Hyperkalemia Associated with Angiotensin Converting Enzyme Inhibitor or Angiotensin Receptor Blockers in Chronic Kidney Disease.

Inhibition of the renin-angiotensin-aldosterone system (RAAS) is a key strategy in treating hypertension in cardiovascular and renal diseases. However, RAAS inhibitors (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors) increase the risk of hyperkalemia (serum potassium >5.5 mmol/L). This poses a therapeutic challenge because these patient groups comprise in whom the drugs are therapeutically indicated. Important considerations when initiating ACEI or ARB therapy include obtaining an estimate of glomerular filtration rate and a baseline serum potassium concentration, as well as assessing whether the patient has excessive potassium intake from diet, supplements, or drugs that can also increase serum potassium. Serum potassium monitoring shortly after initiation of therapy can assist in preventing hyperkalemia. If hyperkalemia does develop, prompt recognition of cardiac dysrhythmias and effective treatment to antagonize the cardiac effects of potassium, redistribute potassium into cells, and remove excess potassium from the body is important. Understanding the mechanism of action and monitoring of ACEI and ARB coupled with judicious drug use and clinical vigilance can minimize the risk to the patient of developing hyperkalemia.

Dose-Dependent Hyperkalemia Among Hospitalized, HIV-Infected Patients Receiving Sulfamethoxazole/Trimethoprim.

Background: Sulfamethoxazole-trimethoprim (SXT) therapy is commonly used in HIV-infected patients and is associated with hyperkalemia and elevated serum creatinine (SCr). Objective: The purpose of this study was to examine the frequency of hyperkalemia and elevated SCr in hospitalized, HIV-infected patients receiving SXT. Methods: This was a retrospective, single-center cohort study. HIV-infected hospitalized patients receiving a minimum of 3 consecutive days of SXT were included. Patients were grouped according to high dose (≥10 mg/kg/d) and low dose (<10 mg/kg/d) trimethoprim. The primary end point was the frequency of hyperkalemia, severe hyperkalemia, and elevated SCr. Secondary end points included an evaluation of concomitant potassium-altering medications and concomitant nephrotoxic drugs. Results: A total of 100 consecutive patients were selected from all possible patients who met inclusion criteria. Overall, 47 patients experienced at least 1 adverse drug event (ADE) of either hyperkalemia or increased SCr, with 20 patients experiencing these ADEs in the low-dose group and 27 patients experiencing these ADEs in the high-dose group (P = 0.229). The ADEs of hyperkalemia or increased SCr occurred after a shorter period (5.5 vs 8.7 days) in the high-dose group (P = 0.049). Overall frequency of elevated SCr was 24% and of elevated serum K was 36%. Hyperkalemia requiring a therapeutic intervention occurred in 12 patients in the high-dose group compared with 2 in the low-dose group (P = 0.009). Conclusion and Relevance: Rates of elevated SCr and hyperkalemia in hospitalized HIV-infected patients receiving SXT are significant. Hyperkalemia requiring intervention is more common in patients receiving high-dose SXT.

Salt intake in mineralocorticoid receptor antagonist-treated primary aldosteronism: foe or ally?

