Potassium Homeostasis in Dialysis Patients

Potassium homeostasis is remarkably well preserved in the majority of patients on dialysis, despite the loss of the normal major route of potassium elimination. Nonetheless, the new major pathways for potassium removal (dialysis and gastrointestinal) are clearly less able to adapt to changes in potassium intake than is the healthy kidney. Therefore, disturbances in the plasma potassium concentration, most commonly hyperkalemia, remain a constant threat to the health of dialysis patients. A recent survey of outpatients on chronic hemodialysis found about a 10% incidence of severe predialysis hyperkalemia (serum potassium concentration greater than 6.0 mmol/L). Several causes of this potentially lethal problem must be considered when it occurs (Table 2). We hope that through a sound understanding of potassium homeostasis, the incidence of such serious disturbances in plasma potassium concentration can be reduced.     

Extrarenal potassium tolerance in chronic renal failure: implications for the treatment of acute hyperkalemia

The role of extrarenal potassium homeostasis is well recognized as a major mechanism for the acute defense against the development of hyperkalemia. The purpose of this report is to examine whether or not the various mechanisms of extrarenal potassium regulation are intact in patients with end-stage renal disease (ESRD). The available data suggest that with the development of ESRD and the uremic syndrome there is impaired extrarenal potassium metabolism that is related to a defect in the Na,K-adenosine triphosphatase (ATPase). The responsiveness of uremic patients to the various effector systems that regulate extrarenal potassium handling is discussed. Insulin is well positioned to play an important role in the regulation of plasma potassium concentration in patients with impaired renal function. The role of basal insulin may be even more important than previously appreciated, since somatostatin infusion causes a much greater increase in the fasting plasma potassium in rats with renal failure than in controls. Furthermore, stimulation of endogenous insulin by oral glucose results in a greater intracellular translocation of potassium in uremic rats than in controls. Under at least two common physiologic circumstances, feeding and vigorous exercise, endogenous catecholamines might also act to defend against acute increments in extracellular potassium concentration. However, it is important to appreciate that the response to beta 2-adrenoreceptor-mediated internal potassium disposal is heterogeneous as judged by the variable responses to epinephrine infusion. Based on the evidence presented in this report, a regimen for the treatment of life-threatening hyperkalemia is outlined. Interpretation of the available data demonstrate that bicarbonate should not be relied on as the sole initial treatment for severe hyperkalemia, since the magnitude of the effect of bicarbonate on potassium is variable and may be delayed. The initial treatment for life-threatening hyperkalemia should always include insulin plus glucose, as the hypokalemic response to insulin is both prompt and predictable. Combined treatment with beta 2-agonists and insulin is also effective and may help prevent insulin-induced hypoglycemia.     

Acute increase in plasma osmolality as a cause of hyperkalemia in patients with renal failure

These studies were performed in patients with chronic renal failure to understand the mechanism(s) of hyperkalemia secondary to hypertonic NaCl infusion. In 10 patients, after intravenous infusion of either 5% or 2.5% NaCl (6 mEq per kg body wt for 120 minutes in both solutions), the maximum increase in plasma potassium averaged 0.6 (range 0.3 to 1.3) mmol/liter (P less than 0.01) or 0.3 (range 0.2 to 0.6) mmol/liter (P less than 0.01), respectively. The rise of both plasma potassium and osmolality was significantly higher during 5% NaCl than during 2.5% NaCl infusion (P less than 0.01). A significant linear correlation (P less than 0.01) between plasma potassium and osmolality was observed. Urinary potassium excretion was increased to a similar extent by 5% NaCl and 2.5% NaCl infusion. The observed hyperkalemia, secondary to NaCl infusion, was independent of venous pH, plasma bicarbonate, anion gap, insulin levels, and urinary norepinephrine and epinephrine excretion, and was associated with a fall in plasma aldosterone concentration. In separate studies, nine patients were treated with desoxycorticosterone acetate (DOCA; 20 mg i.m. for three days) before receiving saline (5%) infusion. DOCA did not prevent the level increase in plasma potassium that remained significantly correlated with plasma osmolality (P less than 0.01). In conclusion, hypertonic NaCl infusion in patients with renal failure causes a clinically relevant hyperkalemia despite increased renal excretion of potassium. This hyperkalemia is independent of acid-base or hormonal mechanisms known to regulate extrarenal homeostasis of potassium, and is strictly correlated with a rise in plasma osmolality.     

