Cause Of Hyperkalemia Research Articles

Gas repellents herbal drugs could induce hyperkalemia in infants: case series in tertiary centers in Saudi Arabia

This is a case series involving four infants who experienced hyperkalemia (high levels of potassium in the blood) after using herbal gas repellents that contained potassium sorbate as an antimicrobial preservative. The first patient was a ten-day-old male who presented with jaundice and incidental hyperkalemia, which resolved with treatment. The second patient was a three-month-old male who had a history of neonatal critical care admission and presented with vomiting and incidental hyperkalemia, which resolved spontaneously. The third patient was a two-month-old female who presented with failure to thrive and incidental hyperkalemia, which resolved after discontinuation of the herbal gas repellent. The fourth patient was a one-month-old male who presented with vomiting and incidental hyperkalemia, which also resolved after discontinuation of the herbal gas repellent. All patients underwent investigations to determine the underlying cause of hyperkalemia, but no specific cause was found other than the use of the herbal gas repellents. The abstract highlights the importance of physicians being aware of the potential effects of potassium-containing herbal gas repellents and the occurrence of unexplained hyperkalemia in infants, urging caution in their use.

Severe respiratory acidosis contributing to refractory hyperkalemia: a case series of COVID-19 patients with renal failure

Introduction: Respiratory acidosis (RA) is not known to cause severe hyperkalemia. However, an exception to this general rule was observed in three patients with severe COVID-19 complicated with renal failure in our center. Objectives: The current study investigated the explanation for hyperkalemia refractory to renal replacement therapy in patients with severe COVID-19 with hypercarbia and renal failure in a tertiary care center. Patients and Methods: In this study, we present a case series of three patients with severe COVID-19 with hypercarbia and dialysis-requiring renal failure who developed persistent hyperkalemia refractory to renal replacement therapy. We studied various causes of persistent hyperkalemia, such as acid‒base disorder, a high turnover state, exogenous administration, rhabdomyolysis, and hypoaldosteronism. Results: All three patients initially presented with episodes of severe hyperkalemia, which were ameliorated after RA was corrected. All of these patients had worsening pulmonary function, after which the hyperkalemia could not be corrected, corresponding to persistent RA. The evidence that there was a contribution of RA to hyperkalemia was further strengthened by the observations of patient 1, in whom the hyperkalemia was only corrected after changing ventilator settings and who was unresponsive to dialysis. We studied the dialysate effluent in patient 3, and the results showed satisfactory removal of potassium with no improvement in the high serum potassium levels. Another interesting finding was that although the dialysate sodium concentration was greater than the serum sodium concentration, there was a decrease in the serum sodium concentration, indicating a reduced movement of sodium into the extracellular space. Conclusion: In our study, metabolic acidosis alone could not explain the high serum potassium levels. Moreover, hyperkalemia was corrected after RA was corrected, indicating that the latter might have been the predominant cause of hyperkalemia in these scenarios. The presence of renal failure and low serum bicarbonate levels might have been the factors contributing to decreased Na+-K+-ATPase activity in the setting of RA, which contributed to severe hyperkalemia in all three patients.

Assessment of etiological factors of hyperkalemia development in cats

Hyperkalemia, or elevated potassium levels in the blood, can have a serious effect on the body. High potassium levels can be both a cause and a consequence of impaired cell function, including cells of the heart, nervous system, muscles and other organs. The purpose of the presented study was to identify and evaluate the etiological causes leading to the development of hyperkalemia in cats in St. Petersburg with subsequent statistical processing of the results obtained. The serum levels of total protein, albumin, globulin, urea, creatinine, bilirubin, glucose, potassium, calcium, phosphorus, sodium, chlorine, as well as the activity of the enzymes alanine aminotransferase (AlAt), aspartate aminotransferase (AsAt) and alkaline phosphatase were determined. The study of biochemical parameters was carried out according to generally accepted methods. It was revealed that the most common causes of hyperkalemia in cats include disorders of the urinary system (52%) – acute renal failure, less often chronic kidney disease, as well as diseases of the gastrointestinal tract (24%), oncological processes (19%). It was also revealed that the survival rate for 7 days after diagnosis was approximately the same in groups with different levels of hyperkalemia and amounted to about 60-67%, which indicates the rapid reversibility of adverse reactions resulting from hyperkalemia with timely intervention. In the future, the study is planned to expand with the capture and analysis of individual nosological units and breed characteristics, as well as dietary characteristics, the ratio to the severity of the condition, the analysis of life expectancy and survival.

