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Hyperkalemia is a frequent complication among kidney transplant recipients that can lead to fatal arrhythmias. The causes of hyperkalemia post kidney transplant are multifactorial and often are drug-induced, and include decreased glomerular filtration rate, tubular dysfunction, and impaired sodium delivery in the distal nephron. This review will discuss pathophysiology and recent updates in the management of both acute and chronic hyperkalemia with a focus on kidney transplant recipients., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Continuous renal replacement therapy (CRRT) is used to manage electrolyte and acid-base imbalances in critically ill patients with acute kidney injury. Although a standard solution and prescription is acceptable in most clinical circumstances, specific disorders may require a tailored approach such as adjusting fluid composition, regulating CRRT dose, and using separate intravenous infusions to mitigate and correct these disturbances. Errors in fluid prescription, compounding, or delivery can be rapidly fatal. This article provides an overview of the principles of acid-base and electrolyte management using CRRT., (Copyright © 2016 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Body water, electrolytes, and acid-base balance are important considerations in the evaluation and treatment of small ruminants and camelids with any disease process, with restoration of these a priority as adjunctive therapy. The goals of fluid therapy should be to maintain cardiac output and tissue perfusion, and to correct acid-base and electrolyte abnormalities. Hypoglycemia, hyperkalemia, and acidosis are the most life-threatening abnormalities, and require most immediate correction., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Tumor lysis syndrome (TLS) is an oncologic emergency triggered by the rapid release of intracellular material from lysing malignant cells. Most common in rapidly growing hematologic malignancies, TLS has been reported in virtually every cancer type. Central to its pathogenesis is the rapid accumulation of uric acid derived from the breakdown of nucleic acids, which leads to kidney failure by various mechanisms. Kidney failure then limits the clearance of potassium, phosphorus, and uric acid leading to hyperkalemia, hyperphosphatemia, and secondary hypocalcemia, which can be fatal. Prevention of TLS may be more effective than treatment, and identification of at-risk individuals in whom to target preventative efforts remains a key research area. Herein, we discuss the pathophysiology, epidemiology, and treatment of TLS with an emphasis on the kidney manifestations of the disease., (Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Purpose: To report a case of severe hyperkalemia successfully managed without the use of hemodialysis and to provide a review of the literature regarding the management of severe hyperkalemia., Methods: A clinical case report from the medical-surgical intensive care unit of a teaching hospital and a literature review are presented. The case involves a 59-year old man with diabetes mellitus, essential hypertension, and gout, who presented to hospital with severe hyperkalemia (K(+) = 10.4 mEq/L) and normal renal function. He was treated with intravenous fluids, sodium bicarbonate, calcium chloride, insulin, calcium resonium, and furosemide., Results: The hyperkalemia resolved with conservative treatment within 8 hours, and dialytic therapy was not required. The literature review supported an initial conservative management approach in stable patients with intact renal function., Conclusions: Hemodialysis is not necessary for all cases of severe hyperkalemia and should be reserved for patients with acute or chronic renal failure or those with life-threatening hyperkalemia unresponsive to more conservative measures.

Four patients presented to the emergency room with life-threatening hyperkalemia and concomitant watery diarrhea. Hypovolemia, acidosis, and renal insufficiency were present in all 4 cases. In 2 patients, hyperkalemia followed initiation of angiotensin-converting enzyme (ACE) inhibitor therapy, whereas 1 patient experienced hyperkalemia after a dose increase of an ACE inhibitor, and the fourth patient was on continuous ACE-inhibitor therapy at the time of the hyperkalemia episode. Two of the 3 patients with functioning kidneys required hemodialysis to correct the hyperkalemia, whereas the other patient was on long-term hemodialysis therapy. In the 2 patients in whom transtubular potassium (K+) gradients were available, their values ranged far below normal, indicating tubular failure to secrete K+. This abnormality was attributed to decreased distal delivery of sodium and water and to renin/angiotensin II/aldosterone blockade. It has been proposed that aldosterone blockade impairs the capacity of the colonic epithelial cells to secrete K+. In all 4 patients the watery diarrhea ceased in parallel with the correction of serum K+ to normal values. It is suggested that hyperkalemia, most likely by stimulating intestinal motility, induced the watery diarrhea in all 4 patients. The watery diarrhea, however, failed to compensate for the renal tubular failure to secrete K+.

