Abnormalities of serum potassium concentration in dialysis-associated hyperglycemia and their correction with insulin: a unique clinical/physiologic exercise in internal potassium balance

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.     

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.     

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.     

Pathophysiology and management of fluid and electrolyte disturbances in patients on chronic dialysis with severe hyperglycemia

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.     

Acidosis and coma in adult diabetic maintenance dialysis patients with extreme hyperglycemia

Background

Extreme hyperglycemia (serum glucose ≥ 800 mg/dL or 44.4 mmol/L) is infrequently associated with impaired consciousness in patients on maintenance dialysis. The purpose of this study was to determine features of extreme hyperglycemia that bring about coma in dialysis patients who do not have any of the potential conditions, other than hyperglycemia, that can affect the sensorium.

Methods

We analyzed 24 episodes of extreme dialysis-associated hyperglycemia in men who did not have neurological disease or sepsis. We compared serum parameters related to hyperglycemia between a group of 12 patients (8 on peritoneal dialysis, 4 on hemodialysis) who were alert and oriented (group A) and another group of 12 patients (5 on peritoneal dialysis, 7 on hemodialysis) who displayed varying degrees of impairment of sensorium, ranging from drowsiness to coma (group B).

Results

Group B had, in the serum, lower total carbon dioxide (TCO₂, 8 ± 4 vs. 20 ± 3 mmol/L, P < 0.01) and higher anion gap (AG, 32 ± 8 vs. 15 ± 4 mEq/L, P < 0.01) and potassium (6.3 ± 1.5 vs. 4.6 ± 1.0 mEq/L, P < 0.05) than group A. Serum levels of glucose, chloride, urea nitrogen, calculated osmolarity and tonicity did not differ between the two groups. The test for serum ketone bodies was positive only in group B (all patients). Stepwise multiple linear regression identified serum TCO₂ and AG as the only predictors of impaired sensorium (r ² = 0.74. P < 0.01).

Conclusion

There is a strong statistical association between the severity of diabetic ketoacidosis (DKA) and the level of impairment of consciousness in patients on dialysis with extreme hyperglycemia and no neurological or infectious disease. This association suggests that the presence or absence of DKA is usually the primary etiologic factor in the development of impaired sensorium in these patients.     

The Effects of Angiotensin Converting Enzyme Inhibitors on Potassium Homeostasis in Dialysis Patients With and Without Residual Renal Function

Hyperkalemia is exacerbated by angiotensin converting enzyme inhibitors (ACE‐I). Distal potassium (K⁺) secretion is negligible in anuric patients. ACE‐I therapy may reduce renal, peritoneal, and colonic K⁺ losses. We examined the effect of ACE‐I therapy on serum, urinary, and dialysate K⁺ in a cross‐section of peritoneal and hemodialysis patients. Serum, 24‐h urine K⁺, and peritoneal dialysate excretion K⁺ levels were measured and the results were compared in the various dialysis and treatment groups. Eighty‐one hemodialysis (HD) and 32 peritoneal dialysis (PD) patients were included. Serum K⁺ in HD patients with no residual renal function (RRF) was higher in those receiving ACE‐I therapy (P = 0.02). Serum K⁺ levels in HD patients receiving ACE‐I treatments with RRF was similar to that in oligoanuric HD patients not receiving an ACE‐I. Urinary K⁺ excretion was significantly reduced in those on ACE‐I therapy versus those not on an ACE‐I (P < 0.05). Mean serum K⁺ was lower in PD versus HD patients (P < 0.05). PD patients with no RRF on ACE‐I therapy had higher serum K⁺ concentrations (P = 0.002) and dialysate K⁺ excretion was lower (P = 0.05), in comparison with PD patients not on an ACE‐I. PD patients with RRF on ACE‐I therapy had higher serum K⁺ concentrations compared with those not on ACE‐I therapy (P = 0.03). Both urinary and dialysate K⁺ excretion were reduced (P = 0.001 and P = 0.002, respectively). ACE‐I therapy increases serum K⁺ concentration in dialysis patients. PD patients have relatively lower serum K⁺ levels compared with HD patients. In PD patients, ACE‐I therapy reduces dialysate K⁺. These changes may result from reduced peritoneal movement of K⁺.     

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.     

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.     

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.     

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.     