#2986 Patiromer for hyperkalemia in the early post-transplant period

Abstract Background and Aims Hyperkalemia is a serious condition among kidney transplant (KT) recipients, which can lead to life-threatening complications such as cardiac arrhythmias. Following kidney transplantation, the causes of hyperkalemia are multifactorial owing to graft function, excess potassium repletion, comorbidities, and medications used in the peri- and post-operative setting. The risk for hyperkalemia is increased immediately post-transplantation, particularly in those with suboptimal graft function and higher calcineurin inhibitors levels. A rapidly rising potassium refractory to medical therapy can be an indication for dialysis. Managing hyperkalemia after kidney transplantation is associated with increased morbidity and healthcare costs. In that manner, newer alternatives such as patiromer and sodium zirconium cyclosilicate have emerged due to their potentially superior efficacy and safety profiles. Method This is an observational, retrospective, single-center study aimed to evaluate the efficacy and safety of patiromer for hyperkalemia management in adult transplant recipients over the first 3 months post-transplant period, between January and December 2022 (since patiromer is available in our hospital pharmacy). We included all the kidney transplant recipients of our hospital, with the exception of those with primary graft failure. Information concerning the donor, recipient, graft, drugs pre and post-transplant, fluid therapy, transfusions, and blood tests (ions, blood gases, glycemia, kidney function measurements, anticalcineurin inhibitors levels) were collected. Patiromer was administered in a single-daily dose, diluted in 250 cc of water, in the afternoon, at least 2 hours separated of other drugs. Results In total, 69 recipients were included in the analysis. 94% were from deceased donors and 54% from donation after cardiac death. The average age of the entire cohort was 55 years and 66% were male. Medical history of each KT recipients reveal that 89% has hypertension, 32% diabetes, and 35% previous cardiopathy. Hypertension treatment before the KT included beta-blockers (39%) and angiotensin-converting enzyme inhibitors (37%). The incidence of hyperkalemia (K ≥ 5.5 mmol/L) was 29.7% in the first three months, mostly in the first week (21.6%). Patiromer was administered to 37% of them. For the 88.5% an initial dose of 8.4 g/day was enough. Although, 27% required an increase of the dose to 16.8 g/day and 8% to 25.2 g/day. The changes in serum potassium levels following the first patiromer dose are shown in Graphic 1. The mean time duration of the patiromer treatment was 14.5 days (3.7-36.7). However, 27% continue with patiromer beyond three months. There was no significant difference in the dose/levels of tacrolimus neither in the serum magnesium levels between patients with or without patiromer. No gastrointestinal complications were observed following the use of patiromer. Conclusion Patiromer may play an important role in the management of hyperkalemia over the first weeks after KT, allowing a significant and sustained reduction of the serum potassium levels, although additional long-term studies are necessary to confirm these effects.

Serum Potassium in Thyroid Cancer Patients With Hypothyroidism During Thyroid Hormone Withdrawal: A Retrospective Study.

