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Aims Hypokalaemia is associated with cardiovascular events and mortality in patients with chronic kidney disease (CKD). This exploratory FIDELITY analysis, a prespecified pooled patient-dataset from FIDELIO-DKD and FIGARO-DKD, investigated the incidence and effect of hypokalaemia in patients with CKD and type 2 diabetes (T2D) treated with finerenone vs. placebo. Methods and results Outcomes include the incidence of treatment-emergent hypokalaemia (serum potassium <4.0 or <3.5 mmol/L) and the effect of finerenone on cardiovascular composite outcome (cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, or hospitalization for heart failure) and arrhythmia composite outcome (new diagnosis of atrial fibrillation/atrial flutter, hospitalization due to arrhythmia, or sudden cardiac death) by baseline serum potassium subgroups. In the FIDELITY population, treatment-emergent hypokalaemia with serum potassium <4.0 and <3.5 mmol/L occurred in 41.1% and 7.5%, respectively. Hazards of cardiovascular and arrhythmia composite outcomes were higher in patients with baseline serum potassium <4.0 vs. 4.0–4.5 mmol/L [hazard ratio (HR) 1.16; 95% confidence interval (CI) 1.02–1.32, P = 0.022 and HR 1.20; 95% CI 1.00–1.44, P = 0.055, respectively]. Finerenone reduced the incidence of hypokalaemia with serum potassium <4.0 mmol/L (HR 0.63; 95% CI 0.60–0.66) and <3.5 mmol/L (HR 0.46; 95% CI 0.40–0.53) vs. placebo. Finerenone lessened the hazard of cardiovascular and arrhythmia events vs. placebo, irrespective of baseline serum potassium. Conclusion A substantial proportion of patients with CKD and T2D experienced hypokalaemia, which was associated with an increased hazard of adverse cardiovascular outcomes. Finerenone reduced the incidence of hypokalaemia. Finerenone reduced the hazard of cardiovascular and arrhythmia outcomes irrespective of serum potassium subgroups. Clinical trials registration: FIDELIO-DKD and FIGARO-DKD are registered with ClinicalTrials.gov, numbers NCT02540993 and NCT02545049, respectively (funded by Bayer AG). Graphical Abstract Graphical Abstract Incidence of hypokalaemia in FIDELITY and the effect of finerenone on the incidence of hypokalaemia as well as CV and arrhythmia outcomes. aTime to CV death, non-fatal myocardial infarction, non-fatal stroke, or hospitalization for heart failure. bTime to new diagnosis of atrial fibrillation/atrial flutter, hospitalization due to arrhythmia, or sudden cardiac death. CI, confidence interval; CKD, chronic kidney disease; CV, cardiovascular; FIDELITY, FInerenone in chronic kiDney diseasE and type 2 diabetes: Combined FIDELIO-DKD and FIGARO-DKD Trial programme analYsis; HR, hazard ratio; K+, potassium; and T2D, type 2 diabetes.

In patients with cardiovascular disease and an implantable cardioverter–defibrillator, increasing potassium levels to the high-normal range reduced the risk of arrhythmia events, hospitalizations, and death.

BackgroundPatients with COVID-19 experience multiple clinical conditions that may cause electrolyte imbalances. Hypokalemia is a concerning electrolyte disorder closely associated with severe complications. This study aimed to estimate prevalence, risk factors and outcome of hypokalemia in a cohort of patients with confirmed COVID-19.MethodsA retrospective analysis was conducted on 290 non-ICU admitted patients with COVID-19 at the tertiary teaching hospital of Modena, Italy, from February 16 to April 14, 2020.ResultsHypokalemia was detected in 119 out of 290 patients (41%) during hospitalization. Mean serum potassium was 3.1 ± 0.1 meq/L. The majority of patients (90.7%) patients experienced only a mild decrease in serum potassium level (3–3.4 mEq/L). Hypokalemia was associated with hypocalcemia, which was detected in 50% of subjects. Urine potassium-to-creatinine ratio, measured in a small number of patients (n = 45; 36.1%), revealed an increase of urinary potassium excretion in most cases (95.5%).Risk factors for hypokalemia were female sex (odds ratio (OR) 2.44; 95% CI 1.36–4.37; P 0.003) and diuretic therapy (OR 1.94, 95% CI 1.08–3.48; P 0.027). Hypokalemia, adjusted for sex, age and SOFA score, was not associated with ICU transfer (OR 0.52; 95% CI 0.228–1.212; P = 0.131), in-hospital mortality (OR, 0.47; 95% CI 0.170–1.324; P = 0.154) and composite outcome of ICU transfer or in-hospital mortality (OR 0.48; 95% CI 0.222–1.047; P = 0.065) in our cohort of patients.ConclusionsHypokalemia was a frequent disorder in subjects with COVID-19. Female sex and diuretic therapy were identified as risk factors for low serum potassium levels. Hypokalemia was unrelated to ICU transfer and death in this cohort of patients.

