PubMed Health⌕ Search

Biomedical subjects

P Kildeberg

Publications and source records attributed to P Kildeberg.

At least 19 recordsLinked to original sources
PubMed2004

Renal response to acute acid loading--an organ physiological approach.

OBJECTIVE: In previous studies of the renal response to acute NH4Cl acidosis no correlation was found between systemic acid-base status and the traditionally used quantity, renal net acid excretion (NAE). If NAE is to be considered a physiologically meaningful quantity then this is surprising, as the extracellular acid-base status would be expected to be the key physiological trigger for renal NAE. The object of this study was to investigate the renal response to acute non-carbonic acid loading using a quantitative organ physiological approach. MATERIAL AND METHODS: Five-h NH4Cl loading studies were performed in 10 healthy men using a randomized, placebo-controlled, crossover design. Arterialized capillary blood, serum and urine were collected hourly during the loading studies for the measurement of electrolytes and acid-base status. Concentrations of non-metabolizable base (NB) and acid (NA) were calculated from measured concentrations of non-metabolizable ions according to Kildeberg. RESULTS: In the steady state (placebo) the rate of renal excretion of NA (=-NB) was close to zero, indicating that the net extrarenal input of NA (endogeneous production, gastrointestinal absorption. skeletal release, etc.) was likewise about zero. An inverse correlation was found between blood pH and the rate of renal excretion of NA. Only a small amount of the acid load (approximately 8%) was excreted during the 5-h study period and this was accompanied by massive calciuria, indicating that mobilization of NB from bone contributed substantially to the current net extrarenal NA input. CONCLUSION: From a physiological point of view, NB can be regarded as the actual substrate for renal acid-base control, and measurement of renal turnover of NB may give a more precise description of renal acid-base metabolism during acid loading than previously described methods.

Acid-Base Equilibrium↗
PubMed1993

Pathophysiology of incomplete renal tubular acidosis in recurrent renal stone formers: evidence of disturbed calcium, bone and citrate metabolism.

Urinary acidification, bone metabolism and urinary excretion of calcium and citrate were evaluated in 10 recurrent stone formers with incomplete renal tubular acidosis (iRTA), 10 recurrent stone formers with normal urinary acidification (NUA) and 10 normal controls (NC). Patients with iRTA had lower plasma standard bicarbonate after fasting (P < 0.01) and lower urinary excretion of titratable acid (P < 0.05) and citrate (P < 0.01) compared with NUA patients and NC, and higher urinary excretion of ammonia (P < 0.05) compared with NC (P < 0.05). Hypercalciuria was found in 6 of 10 patients with iRTA compared with 3 of 10 with NUA, and 0 of 10 NC. The citrate/calcium ratio in urine was significantly reduced in iRTA compared with the value in NUA (P < 0.01), and in NUA compared with NC (P < 0.05). Biochemical markers of bone formation (serum osteocalcin) and bone resorption (urinary hydroxyproline) were significantly increased in iRTA compared with NUA and NC (P < 0.01), indicating increased bone turnover in stone formers with iRTA. Stone formers with iRTA thus presented with disturbed calcium, bone and citrate metabolism--the same metabolic abnormalities which characterize classic type 1 RTA. Mild non-carbonic acidosis during fasting may be a pathophysilogical factor of both nephrolithiasis and disturbed bone metabolism in stone formers with iRTA.

Acid-Base Equilibrium↗
PubMed1990

[Testing of a liquid, ready-to-use, breast milk substitute in the county of Funen].

A newly developed liquid ready-to-use cow's milk based formula (BD) was used as the sole nutrient in 314 healthy term infants below the age of 28 weeks--except for supplementary feeding introduced at an average age of 142 days. The incidence of dyspeptic problems (constipation, diarrhea, vomiting), the parents' and visiting nurses' comments on the product, and the causes of "BD failure" (termination of BD feeding because of suspected cow's milk allergy, dyspepsia, etc.) were recorded as were rates of weight gain and linear growth. It is concluded that BD is a valuable alternative to existing powdered milk formulas and that the growth of the infants compared satisfactorily with published reference values.

Animals↗
PubMed1990

[The pH and acidity of feces in colorectal neoplasms].

The pH and faecal titratable acidity in fresh faeces were measured in patients with colo-rectal carcinoma or adenoma and in normal individuals. Significantly higher pH values and lower acidity were found in patients with cancer than in normal individuals. Patients with cancer had pH greater than 6.90 more frequently than normal. Patients with adenomata did not differ significantly from normal individuals. These results support performance of intervention trials with lowering of the pH in the colon with the object of cancer prophylaxis even although the causal connection is obscure.