Several case reports and a few studies have reported that hypothyroid patients have elevated serum potassium levels. However, hypothyroidism has not been widely accepted as a cause of hyperkalemia. This study aims to evaluate the incidence of hyperkalemia and factors influencing serum potassium levels in thyroid cancer patients with hypothyroidism during thyroid hormone withdrawal before radioactive iodine (RAI) treatment. We conducted a retrospective review of electronic medical records from January 2017 to June 2021, involving 956 thyroid cancer patients post-thyroidectomy and undergoing RAI. Laboratory parameters, including serum potassium levels, were collected in both euthyroid (<1 year prior to RAI) and hypothyroid states. Among 508 patients (mean age 52 years, 79.3% female), hyperkalemia (potassium ⩾ 5.0 mEq/L) occurred in 2.8%, without severe hyperkalemia (potassium ⩾ 6.5 mEq/L). The hypothyroid state exhibited significantly higher serum potassium than the euthyroid state [4.16 (IQR, 3.94-4.41) vs 4.10 (IQR, 3.90-4.35) mEq/L, P < .01]. The mean change in potassium levels between the euthyroid and hypothyroid state was 0.05 ± 0.17 mEq/L. Pre-thyroid hormone withdrawal (euthyroid state) factors associated with serum potassium levels in the hypothyroid state included age, use of angiotensin-converting enzyme inhibitors, diabetes mellitus, serum BUN/creatinine, serum potassium levels, hemoglobin A1c (positive correlation); and thiazide use and eGFR (negative correlation). In the hypothyroid state, hyperkalemia was more likely in patients with serum potassium ⩾4.2 mEq/L (OR 9.36, P < .01) or free T4 ⩾1.38 ng/dL (OR 7.05, P < .01) during the euthyroid state. The incidence of hyperkalemia was low in our hypothyroid cohorts. However, physicians should remain vigilant for cases with risk factors for developing hyperkalemia.

Electrolyte Disturbances Related to Sodium and Potassium and Electroconvulsive Therapy: A Systematic Review.

Electrolyte disturbances related to sodium and potassium affect patients with mental disorders undergoing electroconvulsive therapy (ECT). The objective of this study was to systematically summarize the data regarding ECT and electrolyte disturbances related to sodium and potassium. A systematic literature review in accordance with PRISMA guidelines was conducted. Clinical studies of patients receiving ECT with electrolyte disturbances reported before or after treatment were included. We identified nine case reports and two retrospective studies describing electrolyte abnormalities occurring before or after ECT. ECT was effective and safe in patients with hyponatremia and hypernatremia, including the elderly patient population. This treatment was also effective in treating psychiatric symptoms that may persist after ionic equalization. Electrolyte disturbances after ECT were rare. Reports have suggested that succinylcholine used as a muscle relaxant was the main cause of hyperkalemia after ECT. Electrolyte control is a crucial aspect of guiding ECT therapy. In the context of sodium-related disorders, it is critical to control patient hydration as part of therapy. In addition, succinylcholine should not be used in patients with immobilization, such as catatonia or neuroleptic malignant syndrome. It is necessary to conduct further studies to clarify whether electrolyte concentration affects ECT parameters and clinical efficacy. In addition, it is necessary to assess the influence of various anesthetics on these conditions during ECT. The result of this review should be interpreted bearing in mind the small number of studies conducted to date and the low quality of the evidence they provide.

Heparin-induced hyperkalemia, can LMWH cause hyperkalemia? A systematic review.

Hyperkalemia, an elevated blood potassium concentration exceeding 5.0mEq/L, is associated with adverse outcomes and is frequently observed in hospitalized patients. Drug-induced hyperkalemia accounts for a significant proportion of cases, with heparin, commonly used for venous thrombosis prevention, suspected to contribute, though less recognized than other heparin-related side effects. Both unfractionated heparin (UFH) and low molecular weight heparin (LMWH) have been implicated in inducing hyperkalemia, primarily through the suppression of aldosterone levels and modulation of angiotensin II receptors. This systematic review examines the relationship between heparin, particularly LMWH, and hyperkalemia. Thirteen studies involving 1407 patients were analyzed. Findings indicated a lack of highquality evidence, with no significant increase in potassium levels associated with LMWH use. LMWH did not exhibit a dose-response relationship with hyperkalemia incidence. Additionally, mechanisms underlying the hypothetical LMWHinduced hyperkalemia remained inconclusive. While this suggests that LMWH is unlikely to be a primary cause of hyperkalemia, caution is warranted, especially in patients with elevated baseline potassium levels.

