Quiz Page August 2011

Baig, Abdur; Adewale, Adebayo; Borra, Sonia

doi:10.1053/j.ajkd.2011.04.016

Cited by 4 publications

(3 citation statements)

References 13 publications

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“…There are no clear guidelines about when and how to stop the prescription. While not in this case, the beneficial renal effect of discontinuing lithium is observed mainly in patients with moderate chronic kidney disease (creatinine clearance >40 mL/min) (Baig et al 2011 ; McKnight et al 2012 ). Moreover, recent research from a Swedish renal registry suggests that more modern treatment principles of lithium maintenance (i.e., serum levels 0.5 to 0.8 mmol/L vs. 0.8 to 1.2 mmol/L, regular and frequent renal function monitoring) may have reduced this lithium-associated renal event (Aiff et al 2014 ).…”

Section: Correspondencementioning

confidence: 92%

“…Lithium has an acute (nephrogenic diabetes insipidus) and chronic (interstitial fibrosis, segmental glomerulosclerosis, and/or tubulointerstitial changes associated with renal insufficiency) effect on the kidney (Baig et al 2011 ; Bassilios et al 2008 ; Grunfeld and Rossier 2009 ). Lithium interferes with thyroid metabolism and increases the incidence of overt and subclinical hypothyroidism and may cause hyperparathyroidism with a high incidence of multiglandular disease (Hundley et al 2005 ; Kleiner et al 1999 ).…”

Section: Correspondencementioning

confidence: 99%

“…The risk/benefit of end organ toxicity/mood stability must be evaluated in each individual case. Up to 40% of the patients who received long-term lithium experienced nephrogenic diabetes insipidus; whereas the risk of end-stage renal failure is greater than in healthy controls, the absolute risk is low approximately 0.5% (Baig et al 2011 ; McKnight et al 2012 ). The benefit of discontinuing lithium once the kidney begins to fail is a controversial decision.…”

Section: Correspondencementioning

confidence: 99%

See 2 more Smart Citations

Every reason to discontinue lithium

Salgado

Sutor

Albright

et al. 2014

Int J Bipolar Disord

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Lithium as a gold standard therapy for bipolar disorder is well known to have a number of medical comorbidities that impact renal, parathyroid, and thyroid function. Despite these medical comorbidities, there remains a group of lithium-responsive lithium-treated patients who have maintained mood stability for decades. The risk/benefit ratio of end organ toxicity/mood stability must be evaluated in each individual case.

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Section: Correspondencementioning

confidence: 92%

Section: Correspondencementioning

confidence: 99%

Section: Correspondencementioning

confidence: 99%

See 1 more Smart Citation

Every reason to discontinue lithium

Salgado

Sutor

Albright

et al. 2014

Int J Bipolar Disord

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Lithium toxicity and the kidney with special focus on nephrotic syndrome associated with the acute kidney injury: A case‐based systematic analysis

Łukawska

Frankiewicz²,

Izak

et al. 2021

J of Applied Toxicology

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Despite the progress made in treating bipolar and unipolar affective disorders, lithium carbonate is still a common drug in psychiatric practice. Lithium‐related renal side effects include nephrogenic diabetes insipidus, chronic tubulointerstitial nephropathy, and acute kidney injury (AKI). Nephrotic syndrome (NS) is an uncommon but severe complication of lithium treatment. We present a 49‐year‐old female treated with lithium carbonate due to a recurrent depressive disorder who developed NS during this therapy. NS spontaneously remitted after the drug withdrawal. Since her lithium serum levels were within the recommended values, we performed a retrospective analysis of lithium‐induced NS cases trying to determine causes predisposing to the NS development, underlying histopathology, and preservation or irreversible loss of kidney function. This analysis revealed that in lithium‐induced NS with AKI, lithium serum level was the key determinant of AKI development (the β coefficient = 0.8499 with a confidence interval ranging from 0.7452 to 0.9546 and p value < 0.0001). In these cases, the underlying pathology was mainly minimal change disease (MCD), which was quickly reversible upon the drug withdrawal. The development of chronic kidney disease (CKD) seemed to be associated with lithium therapy duration. However, the multiple regression analysis for CKD as the dependent variable showed that the decisive factor was focal segmental glomerulosclerosis (FSGS) as the underlying pathology (the β coefficient = 0.7866 with a confidence interval ranging from 0.600 to 0.9704 and the p value < 0.0001). Thus, we conclude that in lithium‐induced NS/AKI, serum lithium levels contribute to these complications, while FSGS lesions are responsible for CKD's disease progression.

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