Mild hyperkalemia is a common side effect of mineralocorticoid receptor antagonist (MRA) treatment of patients with primary aldosteronism (PA), which can be worsened by instructions to minimize salt intake. Our objective was to evaluate the effect of salt consumption on serum potassium levels and mean, mean minimal, and mean maximal systolic and diastolic blood pressure (BP) in MRA-treated hyperkalemic PA patients under relative salt restriction. Seventeen consecutive mildly hyperkalemic MRA-treated PA patients aged 66.3 ± 8.37 years were recruited. Body mass index (BMI) and BP were assessed, and serum and 24-h urinary sodium and potassium levels, plasma renin, and serum aldosterone were measured, while patients followed a relatively salt-restricted diet, after 1 month of controlled salt supplementation (usual salt-restricted diet plus 4 g salt/day) and after 6 months on instructions for free dietary salt consumption. Baseline salt consumption was additionally evaluated in two more patient groups (normotensive subjects and normokalemic MRA-treated PA patients). One month of controlled salt supplementation (24-h urine sodium (median, min, max): 195.2 (120.30-275.20) vs 110.13 (34.30-139.20) mEq/day, p < 0.001) resulted in increased kaliuresis (62.25 (40.69-97.0) vs 54.0 (23.28-79.60) mEq/day, p = 0.001) and a decrease of serum potassium (5.2 (5-5.70) vs 4.6 (3.8-5.1) mEq/L, p < 0.001), while serum sodium (139 (133-141) vs 1 39 (135-144) mEq/L) and mean systolic (130 (105-141 vs. 130 (106-141) mmHg) and diastolic (76 (53-85) vs75 (53-84) mmHg) BP remained stable. These findings were unchanged after 6 months of free salt consumption. BMI remained constant, while plasma renin and serum aldosterone decreased following salt repletion. Adequate salt consumption attenuates MRA-induced hyperkalemia in relatively salt-restricted PA patients without affecting BP or BMI.

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.

Serial measurement of glyphosate blood concentration in a glyphosate potassium herbicide-intoxicated patient: A case report.

INTRODUCTION: This report describes changes in blood and urine concentrations of glyphosate potassium over time and their correlations with clinical symptoms in a patient with acute glyphosate potassium poisoning. CASE REPORT: A 67-year-old man visited the emergency center after ingesting 250 mL of a glyphosate potassium-based herbicide 5 h before. He was alert but presented with nausea, vomiting, and bradyarrhythmia with atrial fibrillation (tall T waves). Laboratory findings revealed a serum potassium level of 6.52 mEq/L. After treatment with an injection of calcium gluconate, insulin with glucose, bicarbonate, and an enema with polystyrene sulfonate, the patient's serum potassium level normalized and the bradyarrhythmia converted to a normal sinus rhythm. During admission, the blood and urine concentration of glyphosate and urine aminomethylphosphonic acid (AMPA, a glyphosate metabolite) was measured at regular time intervals. The patient's glyphosate blood concentration on admission was 11.48 mg/L, and it had decreased rapidly by 16 h and maintained about 1mgl/L by 70 h after admission. Urine glyphosate and AMPA levels had also decreased rapidly by 6 h after admission. DISCUSSION: Glyphosate potassium poisoning causes hyperkalemia. Blood concentrations of glyphosate were decreased rapidly by 16 h after admission, and urine concentrations were also decreased by 6 h after admission.

Abdominal Wall Pain: A Common Clinical Problem.

Abdominal wall pain (AWP) is a common and underrecognized cause of chronic abdominal pain. The etiology of AWP varies. History and physical examination are critical to an accurate diagnosis of AWP. Trigger point injection using either a corticosteroid, a local anesthetic, or a combination of both often gives relief of pain and is of diagnostic and therapeutic value. Increased awareness of AWP as a cause of chronic, nonvisceral abdominal pain can prevent fruitless searches for intra-abdominal pathology and reduce medical costs.

Peritoneal dialysis can alleviate the clinical course of hungry bone syndrome after parathyroidectomy in dialysis patients with secondary hyperparathyroidism.

