Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article describes concepts of drug treatment for patients with severe renal failure (creatinine clearance less than 10 ml/min), especially in intensive care. These subjects often develop multiorgan failure and require special considerations: 1. Not only should the maintenance dose of digoxin be reduced to 0.05-0.1 mg/day, but the loading or digitalizing dose should also be diminished to 0.4-0.6 mg. 2. Penicillins, cephalosporins, quinolones, and other antibiotics with a high therapeutic ratio can be given as recommended by the manufacturer or reference lists according to renal insufficiency. 3. For drugs with a low therapeutic index, such as aminoglycosides, vancomycin, flucytosine, some antiarrhythmic agents, cardiac glycosides, and theophylline, therapeutic drug monitoring is mandatory. 4. Steroids, insulin, atropine, catecholamines, anticoagulants, thrombolytic agents, antihypertensive drugs, and organic nitrates can be given according to their effect. However, nitroprusside should be discontinued after 2 days because its metabolites may be toxic. 5. The dose of H2-receptor antagonists used for the control of gastric acidity and the treatment of peptic ulcers should be reduced to 20-50% of the normal. The administration of aluminum, magnesium, and bismuth compounds should be avoided. 6. Loop diuretics (e.g., furosemide) can be effective at increased doses in patients with chronic renal failure and fluid overload, particularly when used in combination with a thiazide in refractory edema. Thiazides alone are useless, and potassium-sparing diuretics are contraindicated. 7. Colloid-containing solutions should be infused cautiously at a maximal rate of 2 x 500 ml/week only when the plasma volume is contracted.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Renal failure--concepts for drug therapy in intensive care]. 181 28

The interrelations among fasting serum gastrin, serum creatinine, gastric acid secretion variables, and G-cell densities were analyzed in 47 patients with chronic renal failure (CRF). The patients also underwent gastroscopy and radiologic upper gastrointestinal barium examination. It is suggested that the hypergastrinemia seen in CRF is related to several factors: gastric acidity, grade of renal failure, G-cell density, and basal gastrin secretion rate. With regard to serum gastrin two different populations can be found, the cutting-off point being 300 ng/l. Although the group with high gastrin levels included significantly more patients with gastric body atrophy than the other group (4 of 11 versus of 1 of 36), most of them had no atrophy, which indicates that (an)other mechanism(s) is responsible for the hypergastrinemia. In the relation between serum gastrin and gastric acidity also, two differently behaving subgroups emerged. In the first, strong acidity change corresponded to minor gastrin change, whereas in the other, minor acidity change corresponded to marked gastrin change. The correlation coefficients between gastrin and acidity were high within both subgroups. During regular dialysis patients preserve the characteristics delineated from non-dialyzed values. Patients with signs of duodenal ulcer disease had high maximal acid output and low serum gastrin. Otherwise no associations were found between GI findings and the variables studied.
 ...
PMID:Serum gastrin in chronic renal failure: its relation to acid secretion, G-cell density, and upper gastrointestinal findings. 259 56

A dose-response gastric secretion test was performed in 87 nondialyzed patients with chronic renal failure (CRF) and in 87 age- and sex-matched controls without renal disease. Twenty-six of the CRF patients were reexamined, 18 undergoing regular hemodialysis and 8 after successful transplantation. The gastric acidity, acid output, and volume output of the nondialyzed CRF subjects were decreased when compared with those of the controls or of patients in the posttransplant phase. This decrease was more marked with low than with high stimulant doses. The decrease in acid output was significantly greater than that in volume output. Moreover, when compared with the dialysis phase the nondialyzed patients had lowered gastric acidity and acid output, but no decrease in volume output was evident. The results indicate that there is an inhibition of gastric secretion in CRF. This inhibition is dependent on strength of stimulation and is abolished by active treatment of CRF, more clearly by transplantation than by maintenance dialysis. In addition, the inhibition is predominantly on the secretion of acid, the output of gastric juice being less affected.
 ...
PMID:Gastric secretion kinetics in chronic renal failure. 332 96

In the normal human body, the extracellular fluid pH of 7.40 is closely protected. Any increase in acidity or alkalinity summons forth three lines of defense, starting immediately with the blood buffers, followed soon by the respiratory system's control of CO2, and finally purged by the renal excretion of the excess acid or base. The complex interrelated processes of the renal responses require a few days to accomplish maximum compensation. We have presented the fundamental principles governing maintenance of the acid-base equilibrium to provide a conceptual framework for understanding the clinical disorders of hydrogen ion metabolism. The somewhat elusive concepts of endogenous acid production and net acid balance have also been reviewed to help reveal the pathophysiology of metabolic acidosis caused by renal tubular acidosis, chronic renal failure, certain infant feedings, and total parenteral nutrition. The development and perpetuation of metabolic alkalosis in relationship to chloride and potassium deficiency have been examined. In the delineation of a clinical acid-base disorder, the clinician must bear in mind the continual interactions of electrolytes and hormonal systems and should be prepared to reevaluate frequently the elected therapy against the changing responses, based on a thorough understanding of physiology. The various types of renal tubular acidosis have manifold facets but the basic understanding of their pathophysiology begins with the concept of the "anion gap," a point of reference that can be used in the differential diagnosis and treatment. In this chapter a number of new causes of type IV renal tubular acidosis--currently considered to be the most common form of renal tubular acidosis--have been pointed out, along with special reference to the mineral, electrolyte, and aldosterone metabolism in the various acidoses and current means of reversing growth failure in the child, especially through bicarbonate treatment. The mechanism of metabolic acidosis in chronic renal failure including metabolic acidosis in children undergoing dialysis and in recipients of kidney transplantation, and its relationships to mineral and electrolyte metabolism have been presented. The pathophysiology of the acidosis related to certain infant formulas and the acidogenic properties of some amino acid solutions employed in total parenteral nutrition have been briefly reviewed. Finally, the metabolic alkalosis seen in a variety of chloride deficiency syndromes, such as Bartter's syndrome and dietary chloride deprivation, has been discussed and a rational approach to evaluation and treatment outlined.
 ...
PMID:Acid-base disorders and the kidney. 642 18

