Cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases

Çalışkan, Yaşar; Kalayoğlu-Beşışık, Sevgi; Sargin, Deniz; Ecder, Tevfik

doi:10.1097/01.tp.0000057241.69355.59

Cited by 21 publications

(9 citation statements)

References 17 publications

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“…50 Hyperkalemia in the setting of normal renal function can occur and is most likely caused by tubular dysfunction and secondary hypoaldosteronism. 155 If fluid intake and a low potassium diet do not restore normal serum potassium levels, dose reduction is necessary. 50 Increased levels of serum alkaline phosphatase (ALP) have been reported in up to 8% of psoriasis patients undergoing treatment, generally in the setting of normal liver function tests.…”

Section: Other Laboratory Abnormalitiesmentioning

confidence: 99%

The use of cyclosporine in dermatology: Part II

Ryan¹,

Amor²,

Menter³

2010

Journal of the American Academy of Dermatology

121

135

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Section: Other Laboratory Abnormalitiesmentioning

confidence: 99%

The use of cyclosporine in dermatology: Part II

Ryan¹,

Amor²,

Menter³

2010

Journal of the American Academy of Dermatology

121

135

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“…1,2 Acute GVHD can cause various metabolic derangements because it requires systemic Table 3 Nonrelapse mortality at post-transplant day 100 and 5-year overall survival according to the occurrence of grades III-IV metabolic abnormalities immunosuppressive treatments, which may be complicated by gastrointestinal symptoms or severe infections. Cyclosporine and tacrolimus, the most widely used immunosuppressants for the prophylaxis and treatment of GVHD, have been associated with hyperkalemia, 3,4,13,14 hyperglycemia, 3,4,15,16 hypomagnesemia, [17][18][19] and hypertriglyceridemia 20,21 in HCT recipients. Glucocorticoid, another frequently used immunosuppressant for GVHD, also causes hyperglycemia.…”

Section: Discussionmentioning

confidence: 99%

Severe metabolic abnormalities after allogeneic hematopoietic cell transplantation

Choi

et al. 2004

Bone Marrow Transplant

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Summary:Severe metabolic abnormalities occurring within 100 days after allogeneic hematopoietic cell transplantation (HCT) were investigated in 311 patients. The metabolic abnormalities included hyper-and hypocalcemia, hypophosphatemia, hyper-and hypokalemia, hyper-and hyponatremia, hyper-and hypomagnesemia, hypercholesterolemia, hyper-and hypoglycemia, and hyperuricemia. Severe abnormalities, defined as grades III-V by NCI CTCAE v3.0, occurred in 269 patients (86.5%). Multivariate analysis revealed that patients with moderate-to-severe hepatic veno-occlusive disease had significantly higher risk for the occurrence of severe metabolic abnormalities. Grades III-IV acute graft-versus-host disease was the most frequently associated with individual metabolic abnormalities. Patients with at least one severe metabolic abnormality had significantly higher day 100 nonrelapse mortality (P ¼ 0.015) and lower 5-year overall survival (P ¼ 0.002) than those without severe abnormalities. The number of metabolic abnormalities also stratified the patients with different clinical outcomes. In conclusion, severe metabolic abnormalities occurring within 100 days after allogeneic HCT were common, and their occurrence was significantly associated with inferior clinical outcomes. These results indicate that metabolic parameters should be monitored in patients undergoing allogeneic HCT and that the occurrence of severe metabolic abnormalities should be considered an important toxicity parameter in prospective clinical trials regarding allogeneic HCT.

