Glucosuria: Diabetes Mellitus

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1 172 PHYSIOLOGY CASES AND PROBLEMS Case 30 Glucosuria: Diabetes Mellitus David Mandel was diagnosed with type I (insulin-dependent) diabetes mellitus when he was 12 years old, right after he started middle school. David was an excellent student, particularly in math and science, and had many friends, most of whom he had known since nursery school. Then, at a sleepover party, the unimaginable happened: David wet his sleeping bag! He might not have told his parents if he had not been worried about other symptoms he was experiencing. He was constantly thirsty (drinking a total of 3-4 quarts of liquids daily) and was urinating every minutes. (The night of the accident, he had already been to the bathroom four times.) Furthermore, despite a voracious appetite, he seemed to be losing weight. David's parents panicked: they had heard that these were classic symptoms of diabetes mellitus. A urine dipstick test was positive for glucose, and David was immediately seen by his pediatrician. Table 4-4 shows the findings on physical examination and the results of laboratory tests. TABLE 4-4 David's Physical Examination Findings and Laboratory Values Height Weight Blood pressure Fasting plasma glucose Plasma Na. Urine glucose Urine ketones Urine Na* 5 feet, 3 inches 100 lb (115 lb at his annual checkup 2 months earlier) 90/55 (lying) 75/45 (standing) 320 mg/dl (normal, mg/dl) 143 meq/l (normal, 140 meq/l) 4+ (normal, none) 2+ (normal, none) Increased In addition, David had decreased skin turgor, sunken eyes, and a dry mouth. All of the physical findings and laboratory results were consistent with type I diabetes mellitus. David's pancreatic beta cells had stopped secreting insulin (perhaps secondary to autoimmune destruction after a viral infection). His insulin deficiency caused hyperglycemia (an increase in blood glucose concentration) through two effects: (1) increased hepatic gluconeogenesis and (2) inhibition of glucose uptake and utilization by his cells. Insulin deficiency also increased lipolysis and hepatic ketogenesis. The resulting ketoacids (acetoacetic acid and (3-0H butyric acid) were excreted in David's urine (urinary ketones). David immediately started taking injectable insulin and learned how to monitor his blood glucose level. In high school, he excelled academically and served as captain of the wrestling team and as class president. Based on his extraordinary record, he won a full scholarship to the state university, where he is currently a premedical student and is planning a career in pediatric endocrinology. rin QUESTIONS 1. How is glucose normally handled in the nephron? (Discuss filtration, reabsorption, and excretion of glucose.) What transporters are involved in the reabsorption process?

2 RENAL AND ACID-BASE PHYSIOLOGY At the time of the diagnosis, David's blood sugar level was significantly elevated (320 mg/dl). Use Figure 4-3, which shows a glucose titration curve, to explain why David was excreting glucose in his urine (glucosuria). Does the fact that David was excreting glucose in his urine indicate a defect in his renal threshold for glucose, in his transport maximum (T m) for glucose, or in neither? E E o o 8 2 t, U x Plasma [glucose) (mg/dl) Figure 4-3 Glucose titration curve. Glucose filtration, excretion, and reabsorption are shown as a function of plasma glucose concentration. Shaded areas indicate the "splay." T transport maximum. (Reprinted with permission from Costanzo LS: RRS Physiology, 3rd ed. Baltimore, Lippincott Williams & Wilkins, 2003, p 172.) 3. David's glucosuria abated after he started receiving insulin injections. Why? 4. Why was David polyuric (increased urine production)? Why was his urinary Na' excretion elevated? 5. Plasma osmolarity (mosm/l) can be estimated from the plasma Na* concentration (in meq/l), the plasma glucose (in mg/dl), and the blood urea nitrogen (BUN, in mg/dl), as follows: Plasma omolarity a 2 x plasma [Nal + glucose + BUN Why does this formula give a reasonable estimate of plasma osmolarity? Use the formula to estimate David's plasma osmolarity (assuming that his BUN is normal at 10 mg/dl). Is David's plasma osmolarity normal, increased, or decreased compared with normal? 6. Why was David constantly thirsty? 7. Why was David's blood pressure lower than normal? Why did his blood pressure decrease further when he stood up?

3 174 IPHYSIOLOGY CASES AND PROBLEMS ANSWERS AND EXPLANATIONS 1. The nephron handles glucose by a combination of filtration and reabsorption, as follows. Glucose is freely filtered across the glomendar capillaries. The filtered glucose is subsequently reabsorbed by epithelial cells that line the early renal proximal tubule (Figure 4-4). The luminal membrane of these early proximal tubule cells contains an Na +-glucose cotransporter that brings both Nola' and glucose from the lumen of the nephron into the cell. The cotransporter is energized by the Na' gradient across the cell membrane (secondary active transport). Once glucose is inside the cell, it is transported across the basolateral membranes into the blood by facilitated diffusion. At a normal blood glucose concentration (and normal filtered load of glucose), all of the filtered glucose is reabsorbed, and none is excreted in the urine. Lumen Cell of early proximal tubule Peritubular capillary blood Na+ Glucose Figure 4-4 Mechanism of glucose reabsorption in the early proximal tubule. 2. The glucose titration curve (see Figure 4-3) shows the relationship between plasma glucose concentration and rate of glucose reabsorption. Filtered load and excretion rate of glucose are shown on the same graph for comparison. By interpreting these three curves simultaneously, we can understand why David was "spilling" (excreting) glucose in his urine. The filtered load of glucose is the product of GFR and plasma glucose concentration. Therefore, as the plasma glucose concentration increases, the filtered load increases in a linear fashion. In contrast, the curves for reabsorption and excretion are not linear. (1) When the plasma glucose concentration is less than 200 mg/dl, all of the filtered glucose is reabsorbed because the Nay-glucose cotransporters are not yet saturated. In this range, reabsorption equals filtered load, and no glucose is "left over" to be excreted in the urine. (2) When the plasma glucose concentration is between 200 and 250 mg/dl, the reabsorption curve starts to "bend." At this point, the cotransporters are nearing saturation, and some of the filtered glucose escapes reabsorption and is excreted. The plasma glucose concentration at which glucose is first excreted in the urine (approximately 200 mg/dl) is called the threshold, or renal threshold. (3) At a plasma glucose concentration of 350 mg/dl, the cotransporters are fully saturated and the reabsorption rate

