Chronic acidification

Regulation of NHE3 involves many hormonal and physical mechanisms. Acutely, NHE3 activity is promoted by an increase in intracellular pH and this response is rapid. Furthermore, the increase in activity is proportional to the duration of acidification. Chronic acidification promotes recycling of NHE3 from subapi-cal endosomes to the plasma membrane. 

The Critical concentrations with respect to the soil organisms should be related to a low effect level on the most sensitive species. The effects on the process of metabolism and other processes within the organisms should be considered and also the diversity of the species, which is most sensitive to the heavy metals, has to be accounted. Critical limits must refer to the chronic or accumulated effects. For assessment of the critical concentrations in crops and in drinking water, human-toxicological information is required. In general, for establishing critical loads we should also account the additive effects of the different metals and combination effect between the acidification and biogeochemical mobilization of the heavy metals in soils and bottom sediments. 

It has been estimated that 1.4-7.4 times as many streams in the eastern United States undergo episodic acidification than are chronically acidic (108). Similarly, the number of episodically acidic Adirondack lakes is estimated to be 3 times higher than the number of chronically acidic lakes (108). Wigington et al. (109) reported that acidic episodes occur in a wide range of geographic locations in the northeastern, southeastern, and western United States, as well as in Scandinavia, Europe, and Canada. 

Acid rain primarily affects sensitive bodies of water, that is, those that rest atop soil with a limited ability to neutralize acidic compounds (called buffering capacity ). Many lakes and streams examined in a National Surface Water Survey (NSWS) suffer from chronic acidity, a condition m which water lias a constant low (acidic) pH level. The survey investigated tlie effects of acidic deposition in over 1,000 lakes larger than 10 acres and in thousands of miles of streams believed to be sensitive to acidification. Of the lakes and streams surveyed in the NSWS, arid rain has been determined to cause acidity in 75 percent of the acidic lakes and about 50 percent of tlie acidic streams. Several regions in the U.S. were identified as containing many of the surface waters sensitive to acidification. They include, but are not limited to, the Adirondacks. the mid-Appalachian highlands, the upper Midwest, and the high elevation West. 

Emissions from U.S. sources also contribute to acidic deposition in eastern Canada, where the soil is very similar to the soil of the Adirondack Mountains, and the lakes are consequently extremely vulnerable to chronic acidification problems. The Canadian government has estimated that 14,000 lakes in eastern Canada are acidic. 

For example, approximately 70 percent of sensitive lakes in the Adirondacks are at risk of episodic acidification. This amount is over three limes the amount of chronically acidic lakes. In the mid-Appalachians, approximately 30 percent of sensitive streams are likely to become acidic during an episode. This level is seven times the number of chronically acidic streams in that area,... 

A 70-year-old woman with a 2-year history of primary biliary cirrhosis confirmed by histological and immunological criteria took colestyramine sachets twice daily for 2 months and developed lethargy, confusion, and drowsiness (3). She had signs of chronic liver disease, portal hypertension, and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis, and a urinary pH of 4.85 together with tests of renal acidification excluded renal tubular acidosis. No other cause was found and she responded to 600 mmol of sodium bicarbonate intravenously over 36 hours. 

Figure 2. The role of the Na+/H+ exchanger in pHi regulation. A steady state pHi is attained when the rate of cellular acidification is equal to the rate of cellular alkalinization. In resting cells, the rate of intracellular acidification is low and low activity of the Na+/H+ exchanger is sufficient to maintain a stable pHi. An acute acid load activates H+ efflux, thus allowing cel Is to recover their basal pHi. When, however, cells face chronic intracellular acidification (for instance as a result of an increased metabolic activity), a lower steady state is attained. Sensitization of the Na+/H+ exchanger to H+ following its phosphorylation increases H+ efflux and provides a mechanism for maintaining a stable pHi in spite of the increased acid load.

Acute poisoning is manifested by excitement and peripheral sympathomimetic effects convulsiorrs may occur also, in acute or chronic overuse, a state resembling hyperactive paranoid schizophrenia with hallucinations develops. Hyperthermia occurs with cardiac arrhythmias, vascular collapse and death. Treatment is chlorpromazine with added antihypertensive, e.g. labetalol, if necessary these provide sedation and a- and P-adrenoceptor blockade (not a P-blocker alone), rendering unnecessary the enhancement of elimination by urinary acidification. 

Hyperkalemic distal (type IV) RTA resulting from generalized distal tubule defects is less common than hyporeninemic hypoaldosteronism, but is more common than classic distal (type I) RTA. Patients with this defect have impaired tubular potassium secretion in addition to impaired urinary acidification (urine pH >5.5 despite acidemia or acid loading). Urinary obstruction is the most frequent cause of this disorder, which may also be associated with sickle-cell nephropathy, systemic lupus erythematosus, HIV nephropathy, analgesic abuse nephropathy, amyloidosis, renal transplant rejection, and chronic cyclosporine nephrotoxicity. 

While alcohol abuse may be associated with a variety of electrolyte and acid-base disorders, the role of the kidneys in this process has only recently been fully defined [164]. Renal functional abnormalities have now been related to chronic alcoholism in patients without liver disease and these defects have reverted to normal with abstinence from alcohol abuse. These abnor-mahties include decreases in the maximal reabsorptive abihty and threshold for glucose, a decrease in the threshold for phosphate excretion, and increases in the fractional excretion of P2-microglobulin, uric acid, calcium, magnesium, and amino acids. Defective tubular acidification and impaired renal concentrating ability... 

All patients developed a compensatory metabolic acidosis due to chronic hyperventilation. Respiratory alkalosis was thought to have developed because of capillary leak into the lungs producing borderline or frank pulmonary edema. After several days a superimposed normal anion gap acidosis developed from dilution by large volumes of saline fluid resuscitation. The authors found no defects in renal handling of calcium, phosphorous, or magnesium. There was no evidence of a renal acidification defect or renal tubular acidosis. 

Ascorbic acid, a water-soluble vitamin (1(X) to 250 mg p.o. daily), is indicated in the treatment of frank and subclinical scurvy in extensive bums, delayed fracture or wound healing, postoperative wound healing severe febrile or chronic disease states and in prevention of ascorbic acid deficiency in those with poor nutritional habits or increased requirements. In addition, ascorbic acid has been used for potentiation of meth-enamine in urine acidification and as an adjunctive therapy in the treatment of idiopathic methemoglobinemia. 

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