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Renal glycosuria is a rare condition in which the simple sugar glucose is excreted in the urine [1] despite normal or low blood glucose levels. With normal kidney (renal) function, glucose is excreted in the urine only when there are abnormally elevated levels of glucose in the blood.
This point is called the renal threshold for glucose (RTG). [5] Some people, especially children and pregnant women, may have a low RTG (less than ~7 mmol/L [5] glucose in blood to have glucosuria). If the RTG is so low that even normal blood glucose levels produce the condition, it is referred to as renal glycosuria.
Renal glucose reabsorption is the part of kidney (renal) physiology that deals with the retrieval of filtered glucose, preventing it from disappearing from the body through the urine. If glucose is not reabsorbed by the kidney, it appears in the urine, in a condition known as glycosuria. This is associated with diabetes mellitus. [1]
Nephrocalcinosis, renal failure, ocular/hearing defects, polyruria, polydipsia, recurrent urinary tract infections, recurrent renal colic, normotensive Plasma: ↓Mg, ↑PTH; Urine: ↑Ca, ↑Mg Distal Tubule / Collecting Duct
Fanconi syndrome or Fanconi's syndrome (English: / f ɑː n ˈ k oʊ n i /, / f æ n-/) is a syndrome of inadequate reabsorption in the proximal renal tubules [1] of the kidney.The syndrome can be caused by various underlying congenital or acquired diseases, by toxicity (for example, from toxic heavy metals), or by adverse drug reactions. [2]
Diabetic nephropathy is the most common cause of end-stage renal disease and is a serious complication that affects approximately one quarter of adults with diabetes in the United States. [ 13 ] [ 14 ] Affected individuals with end-stage kidney disease often require hemodialysis and eventually kidney transplantation to replace the failed kidney ...
Dent's disease (or Dent disease) is a rare X-linked recessive inherited condition that affects the proximal renal tubules [1] of the kidney.It is one cause of Fanconi syndrome, and is characterized by tubular proteinuria, excess calcium in the urine, formation of calcium kidney stones, nephrocalcinosis, and chronic kidney failure.
Metabolic abnormalities such as diabetes, renal glycosuria, or glycogen storage disease. Dietary conditions such as starvation, fasting, low-carbohydrate diets, prolonged vomiting, and anorexia including caused by hyperemesis gravidarum. Conditions in which metabolism is increased, such as hyperthyroidism, fever, pregnancy or lactation.
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