Nephrotic syndrome and renal insufficiency associated with lithium therapy

Tam, Vincent K.; Green, Jacob; Schwieger, Jeremy; Cohen, Arthur H.

doi:10.1016/s0272-6386(96)90108-0

Cited by 53 publications

(30 citation statements)

References 36 publications

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“…Rarely, nephrotic syndrome secondary to minimal change disease or focal segmental glomerulosclerosis have been shown to occur after lithium therapy. 92,93 Lithium use has also resulted in hypercalcemia secondary to hyperparathyroidism. 94 The exact mechanism leading to hyperparathyroidism is not clear at this time.…”

Section: Immunosuppressive Agents Calcineurin Inhibitorsmentioning

confidence: 99%

Drug-induced impairment of renal function

Pazhayattil¹,

Shirali²

2014

IJNRD

117

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Pharmaceutical agents provide diagnostic and therapeutic utility that are central to patient care. However, all agents also carry adverse drug effect profiles. While most of these are clinically insignificant, some drugs may cause unacceptable toxicity that impacts negatively on patient morbidity and mortality. Recognizing adverse effects is important for administering appropriate drug doses, instituting preventive strategies, and withdrawing the offending agent due to toxicity. In the present article, we will review those drugs that are associated with impaired renal function. By focusing on pharmaceutical agents that are currently in clinical practice, we will provide an overview of nephrotoxic drugs that a treating physician is most likely to encounter. In doing so, we will summarize risk factors for nephrotoxicity, describe clinical manifestations, and address preventive and treatment strategies.

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Section: Immunosuppressive Agents Calcineurin Inhibitorsmentioning

confidence: 99%

Drug-induced impairment of renal function

Pazhayattil¹,

Shirali²

2014

IJNRD

117

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“…The mechanism of glomerular injury may be secondary to direct cellular toxicity of lithium, resulting in minimal change disease or secondary focal segmental glomerulosclerosis 6 . In minimal change disease, some patients recover after lithium withdrawal, suggesting a strong etiologic relationship 23 .…”

Section: Lithium-induced Nephropathymentioning

confidence: 99%

“…Thus, accumulation of lithium in cells of the distal nephron via ENaC could account for chronic tubulointerstitial damage 7 . Tam et al 23 proposed that the modulation of the phosphoinositol pathway may also play a role in the pathogenesis of minimal change disease after lithium treatment.…”

Section: Pathogenesis Of Lithium-induced Nephropathymentioning

confidence: 99%

Nefrotoxicidade por lítio

Oliveira¹,

Júnior²,

Abreu³

et al. 2010

Rev. Assoc. Med. Bras.

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Lithium has been widely used in the treatment of bipolar disorder. Its renal toxicity includes impaired urinary concentrating ability and natriuresis, renal tubular acidosis, tubulointerstitial nephritis progressing to chronic kidney disease and hypercalcemia. The most common adverse effect is nephrogenic diabetes insipidus, which affects 20-40% of patients within weeks of lithium initiation. Chronic nephropathy correlates with duration of lithium therapy. Early detection of renal dysfunction should be achieved by rigorous monitoring of patients and close collaboration between psychiatrists and nephrologists. Recent experimental and clinical studies begin to clarify the mechanisms by which lithium induces changes in renal function. The aim of this study was to review the pathogenesis, clinical presentation, histopathological aspects and treatment of lithium-induced nephrotoxicity.

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“…Su administración ha sido vinculada a diversos efectos adversos a nivel renal: diabetes insípida nefrogénica (el más frecuente), toxicidad aguda (con poliuria y acidosis tubular), nefropatía túbulo-intersticial crónica (con deterioro progresivo del filtrado glomerular), y lesión glomerular directa [1][2][3] . La aparición de un síndrome nefrótico (SN) supone una complicación más infrecuente, con una primera descripción en la literatura en 1973 [3][4][5][6][7][8][9][10][11][12][13] . Su sustrato morfológico es variable, como demuestra una revisión de los 19 casos publicados anteriormente a 1997, con predominio de la enfermedad por mínimos cambios 3,4,7-9,11 y, en menor medida, glomeruloesclerosis focal y segmentaria 6,10 .…”

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“…Su evolución hacia un SN secundario a lesión glomerular resulta más infrecuente, si bien dicha complicación aparece bien documentada en la literatura, en la que se describe la rápida desaparición de la proteinuria tras la interrupción del tratamiento 5,9 y su recidiva en una segunda exposición 4,13 . El mecanismo íntimo de esta asociación permanece mal caracterizado, habiéndo-se sugerido en la patogenia de la enfermedad por míni-mos cambios un fenómeno de lesión podocitaria directa mediada por linfocitos T y citoquinas (interleuquina 2 y factor de necrosis tumoral α) 3,5,8 . También se ha invocado la posible interacción entre este catión y la carga aniónica de la membrana basal glomerular, resultando en un aumento de su permeabilidad a determinadas macromoléculas como las proteínas plasmáticas.…”

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