Risk Factor | Proposed Mechanism |
---|---|
Duration of lithium therapy | Prolonged lithium exposure leading to irreversible structural changes within the kidney parenchyma |
Age | Age related decline in eGFR, polypharmacy, medical comorbidity |
Lower initial eGFR | Reduced nephron mass, background tubulointerstitial damage |
Female gender | Unclear mechanism |
Cumulative lithium dose | Prolonged lithium exposure leading to irreversible structural changes within the kidney parenchyma |
Other concomitant CKD risks (hypertension, diabetes mellitus) | Concomitant tubulointerstitial damage, nephrosclerosis |
Concomitant use of nephrotoxic medications | Disruption of tubulo-glomerular feedback, volume contraction, drug-interactions |
Prior episodes of lithium toxicity | Higher lithium concentrations, induction of acute kidney injury with subsequent chronic damage |
NDI | Volume contraction leading to elevated lithium concentrations, may be surrogate marker for morphological changes occurring within the kidney tubules |