Assessment of the etiological causes of hyperkalemia in dogs

Hyperkalemia is a marker of many disorders in different species of animals and birds, leading to a significant number of pathophysiological abnormalities. However, dogs have no literature data on the features of potassium metabolism and etiological causes of hyperkalemia in different breeds, especially when taking into account significant differences in size and conditions of keeping. The purpose of the presented study was to identify and assess the frequency of occurrence of etiological causes leading to the development of hyperkalemia in dogs of different breeds in the territory of the city. St. Petersburg with subsequent statistical processing of the obtained results.In the presented study, the analysis of biochemical blood parameters of dogs of small breeds (Yorkshire Terrier, Toy Terrier, Pomeranian, dachshund, tsvergpincher, Chihuahua, Shih Tzu), large breeds (Labrador Retriever, German Shepherd, Dalmatian, American Staffordshire Terrier, Central Asian Shepherd, Husky) enrolled in private veterinary clinic of St. Petersburg in the summer-autumn period.It was found that the most common causes of hyperkalemia in small breed dogs include chronic kidney disease (25%), oncological diseases (18%), infectious processes (pyometra) (14%), heart disease (14%). In dogs of large breeds, the main role in the development of hyperkalemia is played by diseases of the urinary system – 24% (of which chronic kidney disease - 14%, acute renal insufficiency – 5%, bacterial cystitis - 5%), endocrinopathy - 19% (of which diabetes mellitus – 14%, hypothyroidism - 5%), oncological diseases (19%), orthopedic disorders (19%), neurological disorders (14%).

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Hyperkalaemia can be an emergency presentation and refers to a blood potassium concentration of &gt;5.5 mmol/l. Olivia Walesby, an ECC resident at the University of Edinburgh, discusses the causes of hyperkalaemia, clinical presentation and acute treatment.

Unanticipated hyperkalaemia and associated perioperative complications in three captive grey wolves (Canis lupus) undergoing general anaesthesia

AbstractIntraoperative hyperkalaemia has been described in dogs, cats, non‐domestic felids and in a calf. This case series reports the occurrence and associated complications in three captive‐held grey wolves anaesthetised for root canal treatment. Severe bradyarrhythmia associated with hypotension was detected in two cases before hyperkalaemia was confirmed. These also presented with signs compatible with malignant hyperthermia and rhabdomyolysis. In the third wolf, regular arterial blood gas analysis revealed a progressive increase in plasma potassium exceeding reference values 240 min after premedication. Hyperkalaemia was treated symptomatically with standard protocols, and the recovery was uneventful in all three wolves. The cause of hyperkalaemia in the described cases remains unknown and is most likely multifactorial. Prolonged recumbency, long anaesthetic duration and the administration of α2‐adrenoceptor agonists are potential influencing factors. Additionally, malignant hyperthermia, rhabdomyolysis, acidaemia and drug effects are discussed for their potential of causing the described intraoperative hyperkalaemia.

Marked hyperkalemia due to inappropriate blood sample storage in two suspected cases of familial pseudohyperkalemia.

We herein report two suspected cases of pseudohyperkalemia who presented with severe hyperkalemia examined at small primary care clinics; however, re-exams at a tertiary care hospital showed normal potassium levels. We reproduced the laboratory examination conditions of the clinics and found that hyperkalemia was due to sampling/storage condition of serum, which is strongly suggestive of familial pseudohyperkalemia (FP). FP is a possible but under-appreciated cause of hyperkalemia, which does not require treatment, so it is important to include FP in the differential diagnosis of hyperkalemia especially in cases with discrepant of serum potassium levels at different settings.

Sustained hyperkalemia in an asymptomatic primary care patient. When to suspect familial pseudohyperkalemia.