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“…Uno de los hallazgos más significativos relativos a la nefrotoxicidad por CsA en clínica humana, relacionada con potenciales efectos tubulares distintos de los efectos descritos a nivel proximal, es la aparición precoz de hiperpotasemia, acompañada o no de acidosis, con bajas excreciones urinarias de K + . Cuando la hiperpotasemia acompaña a una reducción en el FG de pacientes trasplantados sometidos a tratamiento con CsA, suele considerarse como un signo altamente sugestivo de toxicidad por CsA 16 . Después de 15 días de tratamiento con CsA, no observamos cambios en el K + plasmático, pero la excreción media de K + fue próxi-ma a la mitad.…”

Section: Discussionunclassified

Papel del túbulo en la vasoconstricción renal inducida por ciclosporina

et al. 2008

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RESUMENPAPEL DEL TÚBULO EN LA VASOCONSTRICCIÓN RENAL INDUCIDA POR CICLOSPORINA Introducción: Ciclosporina es el primero de una familia de potentes inmunosupresores con capacidad anticalcineurínica que, sin embargo, presentan como limitación terapéutica una nefrotoxicidad que puede aparecer desde periodos tempranos. Los primeros datos funcionales sugerían la existencia de vasoconstricción renal, si bien estudios posteriores han mostrado un efecto tóxico directo de ciclosporina sobre el túbulo proximal.Materiales y Métodos: En este artículo se presenta un modelo porcino de nefrotoxicidad por ciclosporina a medio plazo, analizándose los cambios hemodinámicos intrarrenales y las funciones tubulares, así como la relación entre ambos.Resultados: Ciclosporina produce específicamente una internalización e inactivación de la Na + , K + -ATPasa basolateral del túbulo proximal, determinando el desplazamiento axial de la carga filtrada hacia regiones distales (asa de Henle), con transportes activos más intensos y no modificados por ciclosporina. El resultado es un aumento en la reabsorción fraccional distal de cloro que condiciona un estímu-lo del "feed-back" túbulo glomerular, vasoconstricción aferente pero no eferente, aumento de las resistencias renales y caída de la presión intraglomerular. Furosemida restaura parcialmente la situación basal. La consecuencia inmediata es un aumento en el consumo de O 2 por unidad de sodio trasportado. A nivel del túbulo colector no se observan cambios en la secreción de agua libre, pero la secreción de K + parece limitada, y no se corrige al aumentar la oferta distal de sodio con furosemida, ni con aldosterona, cuyos valores fueron más altos en los animales tratados con ciclosporina.Conclusión: En resumen, el efecto vasoconstrictor de ciclosporina sobre el riñón se debe en parte a una retroalimentación túbulo glomerular activada por el desplazamiento de solutos filtrados de sus sitios de reabsorción proximal a otros sitos más distales. Las dietas con alto contenido en sodio pueden aumentar el efecto deletéreo de ciclosporina sobre el filtrado glomerular.Palabras clave: Ciclosporina. Nefrotoxicidad. Furosemida. Na + , K + -ATPasa. ABSTRACT STUDY ON THE ROLE OF THE TUBULE IN RENAL VASOCONSTRICTION INDUCED BY CYCLOSPORINEIntroduction: Cyclosporine (CyA) has proved to induce cell apoptosis on cultured proximal tubule cells. However, there is no much data about the in vivo functional consequences of this injury or the long time observed CyA-induced renal vasoconstriction.Material and Methods: In a swine model of subacute CyA nephrotoxicity (10 mg/ Kg. d x 15 days), we performed a right nephrectomy, followed by left renal artery, vein and ureter catheterisation. After inducing water diuresis, three clearance periods of 15 minutes were performed before and after a furosemide 1 mg/kg infusion. Plasma and urine electrolytes, blood gas, acid excretion, plasma renin activity and aldosterone concentration, GFR, RPF, RBF, intra-renal vascular resistances, glomerular filtration pressure, distal Cl -d...

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Cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases

Cited by 21 publications

References 17 publications

The use of cyclosporine in dermatology: Part II

The use of cyclosporine in dermatology: Part II

Severe metabolic abnormalities after allogeneic hematopoietic cell transplantation

Papel del túbulo en la vasoconstricción renal inducida por ciclosporina

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