The effect of a meat load on the renal handling of acid-base balance was studied in ten healthy subjects (GFR by inulin clearance = 98.5 +/- 8.14 ml.min-1.1.73 m-2) and in ten patients affected by chronic renal failure (CRF) (GFR = 39.9 +/- 5.3 ml.min-1.1.73 m-2). After the meat load (2 g.kg-1 body weight of cooked unsalted red meat), GFR increased by 26.9% (peak value) over baseline in healthy subjects and by 32% in CRF patients. The acid-base status of the healthy subjects was in the normal range, whereas the CRF patients disclosed a slight metabolic acidosis. After a meat load, there was, in the healthy subjects, an increase in the filtered load of bicarbonate coupled to an enhanced tubular reabsorption and urinary excretion. The time course between bicarbonate load and urinary excretion was coincident. In CRF patients, the increase of bicarbonate tubular load after the meal was associated with an increase in tubular reabsorption but not in urinary excretion of this anion. The relationship between bicarbonate load and reabsorption was linear in both groups up to the highest filtered loads. Baseline titratable acidity (TA) and ammonium (NH4+) excretion (expressed per ml GFR) were increased in CRF patients as compared with control subjects, but no changes were found after the meat load in both groups in these experimental conditions. The data indicate that the renal tubules contribute to the maintenance of acid-base balance both in healthy subjects and in CRF patients by reabsorbing most of the additional bicarbonate load. The transient, but significant, increase in bicarbonate excretion observed in healthy subjects could be related to the increased tubular load of bicarbonate. In CRF patients, tubular bicarbonate reabsorption was more complete, possibly because of the stimulation of H+ secretion by the mild metabolic acidosis. TA and NH4+ did not participate in tubular compensation of the increased buffer load.
 ...
PMID:Effect of an acute oral protein load on renal acidification in healthy humans and in patients with chronic renal failure. 917 48

Hypophosphatemia caused by renal phosphate loss occurs frequently after kidney transplantation. In assumption of systemic phosphorus depletion, the presumed deficit commonly is replaced by oral phosphate supplements. However, such treatment is debatable, because intracellular phosphorus stores have not been assessed in this setting and may not be accurately reflected by serum phosphate concentrations. Moreover, disturbances in mineral metabolism from chronic renal failure, such as hypocalcemia and hyperparathyroidism, may be prolonged with oral phosphate supplements. Conversely, a neutral phosphate salt might improve renal acid excretion and systemic acid/base homeostasis for its properties as a urinary buffer and a poorly reabsorbable anion. Twenty-eight patients with mild early posttransplantation hypophosphatemia (0.3-0.75 mmol/L) were randomly assigned to receive either neutral sodium phosphate (Na(2)HPO(4)) or sodium chloride (NaCl) for 12 weeks and examined with regard to (1) correction of serum phosphate concentration and urinary phosphate handling; (2) muscular phosphate content; (3) serum calcium and parathyroid hormone (PTH); and, (4) renal acid handling and systemic acid/base homeostasis. Mean serum phosphate concentrations were similar and normal in both groups after 12 weeks of treatment; however, more patients in the NaCl group remained hypophosphatemic (93% versus 67%). Total muscular phosphorus content did not correlate with serum phosphate concentrations and was 25% below normophosphatemic controls but was completely restored after 12 weeks with and without phosphate supplementation. However, the percentage of the energy-rich phosphorus compound adenosine triphosphate (ATP) was significantly higher in the Na(2)HPO(4) group, as was the relative content of phosphodiesters. Also, compensated metabolic acidosis (hypobicarbonatemia with respiratory stimulation) was detected in most patients, which was significantly improved by neutral phosphate supplements through increased urinary titratable acidity. These benefits of added phosphate intake were not associated with any adverse effects on serum calcium and PTH concentrations. In conclusion, oral supplementation with a neutral phosphate salt effectively corrects posttransplantation hypophosphatemia, increases muscular ATP and phosphodiester content without affecting mineral metabolism, and improves renal acid excretion and systemic acid/base status.
 ...
PMID:Metabolic aspects of phosphate replacement therapy for hypophosphatemia after renal transplantation: impact on muscular phosphate content, mineral metabolism, and acid/base homeostasis. 1056 Nov 44