PURPOSE: It is unclear whether clinical courses of hungry bone syndrome (HBS) after parathyroidectomy (PTX) in peritoneal dialysis (PD) and hemodialysis (HD) patients are different. The present study aimed to investigate the possible differences of postoperative hypocalcemia and hyperkalemia between PD and HD patients. METHODS: We performed retrospectively 29 PD patients as the PD group and 169 HD patients as the HD group undergoing successful total PTX with autotransplantation. Calcium supplement after surgery was recorded. Higher levels of serum potassium during and immediately after surgery were recorded as K+d0. K+d3 was recorded as peak pre-dialysis serum potassium level 3 days post-surgery. RESULTS: There were 157 (92.90%) patients in HD group and 22 (75.86%) patients in PD group suffered from HBS after surgery, with significant difference between the groups (P = 0.004). Patients in PD group had significantly shorter intravenous calcium supplement duration (P = 0.037) and significantly smaller intravenous calcium supplement dosage (P = 0.042) and total calcium supplement dosage during hospitalization (P = 0.012) than patients in HD group. The levels of serum K+d0 (P < 0.001) and K+d3 (P < 0.001) were both significantly lower in PD group than those in HD group. Peritoneal dialysis was one of the independent influencing factors with negative correlation for calcium supplement, serum K+d0 and serum K+d3. CONCLUSIONS: Compared with HD patients, the clinical course of HBS after PTX in PD patients was alleviated. Efforts should be devoted to individual perioperative management for PD patients undergoing PTX.

Perioperative hyperkalemia in hemodialysis patients undergoing parathyroidectomy for renal hyperparathyroidism.

The present study investigates the incidence of perioperative hyperkalemia and the influence factors of serum potassium levels during and after parathyroidectomy (PTX) in hemodialysis patients with renal hyperparathyroidism (rHPT). A total of 204 hemodialysis patients with refractory rHPT undergoing successful total parathyroidectomy with autotransplantation (tPTX + AT) were analyzed retrospectively. Hyperkalemia was defined as serum potassium levels ≥ 5.5 mmol/L. The preoperative baseline level of serum potassium (K base+ ) was defined as a mean of the three preoperative prehemodialysis serum potassium levels. The higher levels of serum potassium during and immediately after surgery were recorded as K d0+ and the peak prehemodialysis serum potassium levels 3 days after surgery as K d3+ . 136/204 (66.7%) patients suffered from hyperkalemia during or immediately after surgery and 65/204 (31.9%) patients were affected with prehemodialysis hyperkalemia 3 days after surgery. K base+ was the only influencing factor for K d0+ . Serum K base+ , preoperative serum alkaline phosphatase, and total calcium supplement dosage during intravenous calcium supplement were the influencing factors for K d3+ . In the case of PTX, the serum potassium levels of patients with higher serum K base+ and severe postoperative hypocalcemia need to be monitored with extended attention perioperatively.

Plasma Potassium Determines NCC Abundance in Adult Kidney-Specific γENaC Knockout.

The amiloride-sensitive epithelial sodium channel (ENaC) and the thiazide-sensitive sodium chloride cotransporter (NCC) are key regulators of sodium and potassium and colocalize in the late distal convoluted tubule of the kidney. Loss of the αENaC subunit leads to a perinatal lethal phenotype characterized by sodium loss and hyperkalemia resembling the human syndrome pseudohypoaldosteronism type 1 (PHA-I). In adulthood, inducible nephron-specific deletion of αENaC in mice mimics the lethal phenotype observed in neonates, and as in humans, this phenotype is prevented by a high sodium (HNa+)/low potassium (LK+) rescue diet. Rescue reflects activation of NCC, which is suppressed at baseline by elevated plasma potassium concentration. In this study, we investigated the role of the γENaC subunit in the PHA-I phenotype. Nephron-specific γENaC knockout mice also presented with salt-wasting syndrome and severe hyperkalemia. Unlike mice lacking αENaC or ßΕΝaC, an HNa+/LK+ diet did not normalize plasma potassium (K+) concentration or increase NCC activation. However, when K+ was eliminated from the diet at the time that γENaC was deleted, plasma K+ concentration and NCC activity remained normal, and progressive weight loss was prevented. Loss of the late distal convoluted tubule, as well as overall reduced ßENaC subunit expression, may be responsible for the more severe hyperkalemia. We conclude that plasma K+ concentration becomes the determining and limiting factor in regulating NCC activity, regardless of Na+ balance in γENaC-deficient mice.

