Bicarbonate renal control

Nephrotoxin administration (e.g., radiocontrast dye) should be avoided whenever possible. When patients require contrast dye and are at risk of contrast dye-induced nephropathy, renal perfusion should be maximized through strategies such as assuring adequate hydration with normal saline or sodium bicarbonate solutions and administration of oral acetylcysteine 600 mg every 12 hours for four doses. Strict glycemic control with insulin in diabetics has also reduced the development of ARF. 

Metabolic acidosis In severe renal disease uncontrolled diabetes circulatory insufficiency due to shock, anoxia, or severe dehydration extracorporeal circulation of blood cardiac arrest and severe primary lactic acidosis where a rapid increase in plasma total CO2 content is crucial. Treat metabolic acidosis in addition to measures designed to control the cause of the acidosis. Because an appreciable time interval may elapse before all ancillary effects occur, bicarbonate therapy is indicated to minimize risks inherent to acidosis itself. 

The bicarbonate ion (HCO3A is the second-largest anionic contributor to maintaining acid-base balance, and its secretion from the pancreas helps to neutralize the contents of the small intestine. Respiration controlling the carbon dioxide concentration of the blood (PaCOj) and renal excretion of bicarbonate are the two main homeostatic influences on plasma bicarbonate. Within the renal tubular lumen, carbonic anhydrase converts carbonic acid into carbon dioxide, which diffuses into the epithelial cells and forms carbonic acid, which later dissociates to bicarbonate. 

The renal system is another major regulator of pH balance. The kidneys can control pH by secreting H+ from the body or retaining it to reverse an acidosis or alkalosis. The renal mechanism can correct an acidosis by reabsorbing CO, which then combines with water to form carbonic acid and bicarbonate, which is released into the bloodstream, and H+, as noted earlier in the carbonic acid-bicarbonate buffer system. The renal system can can correct alkalosis by excreting the CO, resulting in less bicarbonate formation. 

All the available evidence for the use of topiramate as monotherapy in patients with newly or recently diagnosed epilepsy has been examined in a systematic review of three randomized, double-bUnd, controlled trials which recruited more than 1000 patients [302 ]. The most common adverse events associated with topiramate 50-500 mg/day generally occurred early in the course of treatment and were nervous system-related effects headache (15-25%), dizziness (12-19%), fatigue (11-23%), somnolence (10-17%), anorexia (8-10%), insomnia (7—10%), and hyperesthesia (5— 10%). Adverse events that were likely to have been related to the carbonic-anhy-drase activity of topiramate (e.g. paresthesia, changes in serum bicarbonate) were frequent (13-35%) but were not usually considered clinically relevant Renal calculi occurred infrequently (1%). The most frequent adverse events during maintenance therapy were headache (20%), reduced appetite (11%), and weight loss (11%). 

These renal mechanisms are described in more detail in Chapter 7. They are components of control mechanisms, providing the means for lowering or raising the plasma bicarbonate concentration as a compensation for disturbances of the hydrogen ion concentration, as described in Chapter 3. 

Diabetics and patients with borderline renal function should be prehydrated to reduce the chances of contrast-induced nephropathy. A recent randomized controlled trial suggested that prehydration with sodium bicarbonate is more effective than sodium chloride in preventing contrast-induced renal failure [8]. For those patients with contrast allergies, prophy-... 

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