Persistent nephrogenic diabetes insipidus, tubular proteinuria, aminoaciduria, and parathyroid hormone resistance following longterm lithium administration.
We report a patient who developed persistent nephrogenic diabetes insipidus associated with renal tubular acidosis, renal resistance to parathyroid hormone, aminoaciduria and proximal tubule pattern proteinuria in the presence of a reduced glomerular filtration rate (19-24 ml/min). A review of the previous reports of persistent nephrogenic diabetes insipidus revealed that in all patients the glomerular filtration rate had been less than 60 ml/min at presentation. Chronic renal failure may therefore predispose to the development of persistent nephrogenic diabetes insipidus in patients receiving lithium.
Neithercut
W D
WD
Department of Pathological Biochemistry, Western Infirmary, Glasgow, UK.
Spooner
R J
RJ
Hendry
A
A
Dagg
J H
JH
D000141:Acidosis, Renal Tubular / Q000139:chemically induced*; D001714:Bipolar Disorder / Q000188:drug therapy; D000242:Cyclic AMP / Q000652:urine; D003919:Diabetes Insipidus / Q000139:chemically induced*; D004351:Drug Resistance; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications; D008094:Lithium / Q000009:adverse effects*; D008875:Middle Aged; D009395:Nephritis, Interstitial / Q000139:chemically induced; D010281:Parathyroid Hormone / Q000494:pharmacology*; D011507:Proteinuria / Q000139:chemically induced*; D000608:Renal Aminoacidurias / Q000209:etiology
D010281:Parathyroid Hormone; D008094:Lithium; D000242:Cyclic AMP