It is a potassium loss nephropathy caused by chronic hypokalemia. The main causes of hypokalemia are insufficient potassium intake, excessive potassium loss (gastrointestinal and urinary losses), application of various diuretics and steroid hormones, chronic renal diseases such as renal tubular acidosis, Bartter’s syndrome, Liddle’s syndrome, renin-secreting tumor, Cushing’s syndrome and hydroxylase deficiency diseases. The common clinical causes of hypokalemia are: 1. Non-nephrogenic hypokalemia: the renal potassium excretion does not increase, but increased cellular potassium uptake due to various reasons is also a common cause of hypokalemia. Hypokalemia caused by increased cellular potassium uptake is mostly temporary and in most cases does not require special treatment. Hypokalemic periodic paralysis is a rare autosomal dominant disorder in which hypokalemic muscle weakness occurs suddenly, often with a potassium level below 3 mmol/L. The cause of this disease is not fully understood, but acetazolamide is effective in improving muscle weakness. Some patients with hyperthyroidism may also present with periodic paralysis and may have a temporary decrease in potassium. However, the etiology may not be identical and acetazolamide is not effective, whereas beta-blockers can significantly improve the symptoms of muscle weakness. In addition, insufficient potassium uptake or intestinal potassium loss due to acute or chronic diarrhea are the main causes of non-nephrogenic hypokalemia. 2. Nephrogenic hypokalemia: Increased urinary potassium excretion due to various causes is the main cause of hypokalemia, which is collectively referred to as nephrogenic hypokalemia. In addition to the manifestations of hypokalemia, patients often have metabolic acidosis or metabolic alkalosis. Most patients with hypokalemia with metabolic acidosis have normal blood pressure, while most patients with hypokalemia with metabolic alkalosis may have hypertension. (1) Hypokalemia with acidosis: Because hypokalemia compensates for the increase in plasma bicarbonate concentration, most patients have a tendency to be alkalotic. This is because hypokalemia with acidosis is only seen in renal tubular acidosis, both proximal and distal tubular, and diabetic ketoacidosis. Diabetic ketoacidosis is accompanied by a significant decrease in total body potassium due to the osmotic diuretic effect caused by hyperglycemia and the excretion of large amounts of negatively charged ketone bodies from the urine promoting the excretion of urinary potassium. However, in the early stages of acidosis, hypokalemia may not be obvious due to the redistribution of intracellular and extracellular potassium. If insulin and alkaline medications are not supplemented with potassium, it can cause severe or even fatal hypokalemia. (2) Hypokalemia with normal blood pH or metabolic alkalosis: (1) Primary aldosteronism: Increased serum aldosterone level, which leads to a significant increase in sodium ions entering the distal tubule and an increase in urinary potassium excretion due to sodium-potassium exchange. In addition to increased blood aldosterone levels and hypokalemia, patients also have clinical manifestations of hypertension and metabolic alkalosis, while plasma renin activity is mostly decreased. Since hypokalemia can feedback inhibit aldosterone secretion from the adrenal cortex, patients with severe hypokalemia do not have a corresponding increase in serum aldosterone levels. Serum aldosterone should be less than 110.96 nmol/L (4 ng/dl) after saline or fludrocortisone infusion in normal subjects or in patients with other causes of hypertension, and unsuppressed serum aldosterone levels are helpful in the diagnosis of this disease. Adrenal tumors must be treated surgically because of high aldosterone levels and significant hypokalemia. In adrenal hyperplasia, anti-aldosterone therapy with spironolactone can be used first. In most patients, hypokalemia and hypertension can be corrected. Some patients with aldosteronism have increased urinary concentrations of 18-hydroxy and 18-oxycortisone and a positive dexamethasone suppression test, a rare autosomal dominant disorder. The administration of thiazide diuretics in these patients can cause extremely severe hypokalemia, and a small dose of dexamethasone (0.75 mg) is effective in correcting hypokalemia and lowering blood aldosterone. (2) Secondary aldosteronism: This disease is often associated with renal vascular disease, such as renal artery stenosis, renal vasculitis, etc. It can also manifest clinically as hypokalemic alkalosis and hypertension. However, it should be noted that not all secondary aldosteronism is associated with hypokalemia. Robertson-Kihara syndrome is a rare tumor of the paraglomerular apparatus that secretes renin secondary to aldosteronism, and is associated with hypokalemia and hypertension. Some extra-renal malignant tumors can also cause aldosteronism, but the increase in serum levels of inactive renin is the main cause. (③) Congenital salicortinotropic syndrome: The congenital 11β-hydroxysteroid dehydrogenase (11β-OHSD) activity is low, thus blocking the conversion of cortisol to inactive hydroxycortisol in the kidney, resulting in a large amount of cortisol binding to and activating the salicortin receptor, exerting salicortin-like effects, with clinical manifestations of increased aldosterone. Drugs such as licorice, cottonseed phenol, and sodium glycopyrrolate also inhibit 11β-OHSD, resulting in clinical manifestations of increased salt corticosteroids. There have been reports in the literature of hypersalivation caused by the ingestion of foods or drugs containing licorice.