Cases reported "Hyperkalemia"

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1/22. Fatal hyperkalemia related to combined therapy with a COX-2 inhibitor, ACE inhibitor and potassium rich diet.

    We describe the case of a 77-year old mildly hypertensive woman with no underlying renal disease who was admitted to the Emergency Department (ED) in a comatose state with fever. The patient had been on low dose enalapril and a potassium rich diet. Five days before admission, rofecoxib, a new selective COX-2 inhibitor nonsteroidal anti-inflammatory drug (NSAID), was added for leg pain. She was found to have severe hyperkalemia and died 90 min after her arrival. We cannot absolutely determine whether the COX-2 inhibitor was the dominant contributor to the development of hyperkalemia or the combination itself, with an intercurrent infection and some degree of dehydration. physicians should be aware of this possible complication and only prescribe NSAIDs, including the new COX-2 drugs, to the elderly under close monitoring of kidney function and electrolyte tests.
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2/22. Treatment of life-threatening hyperkalemia using hemoconcentration in parallel to venovenous bypass during orthotopic liver transplantation.

    IMPLICATIONS: The elimination of potassium in patients with end-stage kidney failure is limited. An increase in potassium concentrations can lead to lethal arrhythmias. In the described case, a large potassium concentration was treated during a liver transplantation using a new technical approach.
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3/22. Lethal neonatal carnitine palmitoyltransferase II deficiency: an unusual presentation of a rare disorder.

    A term male newborn, appropriate for gestational age, developed hypothermia, severe cardiac dysrrhythmia, and nonoliguric hyperkalemia within 24 hours of birth. Despite the prenatal identification of cystic renal dysplasia without oligohydramnios, at birth, a solitary left leg vascular hemangioma and large palpable kidneys were the only anomalies. Gradually hypotonia, lethargy, and poor feeding developed and by 20 hours of age recurrent cardiac dysrrhythmias, myocardial dysfunction, and renal insufficiency with intermittent hyperkalemia were apparent. Episodes of apnea developed on day 7 followed by respiratory failure, recurrent cardiac dysrrhythmias, and death on day 12. Eventually laboratory and autopsy findings confirmed the diagnosis of lethal neonatal carnitine palmitoyltransferase II deficiency.
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4/22. cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases.

    BACKGROUND: Nephrotoxicity is a well-known effect of cyclosporine (CsA) that causes a reduction in glomerular filtration rate through vasoconstriction of the afferent glomerular arterioles and may result in acute renal failure. Isolated CsA-induced hyperkalemia occurring through different mechanisms is also common. However, there are only a few "case reports" addressing this phenomenon in allogeneic bone marrow transplantation patients. In this report, we propose mechanisms and methods of managing CsA-associated hyperkalemia in allogeneic transplantation. methods: We report on four allogeneic blood stem- cell transplant cases and a review of the literature. RESULTS: Four adult leukemia patients underwent allogeneic peripheral blood stem cell transplantation and received CsA as a part of their graft-versus-host disease prophylaxis. The patients developed hyperkalemia, despite adequate kidney function. CsA seemed to be the only pharmaceutical agent to which this electrolyte abnormality could be attributed. Renal tubule dysfunction and secondary hypoaldosteronism seemed to be the reasons for CsA-associated hyperkalemia. CONCLUSION: This report of four cases demonstrates that CsA should be considered among the possible causes of hyperkalemia in bone marrow transplantation. There may be a need for urgent intervention depending on the severity of hyperkalemia. Monitoring of blood CsA level and dose adjustment are important for the prevention of this complication.
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5/22. Delayed angioplasty after renal thrombosis.

    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.
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6/22. hyperkalemia with concomitant watery diarrhea: an unusual association.

    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 .
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7/22. Rare causes of acute hyperkalemia in the 1st week of life. Three case reports.

    We describe three neonates with hyperkalemia and renal salt wasting during the 1st week of life. Endocrinological evaluation led to the diagnosis of selective hypoaldosteronism (HA) in two neonates and secondary pseudohypoaldosteronism (PHA) in one. The infant with PHA developed a urinary tract infection, and radiological investigation demonstrated a small dysplastic left kidney with vesicoureteral reflux. The electrolyte and hormonal disturbances in this infant persisted throughout the first months of life. The two infants with selective HA improved rapidly after administration of fludrocortisone orally and the electrolytes and renin values returned to normal. Secondary PHA and selective HA should be considered in the differential diagnosis in salt-losing neonates during the first days of life. Renal ultrasonography, urine culture, and assays of aldosterone and plasma renin activity should be performed in any infant presenting with hyperkalemia and salt wasting after the exclusion of congenital adrenal hyperplasia.
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8/22. Isolated hyperkalemia associated with cyclosporine administration in allogeneic stem cell transplantation for renal cell carcinoma.

    Two patients with advanced renal cell carcinoma underwent allogeneic hematopoietic stem cell transplantation and received cyclosporine (CSP) as part of their immunosuppressive therapy. Despite adequate renal function, both patients developed hyperkalemia. CSP was the only pharmaceutical agent to which this electrolyte abnormality could be attributed. Evaluation of renal tubule function suggested that CSP-associated isolated hyperkalemia resulted from tubular resistance to aldosterone. We propose that the presence of a single functional kidney may be a risk factor for isolated hyperkalemia due to CSP.
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9/22. role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.

    We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.
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10/22. Endocrine crises. hyperkalemia.

    Clinical disorders causing hyperkalemia require a basic understanding of normal K homeostasis, which consists of external and internal K balances. The kidney is predominant in maintaining the external balance of K, and a number of mechanisms exist to provide a renal adaptation to defend against K excess. Likewise, several factors are known to modulate internal K balance--i.e., its distribution within the body. Some of these factors may provide defense against hyperkalemia before the kidneys have time to adapt. potassium retention by the kidney causes hyperkalemia when renal failure is advanced, or earlier in the face of impaired tubular function in a variety of disorders. hyperkalemia out of proportion to loss of renal function also occurs in the syndrome of hyporeninemic hypoaldosteronism. Drug-induced hyperkalemia is increasingly common and usually is caused by nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors, cyclosporine, or K-sparing diuretics. Clinical disorders of internal K imbalance include diabetes mellitus, systemic acidosis, and use of beta-blockers. hyperkalemia is usually asymptomatic, but the danger of cardiac arrest or arrhythmia in severe hyperkalemia forces prompt clinical attention. Available treatment choices include agents that antagonize the effect of K on membrane potentials, redistribute it internally into cells, and remove it altogether from the body. The diagnostic work-up can then proceed, first by distinguishing renal and extrarenal causes, then by examining the roles of specific factors outlined in the section on normal K homeostasis.
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