[k] Diabetes Mellitus; Glaucoma

THE KIDNEY

Diabetes Mellitus

A woman with insulin-dependent diabetes is given a ¦Â-adrenergic antagonist for treatment of hypertension.

1. If this woman was given an intravenous infusion of K+, what would you predict would happen to the plasma [K+]? Compare the response with a normal individual.

Intravenous infusion of K+ into a subject with a combination of sympathetic blockade and insulin deficiency would result in greater hyperkalemia than would a similar infusion of K+ in a normal subject. Although aldosterone secretion would be stimulated by the hyperkalemia, this hormone stimulates cell K+ uptake after a one-hour lag period. In this first hour after K+ infusion, less than 50% of the infused K+ is excreted by the kidneys. Because sympathetic activity and insulin release are suppressed, most of the K+ in the body will remain in the extracellular fluid.

Glaucoma and Carbonic Anhydrase Inhibitors

A 50-year-old woman with glaucoma is treated with the carbonic anhydrase inhibitor acetazolamide. 1. What effect would administration of acetazolamide have on urine HCO3- excretion, and by what mechanism? 2. What type of acid-base disorder could result from the use of this drug? Carbonic anhydrase plays a critical role in the reabsorption of [HCO3-] by the cells of the proximal tubule and by intercalated cells of the collecting duct. Inhibition of this enzyme would therefore inhibit the reabsorption of [HCO3-] at these nephron sites. Because of the large fraction of the filtered load of [HCO3-] reabsorbed by the proximal tubule, the effect at this site is quantitatively more important. With decreased reabsorption, more [HCO 3-] would be excreted in the urine, and urine pH would become alkaline. This loss of [HCO3-] from the body would result in the development of a metabolic acidosis.