Differential diagnosis: Renal glycosuria should be differentiated from: (1)
Diabetes mellitus (by glucose tolerance curve); (2) Fanconi's syndrome
(multiple tubular defects not isolated glycosuria); (3) Glucose-Galactose
malabsorption (combined renal and jejunal defect); (4) Gluco-glycinuria;
and (5) phosphate diabetes.
Treatment: No treatment is required.
Renal Tubular Acidosis (RTA)
Is a systemic metabolic acidosis resulting from specific tubular
abnormality in handling of H+. Usually the patient presents with metabolic
acidosis out of proportion to the renal functional impairment. There are
four types of RTA; distal (classic, type I) , proximal (type II) , type III
(distal with bicarbonate wastage), and type IV (hyperkalaemic,
hyporeninaemic, hypoaldosteronaemic).
Distal (classic) RTA
The normal daily production of hydrogen ions (H+) is
approximately 1mmol/kg/d in adults and 3 mmol/kg/d in children. This H+
load is excreted by the kidney, through distal nephron. Failure to secrete
this hydrogen load will result in metabolic acidosis. Normally, there is a
pump mechanism in the distal convoluted tubules pushing H+ to the lumen
(urine). In distal RTA, there is a reduced pump activity or there is back
diffusion of H+ (from lumen to tubular cells and systemic circulation)
resulting in systemic acidosis.
Normally, with systemic accumulation of hydrogen ions the kidney
will secrete these H+ to the urine which will be acidified to a urine pH of
5.2 or less. In distal RTA, this is not possible and urine pH is always above
5.7 even with severe metabolic acidosis.