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In the early stages of the disease, this can result in mild symptoms such as reduced appetite or feelings of fatigue, but as CKD progresses, "complications like high blood pressure, heart disease ...
A small proportion of individuals with analgesic nephropathy may develop end-stage kidney disease. Analgesic nephropathy was once a common cause of kidney injury and end-stage kidney disease in parts of Europe, Australia, and the United States. In most areas, its incidence has declined sharply since the use of phenacetin fell in the 1970s and ...
Milk-alkali syndrome is an illness that is characterized by hypercalcaemia, kidney damage, and metabolic alkalosis. [17] This syndrome was discovered in the early 1900s when people began experiencing adverse effects from Bertrand Sippy's gastric ulcer treatment consisting of milk and alkali.
It is typically caused by kidney failure or is treatment-induced such as from antacids or supplements that contain magnesium. [1] [6] Less common causes include tumor lysis syndrome, seizures, and prolonged ischemia. [2] Diagnosis is based on a blood level of magnesium greater than 1.1 mmol/L (2.6 mg/dL).
Drug-induced glomerular disease is not common but there are a few drugs that have been implicated. Glomerular lesions occur primarily through immune-mediated pathways rather than through direct drug toxicity. Heroin and Pamidronate are known to cause focal segmental glomerulosclerosis; Gold salts therapy can cause membranous nephropathy [4 ...
Very low levels of azotemia may produce few, if any, symptoms. If the disease progresses, symptoms become noticeable (if the failure is of sufficient degree to cause symptoms). Kidney failure accompanied by noticeable symptoms is termed uraemia. [18] Symptoms of kidney failure include the following: [18] [19] [20] [21]
Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate (HCO − 3), or alternatively a direct result of increased bicarbonate concentrations.
Some antacids also inhibit pepsin, an enzyme that can damage the esophagus in acid reflux. [2] [13] Antacids do not directly inhibit acid secretion, and thus are distinct from acid-reducing drugs like H 2-receptor antagonists or proton pump inhibitors. [4] Antacids do not kill the bacteria Helicobacter pylori, which causes most ulcers. [4]
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