Temporal profile of serum potassium concentration in nondiabetic and diabetic outpatients on chronic dialysis

We analyzed routine serum potassium concentration measurements and conditions temporally associated with abnormalities in potassium concentration in outpatients on chronic hemodialysis (136 nondiabetics, 36 diabetics) and continuous ambulatory peritoneal dialysis (16 nondiabetics, 10 diabetics). The following potassium concentration frequencies were found: prehemodialysis, nondiabetics: normal 51.3%, severe hyperkalemia (greater than 6.0 mmol/l) 10%, severe hypokalemia (less than 3.0 mmol/l) 0.3%; diabetics: normal 57.8%, severe hyperkalemia 8.7%, severe hypokalemia 0.5%. Peritoneal dialysis, nondiabetics: normal 73.7%, severe hyperkalemia 0.6%, severe hypokalemia 4.9%; diabetics: normal 72.5%, severe hyperkalemia 0.9%, severe hypokalemia 2.9%. Normokalemia and severe hypokalemia were significantly (chi 2 test) more frequent in peritoneal dialysis than in prehemodialysis, whereas severe hyperkalemia was more frequent in prehemodialysis serum samples. No difference was found between nondiabetics and diabetics for either form of dialysis. 50% of prehemodialysis episodes of hyperkalemia were diet-induced. Hyperkalemic drugs and anuria were not associated with a higher risk of prehemodialysis hyperkalemia, but each one of 3 abnormalities, very high BUN (greater than 40 mmol/l), metabolic acidosis (TCO2 less than 15 mmol/l) and, in diabetics, severe hyperglycemia (serum glucose greater than 30 mmol/l), was associated with a statistically higher risk of hyperkalemia.     

Hyperkalemia associated to hepatitis in a peritoneal dialysis patient

Hyperkalemia is an unusual complication in peritoneal dialysis patients, having a prevalence of around 0.8% among the continuous ambulatory peritoneal dialysis (CAPD) population. The main cause of hyperkalemia in this group is the release of potassium from sources such as gross haematomas and rhabdomyolysis. However, there is no previous report regarding hyperkalemia induced by intracellular potassium shift into the intravascular compartment secondary to drug-induced acute hepatitis in peritoneal dialysis. We present the following case report of a peritoneal dialysis patient, well dialyzed and on a low-potassium diet, who was admitted in our hospital with paralysis secondary to hyperkalemia (serum potassium: 7 mmol/l). Both disorders disappeared using continuous automated peritoneal dialysis (APD) until liver enzymes normalized. We concluded that acute hepatitis can be a cause of hyperkalemia in a properly nourished and well-dialyzed peritoneal dialysis patient.     

Serum potassium in the crush syndrome victims of the Marmara disaster

BACKGROUND: Hyperkalemia is a major cause of mortality in the patients who suffer from crush syndrome in the aftermath of major earthquakes. The aim of this study is to investigate the frequency and effects of hyperkalemia in the 639 victims of catastrophic Marmara earthquake that struck northwestern Turkey, in August 1999. PATIENTS AND METHODS: Within the first week of disaster, questionnaires were sent to 35 reference hospitals that treated the victims. Information on serum potassium which was provided in 595 out of 639 questionnaires was submitted to analysis. RESULTS: In the patients who were admitted within the first 3 days of the disaster (n = 401) serum potassium was 5.4 +/- 1.3 mEq/l, which was higher than in those admitted thereafter (n = 171) (4.5 +/- 1.1 mEq/l) (p = 0.02). Considering the whole series, males (p = 0.01), patients needing dialysis support (p < 0.001) and non-survivors (p = 0.001) were characterized by higher serum potassium at admission. Seventy patients' serum potassium was above 7 mEq/l, while 22 patients were hypokalemic (< 3.5 mEq/l). Admission potassium correlated with many clinical and laboratory variables indicating the severity of the trauma, and a logistic regression model with clinical and laboratory parameters upon admission, revealed potassium as the most significant predictor of dialysis needs in the victims admitted within the first 3 days (p = 0.008, OR = 3.33). Among the victims who were admitted to hospitals 1 week after the disaster, 8 had serum potassium levels above 6.5 mEq/l; among 4 of them were complicated by hyperkalemia even higher than 7.5 mEq/l. These findings undeline the importance of hyperkalemia during clinical course. CONCLUSION: The most important and fatal medical complication in crush syndrome patients is hyperkalemia. Risk of fatal hyperkalemia continues even after hospitalization. Empirical therapy at the scene is indicated especially in male victims with severe soft tissue traumas. Early detection and treatment of hyperkalemia may improve the final outcome of renal disaster victims.     