INTRODUCTION:VIPomas are neuroendocrine neoplasms arising from the pancreas in 90% of the cases reported, while the remaining 10% occur in other tissues of neural crest origin. The symptoms found are secondary to an excessive secretion of vasoactive intestinal peptide (VIP) including profuse watery diarrhea, dehydration, hypokalemia and hypoclorhydria. VIPomas are classically slow-growing, and previously reported cases consistently describe chronic diarrhea and a slowly progressing constellation of associated symptoms. We present a case of acute onset of secretory diarrhea secondary to a VIPoma.CASE DESCRIPTION/METHODS:The patient is a 62 y/o F with PMHx of HTN who presented to the ED w/complaints of abdominal pain, diarrhea, nausea and vomiting for approximately 3 days. Patient reported she was having 5-6 episodes of large volume, pale colored diarrhea. She denied any weight loss, change in diet, recent travel, blood in the stool, foul smell or bulky stool. She was initially found to be hypotensive BP 85/45, MAP 58, HR 88. Labs revealed K+ 3.1 meq/L, HCO3 was 16 meq/L, she had an AGMA measured at 15, and AKI with BUN: Cr 52:3.60 mg/dl respectively. On exam of the stool she was noted to have a stool osmolar gap of -14. Given no obvious underlying cause for these findings she underwent CT A/P which revealed a 7.8 × 6 cm mass contiguous w/both body/tail of the pancreas and posterior wall of the stomach, with no other sites of metastasis. EUS/FNA was done and pathology returned as NET type 1. VIP levels were subsequently sent and were elevated at 1385.8 pg/mL. She was started on octreotide 50 mcg TID with significant improvement in her diarrhea. She underwent surgery with distal pancreatectomy and splenectomy. Pathology confirmed the presence of a grade 2, stage T3 well differentiated NET. She had an uneventful recovery and was discharged home. She continues to be asymptomatic several weeks after surgery.DISCUSSION:Pancreatic VIPoma was first described in 1958 by Verner and Morrison in a patient with chronic refractory diarrhea and hypokalemia. VIPoma is very rare with an estimated incidence of 0.05-0.2 cases per million people. Acute diarrhea resulting from a VIPoma is rare event in an already rare malignancy. Our patient presented with acute secretory diarrhea proven by a stool osmolar gap less than 50, which resulted in acute kidney injury. Her diarrhea, secondary to VIPoma responded well to octreotide. VIPomas are classically rare tumors, but our specific case presents an even more rare presentation.