Elevated potassium levels in patients with chronic kidney disease: occurrence, risk factors and clinical outcomes-a Danish population-based cohort study.

Background: Data on the true burden of hyperkalemia (HK) in patients with chronic kidney disease (CKD) in a real-world setting are scarce. Methods: The incidence rate of HK [first blood test with an elevated blood potassium level level >5.0 mmol/L] in primary or hospital care was assessed in a population-based cohort of all newly diagnosed CKD patients [second estimated glomerular filtration rate (eGFR) measurement <60 mL/min/1.73 m2 or hospital diagnosis] in northern Denmark. Risk factors and clinical outcomes were compared for CKD patients with HK and matched CKD patients without HK. Results: Of 157 766 patients with CKD, 28% experienced HK, for an overall HK incidence rate of 70/1000 person-years. Among patients with Stage 3A, 3B, 4 or 5 CKD, 9, 18, 31 and 42%, respectively, experienced HK within the first year. Important HK risk factors included diabetes {prevalence ratio [PR] 1.74 [95% confidence interval (CI) 1.69-1.79]}, heart failure [PR 2.31 (95% CI 2.23-2.40)] and use of angiotensin-converting enzyme inhibitors [PR 1.45 (95% CI 1.42-1.48)], potassium supplements [PR 1.59 (95% CI 1.55-1.62)] or spironolactone [PR 2.53 (95% CI 2.44-2.63)]. In CKD patients who developed HK, 34% had any acute hospitalization 6 months before the HK event, increasing to 57% 6 months after HK [before-after risk ratio 1.72 (95% CI 1.69-1.74)]. The 6-month mortality following HK was 26%, versus 6% in matched non-HK patients. Compared with non-HK patients, 6-month hazard ratios for any acute hospitalization in HK patients were 2.11-fold higher, including hazard ratios of 2.07 for cardiac diagnoses, 2.29 for ventricular arrhythmias, 3.26 for cardiac arrest, 4.77 for intensive care and 4.85 for death. Conclusions: More than one in four CKD patients develops HK. Patients with severe CKD, diabetes, heart failure or use of spironolactone are at high risk. HK is associated with severe clinical outcomes.

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.

Potassium Chloride Sustained Release Dosing Pathway in an Academic Medical Center.

Potassium supplementation can be administered intravenously or orally with either immediate release or sustained release formulations. Sustained release potassium chloride allows for delayed absorption and peak effects. In the inpatient setting, it is important to monitor and prevent both hypokalemia and hyperkalemia. Our tertiary-care academic hospital created a clinical pathway for sustained release potassium chloride supplementation in the inpatient population. Our clinical pathway for sustained release potassium chloride creates dosing restrictions designed to prevent hyperkalemia, while allowing exceptions for patients with high requirements.

Efficacy and effectiveness of anti-digoxin antibodies in chronic digoxin poisonings from the DORA study (ATOM-1).