A new treatment forInterdialytic hyperkalemia - the use of fosinopril sodium.

Fosinopril sodium is the first of the phosphinic acid class of angiotensin-converting enzyme inhibitors (ACEI). It is used as an antihypertensive agent, but differs from other ACEI in its dual routes of excretion (liver and kidney), and less incidence of hyperkalemia and cough. We conducted a study in known chronic hemodialysis patients who developed interdialytic hyperkalemia in spite of other treatments to control hyperkalemia. We used fosinopril in this group of patients to assess the effect of fosinopril on serum potassium (K) levels. Twenty-four patients were given fosinopril 10 mg at 18:00 h daily for 8 weeks. K levels were measured before and after each dialysis treatment. Interdialytic weight gains were recorded. The average pretrial potassium level was 6.57 mmol/l (+/- 0.47), and the posttrial level was 5.34 (+/- 0.76); p 相似文献   

Sodium polystyrene sulfonate resin candy for control of potassium in chronic dialysis patients.

A stable candy with 5.0 g sodium polystyrene sulfonate resin per piece was developed. In vitro testing indicated decrease in potassium concentration of 1.0 mEq per gram of resin. Six chronic dialysis patients with predialysis serum potassium of 5.2 mEq per liter or greater participated in a two week blind trial. No change in diet or dialysis routine was made during the study. Analysis of serum potassium by paired "t" test showed mean potassium decrease of 0.7 mEq per liter during treatment (P less than 0.001). Patient compliance and acceptance was excellent during the trial. Use in the treatment of chronic hyperkalemia may be worthwhile in the care of long-term dialysis patients.     

Hyperkalemia in a Chronic Hemodialysis Patient

A 65-vear-old hemodial-vsis patient has repeated problems presenting with hyperkalemia (serum potassium concentrations of 7–8 mEq/L befbre dial-vsis; sometimes in association with symptoms of paraly- sis). Although she likes to eat a lot of fruit, she frequently denies excess ingestion preceding these episodes. Is dietary indiscretion the major cause of hyperkalemia in dialysis patients? What other causes should be considered? Is there a preferred way to dialyze these patients to remove more potassium safi1.v and prevent these dangerous episodes?     

Abnormalities of serum potassium concentration in dialysis-associated hyperglycemia and their correction with insulin: review of published reports

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.     

We Use Dialysate Potassium Levels That Are Too Low in Hemodialysis

Sudden cardiac death accounts for a quarter of all deaths in hemodialysis patients. While this group is at high risk for cardiovascular events, there are certain modifiable factors that have been associated with higher risk of sudden cardiac death. These include short dialysis time, high ultrafiltration rate, and dialysate with a low potassium or calcium concentration. While it is impossible to discern the relative contribution of each of these factors, our review focuses on the role of dialysate potassium concentration in sudden cardiac death. Retrospective studies have identified low potassium dialysate (<2–3 mEq/l) as a risk factor for sudden cardiac death, particularly in patients with predialysis serum potassium concentrations <5 mEq/l. However, patients with predialysis hyperkalemia (≥5.5 mEq/l) may be an exception since a significant association of low potassium dialysate with sudden cardiac death was not observed in this subgroup. Dialysis prescribers must employ alternatives to low dialysate potassium concentrations to achieve potassium control such as increasing dialysis time and frequency, dietary restriction of potassium, prevention and treatment of constipation, discontinuation of medications contributing to hyperkalemia and traditional (or newer, better tolerated) potassium binding resins. Finally, one must also address other factors associated with sudden cardiac death such as short dialysis time, high ultrafiltration rate, and low calcium concentration dialysate.     