Severe acute respiratory syndrome coronavirus 2 has caused a global outbreak of coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 binds angiotensin-converting enzyme 2 of the rennin-angiotensin system, resulting in hypokalemia. To investigate the prevalence, causes, and clinical implications of hypokalemia, including its possible association with treatment outcomes, among patients with COVID-19. This cohort study was conducted at Wenzhou Central Hospital and Sixth People's Hospital of Wenzhou, Wenzhou, China, from January 11, 2020, to February 15, 2020. Participants included patients who received a diagnosis of COVID-19 according to the criteria issued by the Chinese Health Bureau and were admitted to the hospital. The patients were classified as having severe hypokalemia (plasma potassium <3 mmol/L), hypokalemia (plasma potassium 3-3.5 mmol/L), and normokalemia (plasma potassium >3.5 mmol/L). The clinical features, therapy, and outcomes were compared between the 3 groups. Data analysis was conducted in March 2020. The patients were given general support and antiviral therapy. Their epidemiological and clinical features were collected. The prevalence of hypokalemia and response to treatment with potassium supplements were measured by analyzing plasma and urine potassium levels. One hundred seventy-five patients (87 female patients [50%]; mean [SD] age, 45 [14] years) were classified as having severe hypokalemia (31 patients [18%]), hypokalemia (64 patients [37%]), and normokalemia (80 patients [46%]). Patients with severe hypokalemia had statistically significantly higher body temperature (mean [SD], 37.6 °C [0.9 °C]) than the patients with hypokalemia (mean [SD], 37.2 °C [0.7 °C]; difference, 0.4 °C; 95% CI, 0.2-0.6 °C; P = .02) and the patients with normokalemia (mean [SD], 37.1 °C [0.8 °C]; difference, 0.5 °C; 95% CI, 0.3-0.7 °C; P = .005). Patients with higher levels of hypokalemia also had higher creatine kinase levels (severe hypokalemia, mean [SD], 200 [257] U/L [median, 113 U/L; interquartile range {IQR}, 61-242 U/L]; hypokalemia, mean [SD], 97 [85] U/L; and normokalemia, mean [SD], 82 [57] U/L), higher creatine kinase-MB fraction (severe hypokalemia, mean [SD], 32 [39] U/L [median, 14 U/L; IQR, 11-36 U/L]; hypokalemia, mean [SD], 18 [15] U/L; and normokalemia, mean [SD], 15 [8] U/L), higher lactate dehydrogenase levels (mean [SD], severe hypokalemia, 256 [88] U/L; hypokalemia, 212 [59] U/L; and normokalemia, 199 [61] U/L), and higher C-reactive protein levels (severe hypokalemia, mean [SD], 29 [23] mg/L; hypokalemia, mean [SD], 18 [20] mg/L [median, 12, mg/L; IQR, 4-25 mg/L]; and normokalemia, mean [SD], 15 [18] mg/L [median, 6 U/L; IQR, 3-17 U/L]). Of 40 severely and critically ill patients, 34 (85%) had hypokalemia. Patients with severe hypokalemia were given potassium at a dose of 40 mEq per day, for a total mean (SD) of 453 (53) mEq potassium chloride, during the hospital stay. The patients responded well to potassium supplements as they recovered. The correction of hypokalemia is challenging because of continuous renal potassium loss resulting from the degradation of angiotensin-converting enzyme 2. The high prevalence of hypokalemia among patients with COVID-19 suggests the presence of disordered rennin-angiotensin system activity, which increases as a result of reduced counteractivity of angiotensin-converting enzyme 2, which is bound by severe acute respiratory syndrome coronavirus 2.

Neonatal hypokalemia (defined as a serum potassium level <3.5 mEq/L) is the most common electrolyte disorder encountered in clinical practice. In addition to common secondary causes, primary genetic etiologies are also closely associated with hypokalemia. Currently, a systematic characterization of these genetic disorders is lacking, making early recognition challenging and clinical management uncertain. This review will aid clinicians by summarizing the genetic background of neonatal hypokalemia from two aspects: (1) increased excretion of K + , whereby genetic factors primarily lead to increased renal Na + influx, decreased H + efflux, or reduced Cl − influx, ultimately resulting in increased K + efflux; and (2) decreased extracellular distribution of K + , whereby genetic factors result in abnormalities in transmembrane ion channels, reducing outward potassium currents or generating inward cation leak currents. We describe over ten genetic diseases associated with neonatal hypokalemia, which involve pathogenic variants in dozens of genes and affect multiple target organs, including the kidneys, intestines, and skeletal muscle. For example, in the renal tubules, pathogenic variants in the SLC12A1 gene encoding the Na + -K + -2Cl - cotransporter lead to renal K + loss, causing Bartter syndrome type I; in intestinal epithelial cells, pathogenic variants in the SLC26A3 gene result in a defective Cl⁻-HCO₃⁻ exchanger, causing congenital chloride diarrhea; and in skeletal muscle, pathogenic variants in the CACNA1S gene impact membrane calcium ion channels resulting in hypokalemic periodic paralysis. Given the wide variety of organs and genetic alterations that can contribute to neonatal hypokalemia, we believe this review will provide valuable insights for clinical diagnosis and treatment. Graphical abstract A higher resolution version of the Graphical abstract is available as Supplementary information

