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Gitelman syndrome (GS) is an autosomal recessive kidney tubule disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. [2] It is the most frequent hereditary salt-losing tubulopathy. Gitelman syndrome is caused by disease-causing variants on both alleles of the ...
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 ...
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]
Acute tubular necrosis is classified as a "renal" (i.e. not pre-renal or post-renal) cause of acute kidney injury. Diagnosis is made by a FENa (fractional excretion of sodium) > 3% and presence of muddy casts (a type of granular cast) in urinalysis.
This leads to the formation of several covalent bonds between caseinate anions, which can ultimately cause the cross-linked caseinate to form pockets of hydrophobic regions. [5] Calcium caseinate forms visco-elastic suspensions which increase remarkably when increasing concentration (50–300 g L−1) and decreasing temperature(10–50 °C). [4]
Additionally, hypercalciuria can contribute to kidney stone formation which may present with flank or back pain that comes and goes. It can be painful to pass kidney stones and in extreme cases cause kidney damage. [2] [3] Patients that both form kidney stones and have hypercalciuria are at increased risk for bone loss leading to osteoporosis. [4]
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