Extreme intraoperative hyperkalemia in a non dialysis patient undergoing kidney transplantation

The majority of patients who present for kidney transplantation have end stage renal disease and are on dialysis. Those patients are known to be at risk for the development of hyperkalemia. A patient who has not required dialysis, and with stable potassium levels would not be expected to acutely develop intraoperative hyperkalemia. Presented here is an unusual case in which a 61-year-old man with chronic renal disease but no history of dialysis developed severe intraoperative hyperkalemia during a renal transplant.     

Lethal hyperkalemia associated with severe hyperglycemia in diabetic patients with renal failure

Two patients with diabetic nephropathy on maintenance hemodialysis developed extreme hyperkalemia (7.9 and 9.3 mmol/L, respectively) in association with severe episodes of hyperglycemia (1,152 and 1,185 mg/dL, respectively). The increase in serum potassium was out of proportion to the degree of metabolic acidosis that both patients had, and no exogenous source of hyperkalemia could be identified. Despite treatment efforts both patients died shortly after arrival as a consequence of cardiac arrest. It is proposed that the hyperosmolality of extracellular fluid produced by severe hyperglycemia drives potassium passively out of the cells, therefore favoring the rapid development of hyperkalemia. Insulin deficiency could also play a role. This situation is particularly dangerous in individuals with impaired renal function. Adequate blood glucose control in diabetic patients on dialysis is important to avoid life-threatening hyperkalemia.     

Correction of hyperkalemia by bicarbonate despite constant blood pH.

Patients having hyperkalemia often are given bicarbonate to raise blood pH and shift extracellular potassium into cells. Blood pH in many hyperkalemic patients, however, is compensated. To determine whether bicarbonate, independent of its pH action, affects plasma potassium, 14 hyperkalemic patients were treated with bicarbonate in 5% dextrose. In five patients (changed pH group), blood pH rose at least 0.08, while in nine (constant pH group), it changed less than 0.04. In the first group, pH rose 0.12, bicarbonate rose 5.9 mEq/liter, and plasma potassium fell 1.6 mEq/liter, and plasma potassium fell 1.4 mEq/liter. The correlation between changes in plasma potassium and bicarbonate was identical in the two groups and independent of urinary potassium excretion. Four additional patients, who were treated with 5% dextrose alone, did not significantly lower their plasma potassium, although subsequent treatment with bicarbonate in 5% dextrose lowered their plasma potassium. Thus, bicarbonate lowers plasma potassium, independent of its effect on blood pH, and despite a risk of volume overload, should be used to treat hyperkalemia in compensated acid-base disorders, even in the presence of renal failure, provided the plasma bicarbonate concentration is decreased.     

Role of the renin-angiotensin-aldosterone system in the regulation of plasma potassium in chronic renal disease.

The relationship between plasma potassium concentration and the renin-angiotensin-aldosterone system was evaluated in ten patients with chronic renal failure (creatinine clearance 10-56 ml/min). Under basal conditions and following various stimulation maneuvers, normokalemic patients demonstrated normal plasma renin and aldosterone levels. Five of six patients with hyperkalemia had diminished function of the renin-angiotensin-aldosterone system; their ability to conserve sodium during salt depletion was less than that of normokalemic patients. The data suggest that the maintenance of plasma potassium levels in these patients is dependent of the presence of a normally functioning renin-angiotensin-aldosterone system; aldosterone activity may be an important determinant of sodium conservation in patients with renal failure.     