Study and management of a case with elevated potassium levels without apparent clinical causes in successive follow-up visits. We present the case of a primary care female patient who persistently exhibited elevated levels of potassium (5.3-5.9mmol/L) in successive control laboratory tests, without an apparent clinical cause. Thepatient was ultimately referred to the Unit of Nephrology, where a potassium-low diet was indicated. Diet did not have any effect on potassium levels. After a thorough study, the cause of hyperkalemia could not be determined. The inconsistency between elevated potassium levels and the reason of consultation, and exclusion of other pre-analytical or pathological causes raised suspicion of familial pseudohyperkalemia. The sample was incubated at different times and temperatures to demonstrate their influence on levels of potassium in blood. Familial pseudohyperkalemia was established as the most probable diagnosis. Finally, the patient was discharged from the Unit of Nephrology and instructed to follow a normal diet.

Sistemik Lupus Eritematozuslu Hastalarda Hiperkalemi Nedenlerinin Değerlendirilmesi: Retrospektif, tek merkez deneyimi

Hyperkalemia is a major electrolyte disturbance with potentially life-threatening consequences. Varying prevalence and causes of hyperkalemia have been reported for study populations. Primary risk factors include renal insufficiency, diabetes mellitus (DM) and use of certain medication such as angiotensin converting enzyme (ACE) inhibitors. So far, causes of hyperkalemia in systemic lupus erythematosus (SLE) have not been investigated. Our aim here is to elaborate the causes underlying hyperkalemia and to determine the prevalence of hyperkalemic Type 4 renal tubular acidosis (RTA) in SLE patients. Among the patients followed up at the Department of Rheumatology due to SLE between January 2010 and February 2020, those with a potassium level of ≥5.5 mEq/L (hyperkalemia) were identified. For hyperkalemia patients, patient charts and digital record system were retrospectively searched for clinical and laboratory findings. Those with a non-SLE diagnosis and without hyperkalemia were excluded. Causes of hyperkalemia were classified as renal failure/insufficiency [acute kidney injury, chronic kidney disease (CKD)], medication, hormonal reasons (Addison’s disease, Type 4 RTA), pseudo-hemolysis, and others. Hyperkalemia was identified in 35 SLE patients, who were 40.1±16.9 years old, on average, and 85.7% of them were female. In 57.1% of the patients (n=20) lupus nephritis was identified. The most common type of renal involvement was Class IV lupus nephritis, at a rate of 68.7% (11/16). At the time of hyperkalemia diagnosis, mean duration of SLE disease was 5.2±5.52 years and mean SLE disease activation index (SLEDAI) was 19.8±13.4. Mean potassium level was 6.6 ±1.08 mEq/L. Metabolic acidosis was detected in 40% of the patients. The most common cause of hyperkalemia was renal failure/disease in 45.7% (n=16), followed by use of medication in 25.7%. In two (5%) patients hyperkalemia was attributed to Type 4 RTA. When patient subsets were compared by their causes of hyperkalemia for clinical and laboratory parameters, subset of renal failure/disease has a higher level of creatinine (p≤0.001), but there was no difference in other parameters. In line with its occurrence in general population, hyperkalemia in SLE most often occurs due to renal failure/disease. In addition, Type 4 RTA is an important reason for hyperkalemia. SLE patients presenting with hyperkalemia should also be queried for hyperkalemic Type 4 RTA, once the common causes for hyperkalemia are ruled out or in the event of persistent hyperkalemia.

Approach to Hyperkalemia

Hyperkalemia is one of the most common electrolytic disorders encountered in clinical practice. Serum potassium concentration is tightly regulated by cellular transfer via insulin, catecholamines, and acid-base equilibrium and secondarily by the kidney via aldosterone and renal flow. Severe hyperkalemia can result in dangerous and potentially life-threatening manifestations, mainly cardiac in nature. It is therefore crucial for physicians to be able to identify the causes of hyperkalemia and provide appropriate treatment. This approach article provides an overview of potassium homeostasis, diagnostic strategies, and treatment guidelines for patients with mild, moderate, and severe hyperkalemia.

