Moffitt AM report PEARLS 9/14: lithium renal toxicity + more!

ADDENDUM: check out just how complicated myoclonus is with the attached article (thanks HH!). Beautiful flow diagram! Myoclonus review

Take-home point: patients on lithium can develop nephrogenic diabetes insipidus AND chronic interstitial nephritis (and, in my quick post-report search, also CKD and nephrotic syndrome! More below). Oftentimes, patients’ nephrogenic DI does not manifest in the community but becomes more apparent in the hospital setting because they are relatively more dehydrated.

Bonus take-home point from HH: myoclonus in neurology is like an LDH in medicine. There is a very broad ddx!!

Other PEARLS from the morning:

  • More on renal toxicity of lithium (ref: great UpToDate article on “renal toxicity of lithium”)
    • Chronic lithium use is a/w nephrogenic DI and less frequently, chronic tubulointerstitial nephropathy
    • ~20-40% of patients taking lithium chronically develop polyuria and polydipsia!
      • *Important to do water deprivation test (see below) to confirm central vs nephrogenic DI b/c pts with bipolar can get central DI!
    • Also a/w insidious onset of CKD in 15-20% of pts (related to chronic interstitial nephritis). This can occasionally lead to ESRD!
    • Infrequently, can be a/w distal RTA, nephrotic syndrome
    • Ref: great uptodate article: “Renal toxicity of lithium”!
  • Diagnosing DI:
    • Hyponatremia + low urine osm (<200) = primary polydipsia
    • Hypernatremia + low urine osm (<200) = DI, but consider confirming with water restriction test
    • Normal Na + urine osm >600 = excludes DI
    • Central vs nephrogenic: perform water restriction test! Measure urine osm hourly, and when 2-3 samples vary by <30 osm, give ADH, then recheck urine osm. If it IMPROVES, then dx is central DI. If no improvement, then dx is nephrogenic DI.
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