Adenoma↗
PubMed1988

Adrenocorticotropic hormone in the control of renal tubular hydrogen ion secretion. Balance of non-metabolizable base in ACTH-stimulated weanling rats subject to acid or base loading.

Groups of weanling rats subject to ACTH-stimulation (tetracosactrin, 1 mg kg-1 day-1) were exposed to heavy oral loads of ammonium chloride (approx. 21 mmol kg-1 day-1) or sodium bicarbonate (approx. 40 mmol kg-1 day-1) for 8 days. During loading with sodium bicarbonate, the animals maintained a normal positive external (whole body) balance of non-metabolizable base (NB), excess NB being excreted quantitatively in the urine, whereas loading with ammonium chloride caused a fall in the mean balance of NB from a reference value of 12.1 mmol per 8 days to about zero. However, in the two groups the concentration in plasma of NB rose from the reference value (41 mmol l-1) to the same level (57 and 59 mmol l-1, respectively; P greater than 0.5) despite extreme differences in rates of gastrointestinal NB absorption, despite a significant rise in the rate of endogenous sulphuric acid production and despite the presence of ample chloride in diet and urine. These results indicate that ACTH determines the extracellular concentration of NB at which exchange of NB takes place by influencing, directly or indirectly, the relative rates of renal tubular H- secretion and Cl- reabsorption at any given rate of tubular reabsorption of Na-. Some cybernetic considerations of the disturbance are presented.

Acid-Base Equilibrium↗
PubMed1987

Methionine-induced acidosis in the weanling rat.

Whole body balances of non-metabolizable base (NB) were studied in weanling rats fed a cereal-based diet with or without added L-methionine. In response to L-methionine loading (2.5 mmol day-1) the rats exhibited a significant reduction in rates of food intake (109 vs. 160 g per 8 days) and body growth (3 vs. 52 g per 8 days); fractional oxidation of absorbed dietary amino acid sulphur increased from 0.28 to 0.64; and mean urinary sulphate excretion increased from 2.3 to 14.8 mmol per 8 days. Mean rates of renal excretion of NB and filtered titratable organic acid decreased from 20 to -11 mmol per 8 days and from 22 to 8 mmol per 8 days. Balances of calcium and NB remained at reference values despite a decrease in whole blood 'base excess' from -1.0 to -6.4 mmol l-1. The concentration of NB in plasma rose but slightly. It is concluded that L-methionine loading in the weanling rat leads to extracellular non-carbonic acidosis subject to renal compensation. This acidosis is due not to retention of H+ released by ionization of endogenous sulphuric acid but possibly to accumulation of (acid) organic metabolites of methionine which are efficiently conserved by the kidneys. The rise in sulphuric acid production leads to an adaptive decrease in fractional reabsorption of filtered sulphate. Even during inhibited growth, absorbed dietary NB is retained and deposited in the skeleton, probably as calcium carbonate.

Acid-Base Equilibrium↗
PubMed1985

Acetate versus lactate in peritoneal dialysis solutions.

The acid-base characteristics of two peritoneal dialysis solutions containing either lactate or acetate are compared and the time course of changes in intraperitoneal pH following instillation into the abdominal cavity is measured. The concentration of titratable acid (cTA) is 5.58 mmol/l or 7 times as high in solutions containing acetate as in those containing lactate (0.79 mmol/l). The buffer capacity, -dcTA/dpH, is 11.43 and 1.82 mmol/l, respectively. Following intraperitoneal instillation of 1.5 liter of the solutions, the time course is 2-3 times as long before intraperitoneal pH reaches 7 using acetate (18 min) as when using lactate (7 min). The above mentioned difference in acid-base characteristics as well as an individual acetate intolerance is supposed to be the cause for the development of abdominal pains and peritoneal irritation observed in some patients using acetate-containing solutions. 123 mmol/l of sodium bicarbonate is to be added to the acetate solution to raise the pH value from 5.6 to 7.4. Neutralization using sodium bicarbonate will thus result in sodium intoxication of the patient. The use of lactate instead of acetate for peritoneal solutions is advocated.

Acetates↗
PubMed1983

Corticotropin-induced alkalosis in the weanling rat and its relation to the balance of non-metabolizable base.