Pseudohyperkalemia after total splenectomy in a dog: a case report

A 16-year-old, 7.4 kg, castrated male Cocker Spaniel presenting anorexia and weight loss was referred due to a splenic mass, and total splenectomy was performed to resolve clinical signs. Following surgery, the dog developed mild hyperkalemia (6.27 mmol/L) without any clinical symptoms. Further investigations were conducted to determine the cause of hyperkalemia. The serum-plasma potassium difference was measured (1.05 mmol/L), and pseudohyperkalemia was diagnosed. The cause of pseudohyperkalemia was considered as thrombocytosis after splenectomy. The dog did not receive any specific treatment to lower blood potassium. To our knowledge, we report the first case of post-splenectomy pseudohyperkalemia in a dog.

Псевдогиперкалиемия в клинической практике. Диагностический поиск при гиперкалиемии

Hyperkalemia could be a serious diagnostic challenge to general practitioners, since it could be a life-threatening condition. The causes of hyperkalemia are diverse. These include preanalytical errors, release of potassium resulting from cell lysis, potassium shifting between intra- and extracellular spaces, decreased renal excretion, administration of medications. Diagnostic search should start with history taking. Initial clinical and laboratory tests are usually scheduled by the general practitioner at the outpatient stage. In case of excluded pseudohyperkalemia and medication effects, when hyperkalemia cannot be explained by the existing patient’s disorders, the search for undiscovered kidney, endocrine or cardiovascular diseases should be carried out.

Prevalence and Clinical Profile of Hypokalemia and Hyperkalemia in Admitted Patients of General Medicine Department at a Tertiary Care Centre of Bihar

Objective: The goal of this study was to look into the occurrence and etiology of potassium abnormalities (hypokalemia and hyperkalemia) in hospitalised patients, as well as treatment options. Subjects and Methods: All hospitalized patients at tertiary care centre who had at least one measurement of serum potassium throughout their stay were included in the study. The hospital records included information on electrolyte levels in the blood, demographic characteristics, admission reasons, drugs, the etiology of potassium abnormalities, and treatment techniques. Results: A blood potassium anomaly was found in 1,265 (14.0%) of the 9,045 hospitalised patients; 604 (6.7%) had hypokalemia and 661 (7.30%) had hyperkalemia. The most important explanations for hypokalemia were gastrointestinal losses in 555 (91.8%) of patients and renal losses in 252 (41.7%) of patients. Correcting the underlying cause and replenishing the potassium shortage were the most common therapy techniques. At hospital release, 319 (52.8%) of the 604 hypokalemic patients were normokalemic. Treatment with renin-angiotensin-aldosterone system blockers was the most common cause of hyperkalemia in 228 (34.4%) patients, followed by renal failure in 191. (28.8 percent ). Patients were observed for 298 days (45.0%) without receiving any specific treatment. At hospital discharge, 324 (49.0 percent) of the 661 hyperkalemic patients were normal. Conclusion: The prevalence of potassium imbalance was found to be high among hospitalised patients in this study. Despite the fact that the majority of the potassium abnormalities were mild/moderate, about half of the patients treated for hypokalemia or hyperkalemia were discharged with persistent dyskalemia.

Hyperkalemia: Major but still understudied complication among heart transplant recipients.

Hyperkalemia is a recognized and potentially life-threatening complication of heart transplantation. In the complex biosystem created by transplantation, recipients are susceptible to multiple mechanisms for hyperkalemia which are discussed in detail in this manuscript. Hyperkalemia in heart transplantation could occur pre-transplant, during the transplant period, or post-transplant. Pre-transplant causes of hyperkalemia include hypothermia, donor heart preservation solutions, conventional cardioplegia, normokalemic cardioplegia, continuous warm reperfusion technique, and ex-vivo heart perfusion. Intra-transplant causes of hyperkalemia include anesthetic medications used during the procedure, heparinization, blood transfusions, and a low output state. Finally, post-transplant causes of hyperkalemia include hemostasis and drug-induced hyperkalemia. Hyperkalemia has been studied in kidney and liver transplant recipients, but there is limited data on the incidence, causes, management, and prevention in heart transplant recipients. Hyperkalemia is associated with an increased risk of hospital mortality and readmission in these patients. This review describes the current literature pertaining to the causes, pathophysiology, and treatment of hyperkalemia in patients undergoing heart transplantation and focuses primarily on post-heart transplantation.

