Renal tubular acidosis is a dysfunction of the tubular acidification of urine in renal tubular lesions, which means that the acid cannot be secreted by the tubules and excreted with the urine, and therefore accumulates in the blood and causes acidosis. The etiology of renal tubular acidosis is not fully understood, but many cases are due to autoimmune diseases. Autoimmune processes occurring in the renal tubules can impair renal tubular function and therefore lead to dysfunction of the tubular acidification of urine. Hyperthyroidism (diffuse goiter with hyperthyroidism) is an autoimmune disease and may have autoimmune lesions not only in the thyroid but also in the renal tubules. Therefore, hyperthyroidism and renal tubular acidosis can coexist. In our clinical work, we have found such cases where renal tubular acidosis was reduced after hyperthyroidism was controlled, thus suggesting a close relationship between renal tubular acidosis and hyperthyroidism. However, the causal relationship between the two diseases cannot be confirmed yet, and perhaps the two diseases are manifestations of two aspects of autoimmune diseases. The main clinical manifestations of renal tubular acidosis are: symptoms related to hypokalemia, such as weakness and limb paralysis, etc.; symptoms related to surgery inability to poison, such as nausea and loss of appetite, etc.; symptoms related to bone decalcification, such as bone pain and bone deformation, etc. Laboratory tests revealed hypokalemia, blood poisoning (decrease in blood pH), hypocalcemia, and alkaline urine (increase in urine pH). x-ray examination revealed decreased bone density.