Potassium metabolism in patients with chronic kidney disease. Part II: Patients on dialysis (stage 5)

Potassium is removed mainly by diffusion during dialysis. In hemodialysis, potassium removal averages 70–150mmol per session, and the presence of glucose-free dialysate, sodium profiling, and hyperkalemia, may increase its removal. The most frequent potassium derangement in hemodialysis patients is hyperkalemia. Hemofiltration removes approximately 60mmol of potassium per treatment. In peritoneal dialysis patients, despite lower potassium removal (about 30–40mmol/day), hypokalemia is the most frequent electrolyte alteration, probably due to movement of potassium into the cells mediated by insulin, secondary to glucose absorption from the dialysis solution.     

Erythrocyte sodium and potassium in patients on peritoneal dialysis

Intracellular sodium and potassium concentrations were determined on erythrocytes obtained, before and after treatment, from patients with end-stage renal disease undergoing 48-hour intermittent peritoneal dialysis. Erythrocyte sodium increased from 7.5 +/- 0.3 to 8.6 +/- 0.4 mmol/L cells with a mean of 1.1 +/- 0.1 mmol/L cells (P less than .001), but erythrocyte potassium and cellular water content were virtually unchanged. Plasma potassium decreased during dialysis from 4.2 +/- 0.2 to 3.3 +/- 0.1 mEq/L (P less than .001). The increase in red-cell sodium correlated with this decrease in plasma potassium (r = .51, P less than .01). In contrast, erythrocyte sodium and potassium in undialyzed control patients with chronic renal failure did not change over a similar period, and plasma potassium was unchanged (4.3 +/- 0.1 mEq/L before and 4.3 +/- 0.2 mEq/L after 48 hours). Incubation of postdialysis erythrocytes from the dialysis patients in their own plasma at varying potassium concentrations showed that the rise in cell sodium was blunted as the plasma potassium was increased from 3.2 +/- 0.1 to 4.5 +/- 0.2 mEq/L. These results suggest that unlike hemodialysis, which is not associated with short-term changes in red-cell electrolytes, intermittent peritoneal dialysis results in a reversible increase in erythrocyte sodium. This change appears to be causally related to the decrease in extracellular potassium concentration.     

Safe general anesthesia in a hyperkalemic infant

A 10-day-old boy treated in the intensive care unit and operating room due to hyperkalemia and renal failure. After admission to the intensive care unit and treatment for hyperkalemia, the patient required insertion of dialysis catheter in the operating room. Treatment for hyperkalemia continued while the patient was under general anesthesia. The operation was carried out successfully and cardiac signs and symptoms of hyperkalemia did not occur despite of potassium blood levels of 8.1 mEq x l(-1). General anesthesia could be safe in hyperkalemic patients as long as the treatment for hyperkalemia is initiated before and during the surgery and hyperkalemia inducing agents are avoided.     

Evaluation of Potassium Levels Before Hemodialysis Access Procedures

Few prospective studies have looked at the incidence of hyperkalemia in outpatient hemodialysis access procedures. Our study prospectively evaluated 167 procedures using a preadmit venous blood gas (VBG) and found that 14.3% had moderate or severe hyperkalemia. When the individual procedures were analyzed it was found that 38% of malfunctioning tunneled dialysis catheter (TDC) patients, 20% of new start TDC patients, 22% of thrombectomy patients, and only 5.8% of the angioplasty patients had moderate or severe hyperkalemia. We have changed our practice and now monitor the preprocedure potassium in all but the routine angioplasty patients and treat with the protocol described in the body of the article.     

Hyperkalemia in Dialysis Patients

Serious hyperkalemia is common in patients with end-stage renal disease (ESRD) and accounts for considerable morbidity and death. Mechanisms of extrarenal disposal of potassium (gastrointestinal excretion and cellular uptake) play a crucial role in the defense against hyperkalemia in this population. In this article we review extrarenal potassium homeostasis and its alteration in patients with ESRD. We pay particular attention to the factors that influence the movement of potassium across cell membranes. With that background we discuss the emergency treatment of hyperkalemia in patients with ESRD. We conclude with a review of strategies to reduce the risk of hyperkalemia in this population of patients.