When renal arterial thrombosis occurs, the etiologic process plays an important role in the impact of ischemia on renal tissue. If the occlusion is caused by trauma, infarction rapidly occurs. However, when renal arterial thrombosis results from other processes, collateral vessels may develop and thus enables a prolonged ischemia without necrosis. The following is a case report of an acute renal failure caused by renal arterial thrombosis of a single functional kidney, which had a favorable outcome despite delayed treatment by percutaneous angioplasty. This report suggests that detection by ultrasonography of a venous renal flow could be of significant value to assess a collateral vascularization and thus should require an arteriography with angioplasty even after a delayed presentation.

Potassium is the predominant intracellular cation and is critical for the maintenance of resting cellular membrane potential. Abnormalities of potassium balance can manifest as skeletal and cardiac muscle dysfunction. Abnormalities of potassium concentration in plasma can result from changes in external potassium balance (intake vs. excretion) or internal balance (intracellular to extracellular). Hyperkalemia can result from renal failure, uroperitoneum, or severe dehydration and acidosis in calves with diarrhea. Hypokalemia occurs due to reduced forage intake, when increased gastrointestinal losses occur as with diarrhea, due to increased renal losses as with metabolic alkalosis or exogenous corticosteroid administration which promote kaliuresis, or with redistribution of potassium into the intracellular compartment with alkalosis or in association with insulin-mediated glucose uptake. Aggressive intravenous and oral therapy are often necessary to correct potassium balance disorders, in addition to therapy aimed at correcting any underlying disorder contributing to the potassium imbalance.

Although extracellular potassium accounts for only 1% to 2% of total body potassium, its concentration, [K+], is critical because it affects the depolarization of electrically excitable tissues such as heart and skeletal muscle. Renal failure is a predisposing factor in three-quarters of cases of hyperkalemia. Drugs contribute to the development of hyperkalemia in half of the cases, and most cases are multifactorial. Because hyperkalemia can lead to fatal arrhythmias, it deserves respect as a genuine electrolyte emergency. Nonetheless, recent data highlight the poor correlation of the EKG with [K+]. When present, however, EKG changes should be rapidly antagonized by infusion of calcium salts. Additional measures include shifting potassium from the extracellular to the intracellular compartment, removing potassium from the body, and eliminating risk factors for recurrence. Insulin is the most reliable agent for promoting transcellular shift of potassium. Albuterol can be used alone or to augment the effect of insulin. Alkalinization with bicarbonate, although formerly recommended as a mainstay of therapy, is not efficacious. Hemodialysis rapidly and reliably removes potassium and lowers [K+]. Exchange resins are also useful in removing potassium. Precise data on the quantity of potassium removed with current hemodialysis techniques or with resin are lacking. Although effective, rapid, and convenient means of treating hyperkalemia are available, physicians frequently fail to use them effectively.

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.

Derangements in potassium homeostasis affect the body's bioelectric processes, including muscle contraction, nerve conduction, and myocardial electric pacing. Changes in extracellular potassium concentration occur with altered routes of elimination (renal or gastrointestinal) or with pathologic shifts in potassium from one body fluid compartment to another. The therapeutic interventions may either restore a normal resting potential for excitable cells or affect the threshold potential. Thus, an understanding of the basic pathophysiology is the foundation for treatment.

Although the electrocardiogram (ECG) is not considered a reliable indicator of mild to moderate hyperkalemia, profound elevations of serum potassium concentration generally produce classic ECG manifestations. We report two cases of severe hyperkalemia (greater than 9.0 mEq/L) in which the ECGs did not reveal the expected manifestations of hyperkalemia. Thus, even with profound serum potassium elevations, the ECG cannot reliably be used to exclude the presence of hyperkalemia or to monitor therapy designed to lower the serum potassium concentration.

Administration of intravenous fluid to infants and children requires an understanding of the normal expenditure of water and electrolytes by the healthy child and the effects of specific illnesses on water and electrolyte turnover.