We aimed to assess the prevalence of and factors associated with Na + /K + imbalances in children hospitalized for febrile urinary tract infection (fUTI). This retrospective Italian multicenter study included children aged 18 years or younger (median age = 0.5 years) who were discharged with a primary diagnosis of fUTI. Na + /K + imbalances were classified as hyponatremia (sodium < 135 mEq/L), hypernatremia (sodium > 145 mEq/L), hypokalemia (potassium < 3.5 mEq/L), hyperkalemia (potassium > 5.5 mEq/L), and concurrent hyponatremia and hyperkalemia, in the absence of evidence of hemolyzed blood samples. Among the 849 enrolled children, 23% had hyponatremia, 6.4% had hyperkalemia, 2.9% had concurrent hyponatremia and hyperkalemia, 0.7% had hypokalemia, and 0.4% had hypernatremia. In the multiple logistic regression analysis, after applying the Bonferroni correction, only C-reactive protein (C-RP) levels were significantly associated with hyponatremia (OR = 1.04; 95% CI: 1.02–1.06; p  < 0.001), only age was significantly associated with hyperkalemia (OR = 1.7; 95% CI: 1.1–2.7; p  = 0.01), and only CAKUT was significantly associated with concurrent hyponatremia and hyperkalemia (OR = 4.3; 95% CI: 1.7–10.8; p  = 0.002). Even after adjusting for the presence of kidney hypoplasia, abnormal renal echogenicity, pelvi-caliceal dilation, ureteral dilation, uroepithelial thickening of the renal pelvis, bladder abnormalities, pathogen other than E. coli , concurrent hyponatremia and hyperkalemia persisted significantly associated with CAKUT (OR = 3.6; 95% CI: 1.2–10.9; p  = 0.02). Conclusion : Hyponatremia was the most common Na + /K + imbalance in children hospitalized for fUTI, followed by hyperkalemia and concurrent hyponatremia and hyperkalemia. C-RP levels were most strongly associated with hyponatremia, age with hyperkalemia, and CAKUT with concurrent hyponatremia and hyperkalemia (suggestive of transient secondary pseudo-hypoaldosteronism). Therefore, in children who develop concurrent hyponatremia and hyperkalemia during the course of a fUTI, an underlying CAKUT could be suspected. What is known: • Na+ and K+ abnormalities can occur in patients hospitalized for febrile urinary tract infection (fUTI). • Concurrent hyponatremia and hyperkalemia during fUTI may suggest transient secondary pseudo-hypoaldosteronism (TPHA), for which limited data on prevalence are available. What is new: • The most common Na+/K+ imbalance in children hospitalized with fUTI was hyponatremia (23%), followed by hyperkalemia (6.4%), concurrent hyponatremia and hyperkalemia (2.9%), hypokalemia (0.7%), and hypernatremia (0.4%). • Concurrent hyponatremia and hyperkalemia were mainly associated with CAKUT, while hyponatremia alone correlated with high C-reactive protein and hyperkalemia alone with younger age. In cases of concurrent hyponatremia and hyperkalemia during fUTI, an underlying CAKUT should be suspected.

Abstract Disclosure: M. Marcelli: Employee; Self; Quest Diagnostics. Stock Owner; Self; Quest Diagnostics. C. Bi: Employee; Self; Quest Diagnostics. J.W. Funder: None. M.J. McPhaul: Employee; Self; Quest Diagnostics. In many practices, the screening for primary aldosteronism (PA) relies on a single blood draw for plasma aldosterone concentration (PAC) and plasma renin activity (PRA) to establish an aldosterone-to-renin ratio (ARR). ARR cut-off levels vary between expert centers and between repeated assays in the same individual, emphasizing the potential variability of this screening approach. We conducted a study in 2 cohorts and used 2 screening approaches to identify probable PA (ARR ≥30 vs PRA suppressed to <1 ng/mL/h). Methods: Cohort A consisted of 94,829 consecutive paired PRA and PAC samples submitted by clinicians to evaluate the presence of PA. Cohort B is a subgroup of cohort A consisting of 27,893 patients in whom serum K was measured on the same day as PRA and PAC. Results: Based on ARR, 13.9% of cohort A (95%CI 13.6-14.1) and 13.9% of cohort B (95%CI 13.4-14.3) tested positive; based on PRA, 45.9% of cohort A (95%CI 45.5-46.2) and 45.2% of cohort B (95%CI 44.6-45.8) tested positive. A range of aldosterone levels was observed in cohort A vs B samples that screened positive using ARR vs PRA. PAC >15 ng/dL was present in a similar proportion of patients in both cohorts, regardless of the screening test used; however, PAC 5 to 15 and <5 ng/dL were present in higher proportions of patients positive for PRA than ARR in both cohorts A (25.2% vs 8.4% and 15.1% vs 0.7%) and B (26% vs 8.6% and 13.3% vs 0.5%), respectively. Hypokalemia was tested in cohort B and was more frequent than in an equal number of random controls not tested for the ARR test code (5.4% vs 1.8%) and when examining specific age groups (eg, age 50-70) in both women (4.9% vs 1.3%) and men (7.5% vs 1.5%). Conclusions•In both cohorts screened for PA, more individuals were identified by focusing on PRA < 1 than on ARR ≥ 30. This finding prompts a reassessment of the screening procedures for PA. •The proportion of positives for PA identified by the 2 screening tools was similar in cohort A vs B, suggesting that serum K should not be a routine test in the workup for PA.•Compared with the ARR test, Tthe PRA screening test identified more patients than the ARR test with PAC with 5 to 15 and <5 ng/dL in both cohorts A and B, while thethe tests identified a similar proportion of patients with PAC >15 ng/dL in both cohorts. This indicates that an ARR test of ≥30 is as effective as the PRA <1 for identifying florid cases of PA, but unlike PRA, is unable to identify less florid (and more common) cases of PA. •Hypokalemia was more frequent in cohort B than random controls, even after controlling for age (50-70) and sex, indicating that this cohort is enriched with a classic biochemical marker of PA. Presentation: 6/1/2024