Effect of hyperglycemia on serum sodium concentration and tonicity in outpatients on chronic dialysis

When serum glucose concentration is nearly normal, serum sodium concentration and tonicity are usually normal in ambulatory outpatient diabetics on chronic hemodialysis or peritoneal dialysis. In hyperglycemia, patients on hemodialysis do not undergo osmotic diuresis and are able to nearly normalize their serum tonicity by increasing the intake of water. Patients on peritoneal dialysis differ from hemodialysis patients because of continued loss of water in the peritoneal dialysate and achieve only partial correction of tonicity by water consumption. The model currently used to predict changes in serum sodium concentration and in tonicity from hyperglycemia assumes no changes in external balance of body water or solute during development of hyperglycemia and, therefore, is not applicable in ambulatory dialysis patients with intact thirst mechanism, because of water retention. In ambulatory patients on chronic dialysis, clinical manifestations of hyperglycemia include thirst, water intake, and weight gain. Neurologic manifestations due to hypertonicity are usually absent.     

INSULIN AND MINERALOCORTICOIDS INFLUENCE ON EXTRARENAL POTASSIUM METABOLISM IN CHRONIC HEMODIALYSIS PATIENTS

Insulin-mineral corticoids effects on extrarenal K⁺ metabolism in dialysis patients. During the inter-dialytic interval in dialyzed patients, hydrogen and potassium ions are regulated by extrarenal mechanisms. We studied the hormonal and acidotic effects on the extrarenal potassium metabolism, in selected, anuric and stable, hemodialysis patients. Fifteen patients, were grouped according to the mean mid-week pre-dialysis K⁺ over the past 12 months: > 6.0 mEq/L (G1, n = 5), = 5.1–6.0 mEq/L (G2, n = 5), ≤5.0 mEq/L (G3, n = 5). After a mid-week hemodialysis session and 12 h fasting, they received 1 g/Kg glucose p.os (A). Insulin, aldosterone, renin, pH, HCO₃^?, glucose, body weight, blood pressure and heart rate were measured before and 60′ after the meal. We recorded the same parameters, except insulin, in 15 patients, similarly grouped, before hemodialysis (T0) and on 3 consecutive off dialysis days (T1–T3); G1 received fluorohydrocortisone (FHC) 0.1 mg–0.3 mg/day, according to body weight and G3 spironolactone (SLT) 200 mg per day. G2 were controls (B). (A) A significant rise in glycemia (81 ± 23 to 157 ± 52 mg/dL, P < 0.001) and insulin (11.8 ± 6.2 to 46.8 ± 19.5 μU/mL, P<0.001), with a drop in K⁺ (5.1 ± 0.6 to 4.8 ± 0.7 mEq/L, P= 0.001) and aldosterone (453 ± 373 to 383 ± 364 pg/mL, P<0.01), were noted at T60 vs. T0, in all groups. Insulin levels correlated negatively (r = ?0.54, P<0.04) to serum K⁺ at T60, in all patients. (B) No major pH, HCO₃ and aldosterone changes were observed in the 3 groups. Despite that, K⁺ dropped in G1 by FHC (6.7 ± 0.9 to 5.9 ± 0.6 mEq/L, P<0.05), rose in G3 by SLT (4.4 ± 0.4 to 5.4 ± 0.3 mEq/L, P<0.05) and remained unchanged in controls (5.8 ± 0.2 to 5.8 ± 0.6 mEq/L), (T0 vs T3 pre-dialysis values). Glucose significantly lowered K^? by promoting adequate insulin secretion. Drugs affecting aldosterone action significantly influenced potassium metabolism. Acid-base balance was not important in K⁺ handling in steady state anuric dialysis patients.     