4 RENAL AND ACID-BASE PHYSIOLOGY 175 levels off at its maximal value (transport maximum, or Tm). Now the curve for excretion increases steeply, paralleling that for filtered load. You may be puzzled as to why any glucose is excreted in the urine before the transporters are completely saturated. Stated differently: Why does threshold occur at a lower plasma glucose concentration than does T, (called splay)? Splay has two explanations. (1) All nephrons don't have the same T. (i.e., there is nephron heterogeneity). Nephrons that have a lower T. excrete glucose in the urine before nephrons that have a higher T m. (Of course, the final urine is a mixture from all nephrons.) Therefore, glucose is excreted in the urine before the average T. of all of the nephrons is reached. (2) The affinity of the Ne-glucose cotransporter is low. Thus, approaching Tm, if a glucose molecule becomes detached from the carrier, it will likely be excreted in the urine, even though a few binding sites are available on the transporters. In healthy persons, the fasting plasma glucose concentration of mg/dl is below the threshold for glucose excretion. In other words, healthy fasting persons excrete no glucose in their urine because the plasma glucose concentration is low enough for all of the filtered glucose to be reabsorbed. Because of his insulin deficiency, David's fasting plasma glucose value was elevated (320 mg/dl); this value is well above the threshold for glucose excretion. His Na'-glucose cotransporters were nearing saturation, and any filtered glucose that escaped reabsorption was excreted in the urine (glucosuria). Now we can answer the question of whether David was "spilling" glucose in his urine because of a defect in his renal threshold (increased splay) or a defect in his Tm. The answer is: neither! David was spilling glucose in his urine simply because he was hyperglycemic. His elevated plasma glucose level resulted in an increased filtered load that exceeded the reabsorptive capacity of his Na--glucose cotransporters. 3. After treatment, David was no longer glucosuric because insulin decreased his plasma glucose concentration, and he was no longer hyperglycemic. With his plasma glucose level in the normal range, he could reabsorb all of the filtered glucose, and no glucose was left behind to be excreted in his urine. 4. David was polyuric (had increased urine production) because unreabsorbed glucose acts as an osmotic diuretic. The presence of unreabsorbed glucose in the tubular fluid draws Na and water osmotically from peritubular blood into the lumen. This back-flux of Na' and water (primarily in the proximal tubule) leads to increased excretion of Na* and water (diuresis and polyuria). 5. Osmolarity is the total concentration of solute particles in a solution (i.e., mosm/l). The expression shown in the question can be used to estimate plasma osmolarity from plasma Nat, glucose, and BUN because these are the major solutes (osmoles) of extracellular fluid and plasma. Multiplying the Na + concentration by two reflects the fact that Na + is balanced by an equal concentration of anions. (In plasma, these anions are Cl and HCO3.) The glucose concentration (in mg/dl) is converted to mosm/l when it is divided by 18. BUN (in mg/dl) is converted to mosm/l when it is divided by 2.8. David's estimated plasma osmolarity (P. ) is: glucose BUN Po,, = 2 x [Nal + = 2 x = = 307 mosm/l The normal value for plasma osmolarity is 290 mosm/l. At 307 mosm/l, David's osmolarity was significantly elevated.

5 176 PHYSIOLOGY CASES AND PROBLEMS 6. There are two likely reasons why David was constantly thirsty. (1) His plasma osmolarity, as calculated in the previous question, was elevated at 307 mosm/l (normal, 290 mosm/l). The reason for this elevation was hyperglycemia; the increased concentration of glucose in plasma caused an increase in the total solute concentration. The increased plasma osmolarity stimulated thirst and drinking behavior through osmoreceptors in the hypothalamus. (2) As discussed for Question 4, the presence of unreabsorbed glucose in the urine produced an osmotic diuresis, with increased Na' and water excretion. Increased Na- excretion led to decreased Na, content in the extracellular fluid (ECF) and decreased ECF volume (volume contraction). ECF volume contraction activates the renin-angiotensin II-aldosterone system. The increased levels of angiotensin II stimulate thirst. 7. David's arterial blood pressure was lower than that of a normal 12-year-old boy because osmotic diuresis caused ECF volume contraction. Decreases in ECF volume are associated with decreases in blood volume and blood pressure. Recall from cardiovascular physiology that decreases in blood volume lead to decreased venous return and decreased cardiac output, which decreases arterial pressure. Other signs of ECF volume contraction were his decreased tissue turgor and his dry mouth, which signify decreased interstitial fluid volume (a component of ECF). David's blood pressure decreased further when he stood up (orthostatic hypotension) because blood pooled in his lower extremities; venous return and cardiac output were further compromised, resulting in further lowering of arterial pressure. Key topics Diabetes mellitus type I Glucose titration curve Glucosuria Hyperglycemia Hypotension Orthostatic hypotension Osmoreceptors Plasma osmolarity Polydipsia Polyuria Reabsorption Splay Threshold Transport maximum (T,,) Volume contraction (extracellular fluid volume contraction)

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