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To identify factors associated with the development of hyperkalemia in patients with chronic kidney disease (CKD), we analyzed conditions present during episodes of hyperkalemia in two patients with insulin-dependent diabetes mellitus who had elevated serum potassium concentration ([K]) in ≥ 20% of the blood samples during both the pre-hemodialysis and the hemodialysis period. In both patients, conditions causing derangements in the internal potassium balance (exchanges of potassium between the intracellular and the extracellular compartment), including severe hyperglycemia (serum glucose concentration ≥ 400 mg/dL) and catabolic illnesses, were present in ≥ 75% of the instances of simple hyperkalemia ([K] ≥ 5.1 mmol/L) and almost all of the instances of severe hyperkalemia ([K] ≥ 6.0 mmol/L) during both the pre-hemodialysis and the hemodialysis periods. Derangements of the internal potassium balance, many of which are potentially preventable, can be a major cause of hyperkalemia in patients with CKD before or after starting chronic hemodialysis. Careful analysis of the conditions associated with and potentially causing hyperkalemia in CKD patients is imperative for both treatment and prevention purposes. Categories: Endocrinology/Diabetes/Metabolism, Internal Medicine

The main difference between dialysis-associated hyperglycemia (DH) and diabetic ketoacidosis (DKA) or nonketotic hyperglycemia (NKH) occurring in patients with preserved renal function is the absence of osmotic diuresis in DH, which eliminates the need for large fluid and solute (including potassium) replacement. We analyzed published reports of serum potassium (K(+)) abnormalities and their treatment in DH. Hyperkalemia was often present at presentation of DH with higher frequency and severity than in hyperglycemic syndromes in patients with preserved renal function. The frequency and severity of hyperkalemia were higher in DH episodes with DKA than those with NKH in both hemodialysis and peritoneal dialysis. For DKA, the frequency and severity of hyperkalemia were similar in hemodialysis and peritoneal dialysis. For NKH, hyperkalemia was more severe and frequent in hemodialysis than in peritoneal dialysis. Insulin infusion corrected the hyperkalemia of DH in most cases. Additional measures for the management of hyperkalemia or modest potassium infusions for hypokalemia were needed in a few DH episodes. The predictors of the decrease in serum K(+) during treatment of DH with insulin included the starting serum K(+) level, the decreases in serum values of glucose concentration and tonicity, and the increase in serum total carbon dioxide level. DH represents a risk factor for hyperkalemia. Insulin infusion is the only treatment for hyperkalemia usually required. Int Urol Nephrol

The absence of significant losses of potassium in the urine makes dialysis-associated hyperglycemia (DH) a model for the study of the internal potassium balance. Studies of DH have revealed that hyperkalemia is frequent at presentation, insulin infusion is usually the only treatment required, and the magnitude of the decrease in serum potassium concentration (K(+)) during treatment of DH with insulin depends on the starting serum K(+) level, the decreases in serum glucose concentration and tonicity, and the increase in serum total carbon dioxide level. We present an analysis of these findings based on previously studied actions of insulin. Calculations of transcellular potassium shifts based on the combined effects of insulin-the increase in the electrical potential differences (hyperpolarization) of the cell membranes and the correction of the hyperglycemic intracellular dehydration through decrease in serum glucose concentration-produced quantitative predictions of the decrease in serum K(+) similar to the reported changes in serum K(+) during treatment of DH with insulin. The lessons from analyzing serum K(+) changes during treatment of DH with insulin are applicable to other conditions where internal potassium balance is called upon to protect serum K(+), such as the postprandial state. The main questions related to internal potassium balance in DH that await clarification include the structure and function of cell membrane potassium channels, the effect of insulin on these channels, and the mechanisms of feedforward potassium regulation. Int Urol Nephrol

Reports of dialysis-associated hyperglycemia (DH) were compared to reports of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH) in patients with preserved renal function. Average serum values in DH (491 observations), DKA (1036 observations), and NKH (403 observations) were as follows, respectively: glucose, 772, 649, and 961 mg/dl; sodium, 127, 134, and 149, mmol/l; and tonicity, 298, 304, and 355 mOsm/kg. Assuming that euglycemic (serum glucose, 90 mg/dl) values were the same (sodium, 140 mmol/l; tonicity, 285 mOsm/kg) for all three states, the hyperglycemic rise in the average serum tonicity value per 100-mg/dl rise in serum glucose concentration was 1.9 mOsm/kg in DH, 3.5 mOsm/kg in DKA, and 8.1 mOsm/kg in NKH. Neurological manifestations in DH patients were caused by coexisting conditions (ketoacidosis, sepsis, and neurological disease) in most instances, and by severe hypertonicity (>320 mOsm/kg), with clearing after insulin administration, in a few instances. In 148 episodes of DH corrected with insulin only, the mean increase in serum sodium per 100-mg/dl decrease in serum glucose (Delta[Na]/Delta[Glu]) was -1.61 mmol/l. In agreement with theoretical predictions, Delta[Na]/Delta[Glu] was numerically smaller in patients with edema than in those with euvolemia. The average hyperglycemic increase in extracellular volume, calculated from changes in serum sodium concentration during correction of DH using insulin alone, was 0.013 l/l per 100-mg/dl increase in serum glucose concentration. A small number of DH patients presented with pulmonary edema rectified by insulin alone. DH causes modest hypertonicity, with few patients having neurological manifestations caused usually by other coexisting conditions. In contrast to DKA or NKH, which usually presents with hypovolemia, DH causes hypervolemia manifested occasionally by pulmonary edema. Insulin is adequate treatment for DH. J Diabetes Complications

