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      Hyperkalemia in Dialysis Patients : HYPERKALEMIA IN DIALYSIS PATIENTS

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      Seminars in Dialysis

      Wiley

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          Compliance in hemodialysis patients: multidimensional measures in search of a gold standard.

           P Kimmel,  K. Kaveh (2001)
          The gold standard to assess the compliance of hemodialysis (HD) patients has not been established. Compliance parameters should be easily measured and verified, reproducible, clearly interpretable, and accurate. They should have meaning for the patient, clear pathophysiological significance unrelated to other factors, and be related to important outcomes. There is poor correlation of subjective and objective measures and poor correlation of laboratory compliance measures. Different factors have been associated with differential compliance in different patient populations, depending on the measures assessed. Recently, behavioral measures of compliance with dialysis prescription, such as shortening or skipping HD treatments, have been developed. New data confirm that many compliance measures, including both laboratory and behavioral compliance indices, are associated with patient outcomes. It is the duty of the nephrologist and staff to make the importance of compliance understandable to patients. It is important for the health care team to understand patients' expectations and attitudes about their illness and their beliefs about the efficacy and importance of the treatment, as well as patients' demographic, medical, psychological, familial, and socioeconomic status, before realistically evaluating compliance. Such knowledge and approaches may be critical in achieving mutually agreed on compliance goals. We suggest that although assessment of indirect indices is useful, behavioral compliance measures that quantify shortening and skipping behaviors generally should be used in HD patients. Hopefully, analyses of results that control for multiple potentially confounding factors and effective interventions to improve compliance will be developed in the near future.
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            Effect of various therapeutic approaches on plasma potassium and major regulating factors in terminal renal failure.

            The development of life-threatening hyperkalemia poses a risk for patients with chronic preterminal renal failure. Various therapeutic options have been suggested for hyperkalemic emergencies in these patients; to date, however, no study has evaluated the relative efficacies of these measures in the presence of renal failure. Our goal was to examine the acute effects of a variety of therapeutic approaches, as well as those of hemodialysis, on plasma potassium levels in a hemodialysis population. Ten patients with terminal renal failure undergoing maintenance hemodialysis were enrolled in the study. Blood gas parameters and plasma sodium, potassium, glucose, osmolality, renin, aldosterone, epinephrine, norepinephrine, dopamine, and insulin were measured before, during, and after 60-minute infusions of bicarbonate, epinephrine, and insulin in glucose, and before, during, and after performance of regular hemodialysis for one hour. Hypertonic as well as isotonic intravenous bicarbonate (2 to 4 mmol/minute) induced a marked rise in plasma bicarbonate and pH, but failed to lower the plasma potassium level (5.66 versus 5.83 mmol/liter before and after). Epinephrine, 0.05 microgram/kg/minute administered intravenously, decreased plasma potassium only slightly from 5.57 to 5.25 mmol/liter, and five patients showed no decline. On the other hand, insulin in glucose, 5 mU/kg/minute intravenously, effectively lowered plasma potassium levels from 5.62 to 4.70 mmol/liter, and hemodialysis induced the most rapid decline from 5.63 to 4.29 mmol/liter. Plasma aldosterone was elevated before treatment; it correlated with plasma potassium and dropped during intravenous bicarbonate administration or hemodialysis. Pretreatment plasma renin activity, insulin, epinephrine, norepinephrine, and dopamine levels were generally normal. We conclude that in patients with terminal renal failure undergoing maintenance hemodialysis, intravenous bicarbonate is ineffective in lowering plasma potassium rapidly, and epinephrine is effective in only half the patients, whereas insulin in glucose is a fast and reliable form of therapy for hyperkalemic emergencies. Plasma aldosterone levels are appropriate in relationship to plasma potassium levels, and levels of other potassium-influencing hormones are generally normal.
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              Determinants of plasma potassium levels in diabetic ketoacidosis.

              The classic proposal of intracellular K+ for extracellular H+ exchange as responsible for the hyperkalemia of diabetic ketoacidosis (DKA) has been questioned because experimentally induced organic anion acidosis fails to produce hyperkalemia. It has been suggested, instead, that the elevated serum [K+] of DKA might be the result of the compromised renal function, secondary to volume depletion, that usually accompanies DKA. However, several metabolic derangements other than volume depletion and acidosis, which are known to alter potassium metabolism, also develop in DKA. This study of 142 admissions for DKA examines the possible role of alterations in plasma pH, bicarbonate, glucose (G), osmolality, blood urea nitrogen (BUN) and plasma anion gap (AG) on the levels of [K+]p on admission. Significant (p less than 0.01) correlations of [K+]p with each of these parameters were found that could individually account for 8 to 15 percent of the observed variance in the plasma potassium levels; however, the effects of some or all of these parameters on the [K+]p could be independent and therefore physiologically additive. Since the parameters under study are themselves interrelated, having statistically significant correlations with each other, their possible independent role on [K+]p was evaluated by multiple regression analysis. Only plasma pH, glucose and AG emerged as having a definite independent effect on [K+]p, with no independent role found for bicarbonate, BUN and osmolality. The equation that best describes [K+]p on admission for DKA was: [K+]p = 25.4 - 3.02 pH + 0.001 G + 0.028 AG, (r = 0.515). These results indicate that the endogenous ketoacidemia and hyperglycemia observed in DKA, which result primarily from insulin deficit, are the main determinants of increased [K+]p. Since exogenous ketoacidemia and hyperglycemia in the otherwise normal experimental animal do not increase [K+]p, it is postulated that insulin deficit itself may be the major initiating cause of the hyperkalemia that develops in DKA. Renal dysfunction by enhancing hyperglycemia and reducing potassium excretion also contributes to hyperkalemia.
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                Author and article information

                Journal
                Seminars in Dialysis
                Wiley
                08940959
                September 2001
                January 13 2002
                : 14
                : 5
                : 348-356
                Article
                10.1046/j.1525-139X.2001.00087.x
                © 2002

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