Hyperkalemia Complicating Cardiopulmonary Bypass: Analysis of Risk Factors

This study was undertaken to assess the hyperkalemic effect of several factors, including cardioplegia containing 25 mEq K⁺ per liter. We measured potassium balance at termination of cardiopulmonary bypass (CPB) in each of 20 patients with hyperkalemia (minimum K⁺, 6.0 mEq/L) and 20 patients with normal potassium levels (K⁺ up to 5.5 mEq/L) by subtracting urinary excretion of potassium from the sum of contributions from cardioplegia, hemolysis, and transfusion. The effects of potassium balance, diabetes, blood glucose, catecholamines, and propranolol on the degree of potassium change during CPB were assessed by multiple linear regression.We found no effect of potassium load on potassium change in either the hyperkalemic or normal group. This suggested that derangement of potassium homeostasis was more important than exogenous potassium loading as a hyperkalemic stimulus. Use of catecholamines reduced the potassium change in the hyperkalemic group (p < 0.048), but any effect of propranolol on potassium change was not significant.A striking finding was the frequency of diabetics in the hyperkalemic group (12 of 20 patients) compared with the control group (2 of 20) (p < 0.001). In addition, the preoperative serum glucose level in the hyperkalemic group (mean, 154 ± 75 mg/dl) exceeded that of the normal group (mean, 103 ± 13 mg/dl) (p < 0.001).It is concluded that dangerous hyperkalemia is related to derangements of potassium homeostasis rather than excessive potassium loads, and that the use of cardioplegic solutions containing 25 mEq/L of potassium is safe. Known diabetics or patients noted preoperatively to have abnormal elevations of serum glucose deserve special attention during CPB, as many hyperkalemic patients require pacing or prolongation of bypass to manage the resulting electromechanical disturbance.     

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?     

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.     

Model-Based Analysis of Potassium Removal During Hemodialysis

Potassium ion (K⁺) kinetics in intra‐ and extracellular compartments during dialysis was studied by means of a double‐pool computer model, which included potassium‐dependent active transport (Na‐K‐ATPase pump) in 38 patients undergoing chronic hemodialysis. Each patient was treated for 2 weeks with a constant K⁺ dialysate concentration (K⁺_CONST therapy) and afterward for 2 weeks with a time‐varying (profiled) K⁺ dialysate concentration (K⁺_PROF therapy). The two therapies induced different levels of K⁺ plasma concentration (K⁺_CONST: 3.71 ± 0.88 mmol/L vs. K⁺_PROF: 3.97 ± 0.64 mmol/L, time‐averaged values, P < 0.01). The computer model was tuned to accurately fit plasmatic K⁺ measured in the course and 1 h after K⁺_CONST and K⁺_PROF therapies and was then used to simulate the kinetics of intra‐ and extracellular K⁺. Model‐based analysis showed that almost all the K⁺ removal in the first 90 min of dialysis was derived from the extracellular compartment. The different K⁺ time course in the dialysate and the consequently different Na‐K pump activity resulted in a different sharing of removed potassium mass at the end of dialysis: 56% ± 17% from the extracellular compartment in K⁺_PROF versus 41% ± 14% in K⁺_CONST. At the end of both therapies, the K⁺ distribution was largely unbalanced, and, in the next 3 h, K⁺ continued to flow in the extracellular space (about 24 mmol). After rebalancing, about 80% of the K⁺ mass that was removed derived from the intracellular compartment. In conclusion, the Na‐K pump plays a major role in K⁺ apportionment between extracellular and intracellular compartments, and potassium dialysate concentration strongly influences pump activity.     

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.     

Storage Age of Transfused Red Blood Cells During Liver Transplantation and Its Intraoperative and Postoperative Effects

Background

Recent studies suggest that the storage age of red blood cells (RBCs) may be associated with morbidity and mortality in surgical patients. We studied perioperative effects of RBC storage age in patients undergoing orthotopic liver transplant (OLT).

Methods

Adult patients who received ≥5?U of RBCs during OLT between January 2004 and June 2009 were studied. The subjects were divided into two groups according to the mean storage age of RBCs they received: new or old RBCs (stored ≤14 or >14?days, respectively). Effects of storage age of transfused RBCs during OLT on intraoperative potassium (K⁺) concentrations, incidence of hyperkalemia (K⁺ ≥5.5?mmol/L), postoperative morbidity, and patient and graft survival were studied.

Results

The mean serum K⁺ concentrations and the incidence of hyperkalemia during OLT were significantly associated with storage age of the RBCs. Logistic analysis showed that storage age of RBCs was an independent risk factor for intraoperative hyperkalemia (odds ratios 1.067–1.085, p?<?0.001) in addition to baseline K⁺ concentration and units of RBCs transfused. Patient and graft survival and postoperative morbidity including postoperative ventilation, reoperation, acute renal dysfunction defined by the RIFLE criteria was not associated with old RBCs.

Conclusions

Transfusion of RBCs stored for a longer time was associated with intraoperative hyperkalemia but not with postoperative adverse outcomes in adult OLT. Prevention and treatment of potentially harmful hyperkalemia should be considered when old RBCs are administered.     

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