Risk factors associated with the incidence and recurrence of hyperkalaemia in patients with cardiorenal conditions.

Hyperkalaemia (HK) is associated with increased mortality risk. Prior studies suggest that the causes of HK are multifactorial. This study aimed to examine risk factors for incident and recurrent HK in six large real-world cohorts of UK patients that could be considered at elevated HK risk because of underlying disease pathology and/or medication use. This retrospective, observational cohort study utilised UK primary and secondary care data from Clinical Practice Research Datalink (CPRD) and linked Hospital Episode Statistics (HES), respectively. Patients were included if they were aged ≥18years and had a record of ≥1 condition of interest (chronic kidney disease [CKD] stage 3+, heart failure, resistant hypertension [RHTN], dialysis, diabetes) and/or renin-angiotensin-aldosterone system inhibitors (RAASi) use between 01 January 2003 and 30 June 2018. Based on their diagnosis/ RAASi prescription record, patients were assigned to overlapping cohorts. The outcomes assessed were HK and recurrent HK, the latter defined as second or subsequent HK episode during follow-up. HK was defined as a serum K+ measurement ≥5.0mmol/L; thresholds of ≥5.5 and≥6.0mmol/L were also explored. Of 931460 meeting the eligibility criteria, 310535 (33.3%) patients experienced ≥1 HK event and 187719 (20.2%) experienced HK recurrence. The probability of subsequent HK events increased with event number from 60.5% for the second event to 76.5% for the sixth and the corresponding time to the next HK event decreased from 15.8months to 6.1months. Amongst the key risk factors, serum creatinine, serum phosphorus, systolic blood pressure, and white cell count demonstrated direct relationships with incidence and recurrence of HK, while inverse relationships were observed for estimated glomerular filtration rate (eGFR), haemoglobin and diastolic blood pressure. The relationship for Charlson's Comorbidity Index was mixed. The use of RAASi and anti-hyperglycaemic agents was associated with an increased risk of HK, while the use of diuretics (non-K+ -sparing) was protective against HK. Several risk factors for HK that are easily measured in routine clinical practice were identified, facilitating the identification of patients who are at the highest risk of experiencing HK, including recurrent HK.

Renal Tubular Acidosis and Management Strategies: A Narrative Review

Renal tubular acidosis (RTA) occurs when the kidneys are unable to maintain normal acid−base homeostasis because of tubular defects in acid excretion or bicarbonate ion reabsorption. Using illustrative clinical cases, this review describes the main types of RTA observed in clinical practice and provides an overview of their diagnosis and treatment. The three major forms of RTA are distal RTA (type 1; characterized by impaired acid excretion), proximal RTA (type 2; caused by defects in reabsorption of filtered bicarbonate), and hyperkalemic RTA (type 4; caused by abnormal excretion of acid and potassium in the collecting duct). Type 3 RTA is a rare form of the disease with features of both distal and proximal RTA. Accurate diagnosis of RTA plays an important role in optimal patient management. The diagnosis of distal versus proximal RTA involves assessment of urinary acid and bicarbonate secretion, while in hyperkalemic RTA, selective aldosterone deficiency or resistance to its effects is confirmed after exclusion of other causes of hyperkalemia. Treatment options include alkali therapy in patients with distal or proximal RTA and lowering of serum potassium concentrations through dietary modification and potential new pharmacotherapies in patients with hyperkalemic RTA including newer potassium binders.