Abstract Context Primary aldosteronism (PA) is a common cause of hypertension (HT). However, diagnosis is often delayed, leading to poorer clinical outcomes. Hypokalemia with HT is characteristic of PA, and is an indication for screening. Objective We evaluated if patients with PA had prolonged hypokalemia before diagnosis, the subsequent biochemical/clinical control, and factors associated with delayed diagnosis. Methods Our study included all PA patients with hypokalemia diagnosed between 2001 and 2022. Delayed diagnosis was defined as duration of hypokalemia of more than 1 year from first occurrence to first evaluation by a PA specialist. Patients were reassessed post adrenalectomy using the Primary Aldosteronism Surgery Outcomes criteria. We performed multivariable analysis to assess for factors associated with delayed diagnosis. Results Among 240 patients with PA who presented with hypokalemia, 122 (51%) patients had delayed diagnosis, with prolonged hypokalemia of median duration 4.5 years (range, 2.4-7.5 years). Patients with delayed diagnosis were older, had longer duration of HT, higher pill burden, lower renal function, and more prevalent cardiovascular disease. Factors associated with delayed diagnosis included older age, presence of hyperlipidemia, and less severe hypokalemia (serum potassium >3.0 mmol/L). Compared to patients with early diagnosis, a lower proportion of those with delayed diagnosis underwent adrenal vein sampling (73% vs 58%) (P < .05). Sixty of 118 (50.8%) nondelayed, and 39 of 122 (32.0%) patients with delayed diagnosis, underwent surgery. Conclusion Despite manifestation of hypokalemia, many patients with PA fail to be promptly screened. Greater emphasis in HT guidelines, and efforts to improve awareness of PA among primary care physicians, are urgently needed.

We investigated the clinical characteristics of primary aldosteronism (PA) screened from patients with hypertension in China. The participants were hypertensive patients who were suspected of PA and registered in the China Primary Aldosteronism Prospective Study. Plasma aldosterone‐to‐renin ratio (ARR) was used as the screening test. In patients screened positive for PA, that is, an ARR exceeding the thresholds and plasma aldosterone concentration (PAC) > 100 pg/mL, a confirmatory test was performed for diagnosis. Patients with PA underwent a CT scan and adrenal venous sampling for subtyping. Of the 1497 screened patients, 754 (50.4%) had an ARR exceeding the diagnostic threshold and 637 (84.5% of those eligible) were registered. These registered hypertensive patients with suspected PA had a mean (standard deviation) age of 52.6 ± 12.1 years, and included 442 (58.6%) women. In multiple stepwise logistic regression, the significant odds ratios for the presence of diagnosed (n = 490) versus suspected and non‐diagnosed PA (n = 147) were 4.54 (95% CI: 2.78‐7.39) for a history of hypokalemia, 0.79 (95% CI: 0.64‐0.98) for a 0.9 mmol/l higher serum total cholesterol, and 2.25 (95% CI: 1.63‐3.10) for a doubling of PAC in the supine or standing/sitting position. In multiple stepwise logistic regression, the significant odds ratios for the presence of unilateral (n = 135) versus bilateral PA (n = 53) were 3.04 (95% CI: 1.90‐4.87) for a 0.4 mmol/l lower minimum serum potassium concentration and 1.86 (95% CI: 1.20‐2.86) for a 0.3 mmol/l higher serum high‐density lipoprotein cholesterol. PA might be a biochemical continuum in the adrenal hypersecretion of aldosterone as well as hypokalemia.