Lower limb or circumferential flaccidity is a symptom in the water and salt metabolism disorder type of Barth syndrome, which is a common disease that easily affects people’s daily life and even leads to a decrease in their resistance, so how to check for lower limb or circumferential flaccidity? The following is an introduction to the examination of lower limb or peripheral flaccid palsy. The examination methods of lower limb or circumferential weakness 1, there is significant hypokalemia, generally below 2.5mmol/l, the lowest can be as low as 1.5mmol/l. Metabolic alkalosis is also a common manifestation, blood hco3- increased (28 to 45mmol/l), blood h+ value by the metabolic mechanism, hypokalemia or renal insufficiency and increased or normal, there can also be hyponatremia or hypochlorhydria, infants and children Hypochlorhydria and alkalosis are most severe, with blood chlorine as low as (62±9) mmol/l. Hyperreninemia, hyperaldosteronism, and insensitivity to angiotensin and pressor are also features of laboratory tests in this disease. 2, blood urine prostaglandin increased, bradykinin and renal vasopressin excretion increased, urine is hypotonic, ph is alkaline kidney concentration dilution function is often reduced, about 30% of patients have proteinuria, some patients have hyperalgesia. Some patients can also appear high blood calcium low blood phosphorus, low blood magnesium increased intra-erythrocyte sodium concentration and sodium outflow is reduced, occasionally hypercalciuria. 3, renal biopsy can be seen in membrane proliferative glomerulonephritis, interstitial nephritis, renal calcification and other pathological changes. Proliferation and hypertrophy of the glomerular parietal organ is the main pathological abnormality of the disease from these cells all signs of increased renin synthesis can be seen. Electron microscopy reveals hypertrophy of the rough endoplasmic reticulum and Golgi complex probably for renin deposition and increased renin synthesis. 4, Immunocytochemistry has confirmed the atrophy of dense spot cells and abnormal structure of apparently flattened dense spots caused by abnormal renin secretion due to the inability of feedback regulation. Glomerular thylakoid cells proliferate and form periglomerular fibrosis, especially the small arteries and tiny arterial smooth muscle cells are replaced by glomerular collateral cells, and the thickening and sclerosis of small renal arteries reduce the perfusion of the inlet arteries, which in turn can lead to an increase in renin secretion, which in turn acts on vascular smooth muscle to cause vasoconstriction, tubular atrophy and vacuole formation, and mesangial cell proliferation can be seen in the renal medulla, but can rapidly disappear after potassium supplementation. However, it disappears rapidly after potassium supplementation.