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21 CASE 21


A 42-year-old woman experiencing peripheral edema is referred to the nephrologist for evaluation of renal function.


The patient was diagnosed with type 1 diabetes mellitus at the age of 12 and has been managing her blood glucose with three daily injections of insulin. Over the past 5 years, the blood glucose has not been as well managed, and 2 years ago urinalysis showed microalbuminuria.






PATHOPHYSIOLOGY OF KEY SYMPTOMS


The hormone insulin stimulates glucose uptake by a number of tissues, especially skeletal muscle and adipose. Diabetes mellitus is a chronic disease characterized by impaired uptake of glucose by the tissues. The disease can be caused either by a deficiency in insulin production or by the loss of tissue responsiveness to insulin. In either case the underlying cause of diabetic neuropathy is the elevated blood glucose levels characteristic of diabetes.


Glucose is a relatively small molecule that is freely filtered at the renal glomerulus. The filtered glucose load, or tubular glucose load, is the product of the glomerular filtration rate (GFR) × plasma glucose concentration. Once filtered, glucose is reabsorbed by the sodium-coupled transport mechanism (secondary active transport) in the proximal tubule.


The renal glucose transport capacity is determined by the number of transport protein molecules. The maximum glucose transport capacity is about twice as high as the normal filtered load of glucose. Consequently, glucose is not normally excreted in the urine. When the filtered load exceeds the glucose reabsorption, some glucose remains in the tubular filtrate and ultimately is excreted in the urine. For most individuals, the glucose renal threshold occurs when plasma glucose levels exceed 250 mg/dL (Fig. 21-1).


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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 21

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