium polystyrene sulfonate.

A rare but severe complication, intestinal necrosis, has been reported after sodium polystyrene sulfonate (SPS; Kayexalate) and sorbitol intake. Some case reports described bowel perforation following calcium polystyrene sulfonate (CPS; Kalimate) administration. We report a case of ileum and colon perforation following peritoneal dialysis-related peritonitis and high-dose Kalimate in a 59-year-old female patient. The patient had a history of hypertension, diabetes mellitus, and end-stage renal disease (ESRD). During hospitalization for peritoneal dialysis-related peritonitis, she developed hyperkalemia, and Kalimate was administered orally. However, severe abdominal distension and pain occurred just one day after Kalimate intake. An urgent surgery disclosed several perforations in the ileum and sigmoid colon. Pathology of the resected gut showed transmural necrosis and perforation with basophilic angulated crystals. The patient finally expired during hospitalization due to refractory septic shock.

Incident hyperkalemia may be an independent therapeutic target in low ejection fraction heart failure patients: insights from the HEAAL study.

BACKGROUND: Angiotensin receptor antagonists (ARBs) improve outcomes in patients with heart failure (HF) with reduced left ventricular ejection fraction, but may induce hyperkalemia (HK) and/or a worsening of renal function (WRF). METHODS AND RESULTS: The incidence and risk factors of HK and its inter-relationship with WRF, as well as associations with clinical outcome (death or admission for HF i.e. the primary outcome) in 3846 HF patients enrolled in the double blind HEAAL trial (losartan 150 mg/d vs. 50 mg/d) were assessed. Worsening of renal function was defined as a decrease in eGFR >20% from baseline and HK as serum K >5.5 or >5 mmol/L. Higher dose of losartan increased serum potassium. Episodes of HK >5 mmol/L or WRF occurred at least once in about half of the patients. WRF was associated with higher occurrence of HK (HR 1.19 (1.06-1.34)) and vice versa (HR 1.35 (1.19-1.53)), but preceded HK in only about half of the events. High dose losartan improved outcome despite more frequent WRF and HK, both being independently associated with adverse outcomes in multivariate analyses. CONCLUSIONS: HK and WRF are common in HF patients. Both can be predicted from baseline risk factors and are therefore potentially preventable. Although associated with worse outcome, occurrence of any does not hinder the efficacy of high dose losartan. HK was associated with WRF and worse outcomes. Whether therapy targeting specifically HK may maximize the survival benefit derived from renin angiotensin aldosterone inhibitor use should be appropriately tested in future trials.

Non-oliguric hyperkalemia in extremely low birth weight infants.

PURPOSE: It is to examine clinical manifestations, early biochemical indicators, and risk factors for non-oliguric hyperkalemia (NOHK) in extremely low birth weight infants (ELBWI). MATERIALS AND METHODS: We collected clinical and biochemical data from 75 ELBWI admitted to Ajou University Hospital between Jan. 2008 and Jun. 2011 by reviewing medical records retrospectively. NOHK was defined as serum potassium≥7 mmol/L during the first 72 hours of life with urine output≥1 mL/kg/h. RESULTS: NOHK developed in 26.7% (20/75) of ELBWI. Among NOHK developed in ELBWI, 85% (17/20) developed within postnatal (PN) 48 hours, 5% (1/20) experienced cardiac arrhythmia and 20% (4/20) of NOHK infants expired within PN 72 hours. There were statistically significant differences in gestational age, use of antenatal steroid, and serum phosphorous level at PN 24 hours, and serum sodium, calcium, and urea levels at PN 72 hours between NOHK and non-NOHK groups (p-value<0.050). However, there were no statistical differences in the rate of intraventricular hemorrhage, arrhythmia, mortality occurred, methods of fluid therapy, supplementation of amino acid and calcium, frequencies of umbilical artery catheterization and urine output between the two groups. CONCLUSION: NOHK is not a rare complication in ELBWI. It occurs more frequently in ELBWI with younger gestational age and who didn't use antenatal steroid. Furthermore, electrolyte imbalance such as hypernatremia, hypocalcemia and hyperphosphatemia occurred more often in NOHK group within PN 72 hours. Therefore, more use of antenatal steroid and careful control by monitoring electrolyte imbalance should be considered in order to prevent NOHK in ELBWI.

Non-Oliguric Hyperkalemia in Extremely Low Birth Weight Infants

PURPOSE: It is to examine clinical manifestations, early biochemical indicators, and risk factors for non-oliguric hyperkalemia (NOHK) in extremely low birth weight infants (ELBWI). MATERIALS AND METHODS: We collected clinical and biochemical data from 75 ELBWI admitted to Ajou University Hospital between Jan. 2008 and Jun. 2011 by reviewing medical records retrospectively. NOHK was defined as serum potassium > or =7 mmol/L during the first 72 hours of life with urine output > or =1 mL/kg/h. RESULTS: NOHK developed in 26.7% (20/75) of ELBWI. Among NOHK developed in ELBWI, 85% (17/20) developed within postnatal (PN) 48 hours, 5% (1/20) experienced cardiac arrhythmia and 20% (4/20) of NOHK infants expired within PN 72 hours. There were statistically significant differences in gestational age, use of antenatal steroid, and serum phosphorous level at PN 24 hours, and serum sodium, calcium, and urea levels at PN 72 hours between NOHK and non-NOHK groups (p-value <0.050). However, there were no statistical differences in the rate of intraventricular hemorrhage, arrhythmia, mortality occurred, methods of fluid therapy, supplementation of amino acid and calcium, frequencies of umbilical artery catheterization and urine output between the two groups. CONCLUSION: NOHK is not a rare complication in ELBWI. It occurs more frequently in ELBWI with younger gestational age and who didn't use antenatal steroid. Furthermore, electrolyte imbalance such as hypernatremia, hypocalcemia and hyperphosphatemia occurred more often in NOHK group within PN 72 hours. Therefore, more use of antenatal steroid and careful control by monitoring electrolyte imbalance should be considered in order to prevent NOHK in ELBWI.

Life threatening hyperkalemia in a neonate with pseudo-hypoaldosteronism.

Pseudohypoaldosteronism type 1 is a rare disorder characterized by renal resistance to aldosterone which may present with a salt wasting crisis in infancy. We report a neonate with hyponatremia, severe dehydration and refractory life threatening hyperkalemia who was treated with dietary sodium chloride supplementation, potassium binding resins and fluid replacement therapy which proved to be lifesaving.