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Discussion This patient presented with muscle weakness and her laboratory reports showed hypokalemia and metabolic alkalosis with normal blood pressure. Her urinary chloride levels were above 20 mEq/L, which ruled out extra-renal causes of metabolic alkalosis. She did not give any history of diuretic use. The presence of hypomagnesemia and absence of hypercalciuria (urinary calcium creatinine ratio Alpelisib purchase hypomagnesemia, absence of hypercalciuria in background of no history of diuretic use favored the diagnosis of Gitelman syndrome. Her clinical and laboratory data suggested presence of SS as well. Tubular involvement in SS is usually distal tubular dysfunction, type I (distal) renal tubular acidosis and nephrogenic diabetes insipidus. Proximal tubular abnormalities are less frequent, and rarely Fanconi's syndrome has been reported in patients with SS.[2,3] Gitelman ADAMTS12 syndrome is usually an inherited disorder. Acquired Gitelman syndrome is relatively rare. To the best of our knowledge, only five cases of acquired Gitelman syndrome have been reported in English literature so far. Among these five cases, four had SS, one was a case of chronic sialoadenitis.[4,5,6,7,8] Acquired Gitelman syndrome secondary to SS presenting with hypokalemic weakness is very rare. Only two cases have been reported so far.[5,7] Though Gitelman syndrome is an inherited disorder, it can be acquired in patients with autoimmune disorders. Given the paucity of reports, we believe that SS presenting as acquired Gitelman syndrome may be relatively rare. Acquired Gitelman syndrome should be considered in differential diagnosis of renal involvement in patients with SS. Footnotes Source of Support: Nil Conflict of Interest: The results presented in this paper have not been published previously in whole or part, except in abstract format.""Multiple myeloma is the second most common form of hematological malignancy after Selleckchem SB431542 non-Hodgkin lymphoma and represents the hematological disease most often associated with acute kidney injury.[1] Comparable to chronic kidney disease (CKD), it increases with age with a male preponderance. Diagnosis is based on the presence of excessive monoclonal plasma cells in bone marrow, monoclonal immunoglobulins or light chains in serum or urine and related organ or tissue damage such as renal insufficiency, anemia, lytic bone lesions or cardiac and neurological involvement. About 18% of patients present light chain multiple myeloma (LCMM). One major cause of renal damage in LCMM is glomerular filtration of immunoglobulin light chains with subsequent overflow proteinuria. The combination of large amounts of monoclonal light chains reabsorbed via the tubules and their unique physicochemical characteristics are responsible for progressive renal damage due to cast nephropathy.