CONTEXT: We hypothesized that in chronic digoxin toxicity, anti-digoxin antibodies (Fab) would be efficacious in binding digoxin, but this may not translate into improved clinical outcomes. OBJECTIVE: This study aims to investigate changes in free digoxin concentrations and clinical effects on heart rate and potassium concentrations in chronic digoxin poisoning when anti-digoxin Fab are given. MATERIALS AND METHODS: This is a prospective observational study. Patients were recruited if they have been treated with anti-digoxin Fab for chronic digoxin poisoning. Data was entered into a standardised prospective form, supplemented with medical records. Their serum or plasma was collected, analysed for free and bound digoxin and free anti-digoxin Fab concentrations. RESULTS: From September 2013 to February 2015, 36 patients (median age, 78 years; 22 females) were recruited from 18 hospitals. Median heart rate (HR) was 49 beats/min. Initial median digoxin and potassium concentrations were 4.7 nmol/L (3.6 µg/L) (range: 2.3-11.2 nmol/L) and 5.3 mmol/L (range: 2.9-9.2 mmol/L) respectively. Beta-blockers (n = 18), calcium antagonists (n = 6), spironolactone and/or angiotensin blocking agents (n = 24) were also used concomitantly. Renal impairment and gastrointestinal symptoms were present in 31 (86%) and 22 (63%) patients respectively. Five patients died from conditions unrelated to digoxin toxicity. Median change in HR was 8 beats/min post-Fab with no effect on blood pressure; they were 4, 10 and 17 beats/min for the 1, 2 and ≥3 vials of anti-digoxin Fab groups respectively. Concomitant treatments with potassium lowering agents (12/36) and inotropic drugs (7/36) were used. Gastrointestinal effects resolved in all 22 patients. The median decrease for potassium was 0.3 mmol/L. Digoxin concentration reduced from 3.8 to 0 nmol/L post-Fab. There was a rebound observed in the free digoxin concentration in 25 patients but none had associated clinical deterioration. CONCLUSIONS: One to two vials of anti-digoxin Fab initially bound all free digoxin confirming Fab efficacy. However, this was associated with only a moderate improvement in HR and potassium, suggesting bradyarrhythmia and hyperkalaemia may be from other co-morbidities.

Evaluation of changes in serum concentration of sodium in a transurethral resection of the prostate.

INTRODUCTION AND OBJECTIVES: The purpose of this study was to evaluate changes in serum electrolytes during Transurethral resection of the prostate (TURP) and to evaluate the degree of correlation of hyponatremia and the factors that affect the incidence of TURP syndrome and to show the impact of the duration of the procedure on the severity of hyponatremia due to absorption of irrigation fluid in the systemic circulation. MATERIALS AND METHODS: This study examined 60 male patients planned for elective TURP. The level of serum electrolytes are determined by taking venous blood samples preoperatively and Postoperatively and when the duration of the operation was longer than 60 minutes, the level of serum electrolytes was determined intraoperative. The amount of used irrigation fluid, the weight of resection prostate, and duration of surgery, were also followed. Patients were divided in two groups according to the length of the surgical procedure: Group 1 (30-60 min) and Group 2 (> 60 min). RESULTS: Statistically significant reduction of serum sodium and the elevation of the potassium level in serum observed postoperatively and was directly proportional to the volume of of the used irrigation fluid, the duration of the procedure and volume of the resected prostate. CONCLUSIONS: To evaluate changes in serum electrolyte during TURP is simple and economical method for the indirect estimation of irrigation fluid absorption into the systemic circulation during TURP and opportunity for early identification of TURP syndrome.

Renal formulas pretreated with medications alters the nutrient profile.

BACKGROUND: Pretreating renal formulas with medications to lower the potassium and phosphorus content is common in clinical practice; however, the effect of this treatment on other nutrients is relatively unstudied. We examine whether nutrient composition is affected by pretreating renal formulas with sodium polystyrene sulfonate (SPS) suspension and sevelamer carbonate. METHODS: Fixed medication doses and treatment times were utilized to determine changes in the nutrient composition of Suplena® and Similac® PM 60/40. The effect of simultaneously adding both medications (co-administration) to the formula on the nutrient composition of Suplena® was also evaluated. RESULTS: Pretreatment of Suplena® with SPS reduced the concentrations of calcium (11-38 %), copper (3-11 %), manganese (3-16 %), phosphorus (0-7 %), potassium (6-34 %), and zinc (5-20 %) and increased those of iron (9-34 %), sodium (89-260 %), and sulfur (19-45 %) and the pH (0.20-0.50 units). Pretreatment of Similac® PM 60/40 with SPS reduced the concentrations of calcium (8-29 %), copper (5-19 %), magnesium (3-26 %), and potassium (33-63 %) and increased those of iron (13-87 %) and sodium (86-247 %) and the pH (0.40-0.81 units). Pretreatment of both formulas with the SPS suspension led to significant increases in the aluminum concentration in both formulas (507-3957 %). No differences in potassium concentration were observed between treatment times. Unexpectedly, the levels of neither phosphorus nor potassium were effectively reduced in Suplena® pretreated with sevelamer carbonate alone or when co-administered with SPS. CONCLUSIONS: Pretreating formula with medications alters nutrients other than the intended target(s). Future studies should be aimed at predicting the loss of these nutrients or identifying alternative methods for managing serum potassium and phosphorus levels in formula-fed infants. The safety of pretreating formula with SPS suspension should also be examined.

