Idiogenic osmols

Uremia results in increased permeability of the blood-brain barrier to sucrose and insulin K+ transport is enhanced whereas Na+ transport is impaired. There is an increase in brain osmolarity in acute renal failure due to the increase in urea concentrations. However, in contrast to acute renal failure, the increase in osmolarity in chronic renal failure results from the presence of idiogenic osmoles in addition to urea. CBF is increased in uremic patients but CMR02 and CMR are decreased. In the brains of rats with acute renal failure, ATP, phosphocreatine and glucose are increased whereas AMP, ADP and lactate are decreased, most probably as a result of decreased energy demands. 

Dehydration may result from primary water deficiency, usually because of decreased intake, but in some instances (e.g., diabetes insipidus) it may result from increased losses of water. In general, the term dehydration implies intracellular and interstitial fluid depletion, in contrast to volume depletion, which implies extracellular, and particularly intravascular, sodium and water loss. In the case of primary water deficit, cell dehydration occurs, with delayed circulatory failure from decreased circulatory volume with ongoing losses. Initially, the patient may be thirsty and possibly have some mental status changes, such as confusion. If the cellular dehydration occurs slowly, intracellular substances, referred to as idiogenic osmols, develop that firnit progressive comphcations (e.g., cerebral edema or coma). With combined water and salt deficiencies, such as might occur with gastrointestinal... 

Dialysis dysequilibrium is not seen often nowadays. It may occur in very uremic patients during the first dialysis, particularly with high-flux dialysis or very rapid blood flow. Its etiology is not clear, but is probably related to increased cerebrospinal fluid pressure and cerebral edema. The possible role of urea has already been discussed (see Section 3.1). Another hypothesis is that the brain cells of uremic patients produce idiogenic osmoles to prevent water loss to the hyperosmolar extracellular fluid. When high-flux dialysis rapidly decreases extracellular fluid osmolality, it may cause a water shift into the brain (B22). 

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