The mechanisms of fluid and solute abnormalities that should be considered in any patient with severe hyperglycemia include changes in the total amount of extracellular solute, osmotic diuresis, intake of water driven by thirst, and influences from associated conditions. The absence of osmotic diuresis distinguishes dialysis-associated hyperglycemia (DH) from hyperglycemia with preserved renal function (HPRF). Mainly because of this absence, comparable degrees of hyperglycemia tend to produce less hypertonicity and less severe intracellular volume contraction in DH than in HPRF, while extracellular volume is expanded in DH but contracted in HPRF. Ketoacidosis can develop in both DH and HPRF. Among DH patients, hyperkalemia appears to be more frequent when ketoacidosis is present than when nonketotic hyperglycemia is present. Among HPRF patients, the frequency of hyperkalemia appears to be similar whether ketoacidosis or nonketotic hyperglycemia is present. Usually patients with severe DH have no symptoms or may exhibit a thirst. Infrequent clinical manifestations of DH include coma and seizures from hypertonicity or ketoacidosis and pulmonary edema from extracellular expansion. Insulin infusion is usually the only treatment required to correct the biochemical abnormalities and reverse the clinical manifestations of DH. Monitoring of the clinical manifestations and biochemical parameters during treatment of DH with insulin is needed to determine whether additional measures, such as administration of saline, free water, or potassium salts, as well as emergency hemodialysis (HD) are needed. Emergency HD carries the risk of excessively rapid decline in tonicity; its benefits in the treatment of DH have not been established. Semin Dial

Hyperglycemic syndromes cause disturbances in the tonicity of body fluids, the distribution of body water between major body fluid compartments, and the external balance of body solute and water. The unique feature of dialysis-associated hyperglycemia (DH) is that, during its development, it can cause changes exclusively in the internal balance of body solute (hypertonicity) and fluids (intracellular volume contraction and extracellular volume expansion) without affecting the external balance of water or solute. This makes DH the proper substrate for studying predictions of the changes in tonicity and extracellular volume caused by hyperglycemia because these predictions fail, by and large, to account for changes in the external balance of sodium, potassium, and water observed in hyperglycemic syndromes occurring in patients with preserved renal function. The predictions suggest that the baseline state of extracellular volume and the degree of hyperglycemia are major factors influencing the magnitude of abnormalities in the tonicity and extracellular volume resulting from DH, while transfers of solute between the intracellular compartment and the extracellular compartment have relatively smaller effects. Edematous patients are at risk for greater hypertonicity and larger increases in their extracellular volume than euvolemic -- or, even less, hypovolemic -- patients with the same degree of hyperglycemia. Studies reporting the treatment of DH with only insulin therapy can be used to test these theoretical predictions and to analyze the relationship between solute and fluid abnormalities and clinical manifestations. J Diabetes Complications

Chest pain is one of the most difficult diagnostic problems for physicians working in an emergency department. In this setting, more malpractice dollars are awarded for missed myocardial infarction than for any other physician error. This problem usually occurs when the patient has atypical symptoms, the physician is inexperienced, or the diagnosis is not considered. The clinical manifestations of myocardial infarction vary greatly, and patients with "atypical" presentations have a poorer prognosis than those with classic symptoms. Although no feature of a patient's history excludes infarction with certainty, pain that is sharp, positional, pleuritic, or reproduced by palpation indicates a lower probability of acute ischemic heart disease. New immunochemical methods and serial sampling strategies have increased the sensitivity of creatine kinase-MB as an indicator for the disorder. Recent investigations have also established the prognostic value of the initial electrocardiogram. These methods allow emergency physicians to assess the risk of complications and to perform triage when there is a shortage of beds in the coronary care unit. Emergency physicians must also consider other diseases for which coronary care might be beneficial.

2, KJ00006741238, 論文, Article