Acute and chronic cardiovascular effects of hyperkalemia: new insights into prevention and clinical management.

The plasma pool of potassium is a partial reflection of the overall body, transient cellular shifts, and potassium elimination regulated by the kidneys. Potassium concentrations elevating above the upper limit of normal (> 5.0 mEq/L) have become more common in cardiovascular practice due to the growing population of patients with chronic kidney disease and the broad applications of drugs that modulate potassium excretion by either reducing production of angiotensin II (angiotensin-converting enzyme inhibitors, direct renin inhibitors, beta-adrenergic receptor antagonists), blocking angiotensin II receptors (angiotensin receptor blockers), or antagonizing the action of aldosterone on mineralocorticoid receptors (mineralocorticoid receptor antagonists). In addition, acute kidney injury, critical illness, crush injuries, and massive red blood cell transfusions can result in hyperkalemia. Progressively more severe elevations in potassium are responsible for abnormalities in cardiac depolarization and repolarization and contractility. Untreated severe hyperkalemia results in sudden cardiac death. Traditional management steps have included reducing dietary potassium and discontinuing potassium supplements; withdrawal of exacerbating drugs; acute treatment with intravenous calcium gluconate, insulin, and glucose; nebulized albuterol; correction of acidosis with sodium bicarbonate for short-term shifts out of the plasma pool; and, finally, gastrointestinal ion exchange with oral sodium polystyrene sulfonate in sorbitol, which is mainly used in the hospital and is poorly tolerated due to gastrointestinal adverse effects. This review explores hyperkalemia as a complication in cardiovascular patients and highlights new acute, chronic, and preventative oral therapies (patiromer calcium, cross-linked polyelectrolyte, ZS-9) that could potentially create a greater margin of safety for vulnerable patients with combined heart and kidney disease.

Onset time of hyperkalaemia after angiotensin receptor blocker initiation: when should we start serum potassium monitoring?

WHAT IS KNOWN AND OBJECTIVE: Angiotensin receptor blockers (ARBs) frequently induce hyperkalaemia in high-risk patients. Early detection of hyperkalaemia can reduce the subsequent harmful effects. This study was performed to examine the onset time of hyperkalaemia after ARB therapy. METHODS: We carried out a retrospective analysis to determine the onset time of hyperkalaemia (serum potassium >5·5 mm) among hospitalized patients newly starting ARB therapy between 2004 and 2012, in a tertiary teaching hospital. Predefined possible risk factors and concomitant medications were evaluated. RESULTS AND DISCUSSION: During the 97-month study period, a total of 4267 hospitalized patients started ARBs as new drugs and 225 patients showed hyperkalaemia. A significantly increased risk of hyperkalaemia was detected among patients with a high baseline potassium [odds ratio (OR) 6·0] and those who took non-potassium-sparing diuretics (OR 2·2) or potassium supplements (OR 1·6). A high glomerular filtration rate (GFR) was associated with a lower risk of hyperkalaemia (OR 0·992). Fifty-two percentage of hyperkalaemic events occurred within the first week after initiation of ARB therapy. The highest frequency of hyperkalaemia occurred on the first day after initiation of ARBs. Hyperkalaemia occurred earlier in patients with a high baseline serum potassium level, reduced GFR, diabetes and in those without heart failure. WHAT IS NEW AND CONCLUSION: Hyperkalaemia occurs most frequently at the beginning of ARB therapy in hospitalized patients. Monitoring of serum potassium and estimated GFR after initiation of ARBs should be started within a few days or not later than 1 week, especially in patients with risk factors.

An evaluation of hyperkalemia and serum creatinine elevation associated with different dosage levels of outpatient trimethoprim-sulfamethoxazole with and without concomitant medications.

BACKGROUND: Adverse events associated with high-dose trimethoprim-sulfamethoxazole (TMP-SMX) for outpatient infections, particularly those likely caused by community-acquired methicillin-resistant Staphylococcus aureus, have not been adequately characterized. OBJECTIVE: Describe hyperkalemia and acute renal injury associated with high-dose TMP-SMX. METHODS: An electronic medical record database retrospective study was conducted of outpatients receiving high-dose or low-dose TMP-SMX, comparing the incidences of hyperkalemia and acute renal injury. RESULTS: Of 6162 patients, more developed hyperkalemia (3.06% vs 1.05%, P < .0001) or acute renal injury (1.99% vs 0.700%, P = .0001) in the high-dose TMP-SMX group. Variables independently associated with hyperkalemia included age >58 years (odds ratio [OR] = 3.44; 95% CI = 1.86-7.0; P < .0001), concomitant receipt of an NSAID (OR = 1.71; 95% CI = 1.02-2.79; P = .044) or an ACE inhibitor (OR = 3.27; 95% CI = 2.06-5.14; P < .0001), high-dose TMP-SMX prescribed (OR = 2.92; 95% CI = 1.85-4.60; P < .0001), and baseline elevated serum creatinine (OR = 45.1; 95% CI = 21.7-93.2; P < .0001). Variables independently associated with acute renal injury included concomitant receipt of an ACE inhibitor (OR = 2.36; 95% CI = 1.01-5.24; P = .048) or a potassium supplement (OR = 4.10; 95% CI = 1.45-10.1; P = .010), high-dose TMP-SMX prescribed (OR = 3.70; 95% CI = 1.70-8.12; P = .0012), and baseline elevated serum creatinine (OR = 2110; 95% CI = 724-7980; P < .0001). CONCLUSIONS: Serum creatinine and potassium concentrations should be monitored in outpatients receiving high-dose TMP-SMX.

Incidence and factors of post-adrenalectomy hyperkalemia in patients with aldosterone producing adenoma.

BACKGROUND: Hyperkalemia is a potentially serious complication following adrenalectomy of aldosterone-producing adenomas (APA). We analyzed the incidence and risk factors for hyperkalemia after adrenalectomy in patients with APA. METHODS: We retrospectively analyzed the records of 55 patients who underwent adrenalectomy for APA between 2002 and 2011. Demographic features, biochemical and hormonal profiles, imaging, and relevant medications were reviewed. RESULTS: Sixteen of 55 APA patients (29.1%) developed hyperkalemia (mean serum K(+) 5.6±0.3 mmol/l) after adrenalectomy and 3 had persistent hyperkalemia requiring mineralocorticoid supplementation for more than nine months. Compared with normokalemic patients, hyperkalemic patients were characterized by male predominance, older age, longer duration of hypertension (12.8±9.3 vs. 6.7±5.0 y, p<0.05), lower nadir serum K(+) (p<0.05), higher preoperative serum creatinine (p<0.01), and higher likelihood of residual hypertension. Using multivariate regression analysis, longer duration of hypertension and impaired renal function were the most important factors of post-adrenalectomy hyperkalemia. CONCLUSIONS: Post-adrenalectomy hyperkalemia in patients with APA is not rare and associated with impaired renal function and longer duration of hypertension. Serum K(+) must be cautiously monitored in patients with long-term hypertension and kidney disease.