Studies of whole body balances of non-metabolizable base (NB) and several electrolytes and of the acid-base status of blood and urine during development of corticotropin-induced alkalosis in the weanling rat were carried out in order to identify the primary source of base and factors instrumental in maintenance of the alkalotic state. The data were compared to baseline and running control values and to the results of whole carcass analysers. Primary accumulation of NB was accounted for by ongoing gastrointestinal NB absorption in the weight-losing animal, distributed to extracellular and non-extracellular compartments of the body. An increase in the rate of renal excretion of non-metabolizable acid (NA), from negative values to zero, corresponded to an increased load of endogenous sulphuric acid and a reduced rate of gastrointestinal NB absorption. Accordingly, the renal response did not per se contribute to the induction of extracellular alkalosis. Maintenance of alkalosis occurred in spite of ample chloride in the renal tubular lumen and a moderate increase in relative extracellular volume. In the absence of evidence of overloading (with base) or malfunction of the kidney, corticotropin-induced alkalosis is classifiable as a 'set-point disturbance' of acid-base metabolism in which fluctuations in the (non-renal) load of NA lead to commensurate changes in renal NA excretion at an elevated extracellular pH. Withdrawal of corticotropin injections was followed by prompt restoration of a normal extracellular acid-base status and a return to reference values for renal NA excretion despite a marked fall in the balance of NB. This observation supports a concept of the extracellular compartment as the immediate reference system of the kidney.

Acid-Base Imbalance↗
PubMed1983

Acid-base status of biological fluids: amount of acid, kind of acid, anion-cation difference, and buffer value.

A formal concept of amount of substance of 'acid' and 'base' is proposed which is based upon the change in extent of protolytic equilibria in an arbitrary reference state for the components of the system concerned and equally consistent with the Brønsted-Lowry terminology, the older medical 'anion-cation' terminology, and the operational principle of titration. It is shown how this concept allows formulations of the 'acid-base status' of biological fluids in accordance with various types of physiological, biochemical, or clinical problems. Finally, a general expression for buffer value is presented which is valid for any acid, base, or ampholyte at any pH.

Acid-Base Equilibrium↗
PubMed1979

Balance of net base in the rat: adaptation to and recovery from sustained hypercapnia.

Net base and mineral balances were evaluated in a group of male 350 g Wistar rats exposed to 10% carbon dioxide in air for 10 days with a view to identifying the source of net base subject to retention during renal compensation of sustained respiratory acidosis. In response to hypercapnia, the rate of renal net acid excretion rose but insignificantly. However, a rise in whole body net base concentration from about 215 mmol/kg to about 250 mmol/kg came about by ongoing gastrointestinal absorption in the weight-losing animal, absorbed net base being distributed to extracellular and non-extracellular compartments of the body, presumably including bone. During an 8-day recovery period, a small decrement in whole body net base concentration was observed.

Acid-Base Equilibrium↗
PubMed1979

Balance of net base in the rat. V. Effects of oral ammonium chloride loading.

The physiology of oral ammonium chloride loading was studied in four groups of male weanling rats weighing about 100 g and fed either standard ground Rostock rat food (containing 317 mmol net base/kg) or ground barley (containing only 20 mmol net base/kg). One group of animals on the Rostock diet received oral supplements of ammonium chloride (approximately 32 mmol . kg-1 . day-1) sufficient to provide a net zero rate of oral net base intake. In this group, ongoing fecal net base excretion caused net acid to be absorbed at an average rate of 15 mmol . kg-1 . day-1. The mean rate of renal net acid excretion rose markedly (by 29.4 mmol . kg-1 . day-1); and over an 8-day balance period the animals were able to maintain near-normal balances of net base. During a subsequent 8-day recovery the pattern of mineral turnover returned to normal. Even in the barley-fed rats, gastrointestinal net acid absorption was observed. These animals suffered a 61% reduction in the rate of body growth, but the overall rate of net base retention, per kilogram of mass gain, was close to the reference value. Finally, the combination of barley and ammonium chloride led to weight loss, positive net acid balances (8.5 mmol . kg-1 . day-1), and a maximal rate of renal net acid excretion (50.8 mmol . kg-1 . day-1). Some implications for the metabolism of organic acids are discussed.

Acid-Base Equilibrium↗
PubMed1978

Balance of net base in the rat. III. Effects of oral sodium bicarbonate and sodium citrate loading.

The balance of net base in groups of male weanling Wistar rats exposed to sustained oral loads of net base were studied. In response to dietary loads of sodium bicarbonate (approx. 50 mmol.kg-1.day-1) an average increment in the mean rate of retention of net base of 21.8 mmol.kg-1.day-1 was observed in the absence of significant changes in the blood 'base excess'. Following withdrawal of sodium bicarbonate, mean rates of gastrointestinal absorption, renal excretion, and retention of net base promptly returned to control values, accumulated net base being retained in the body, presumably as skeletal sodium carbonate. In response to equimolar loads of net base in the form of trisodium citrate, a similar, albeit less pronounced, rise in the rate of retention of net base occurred.

Acid-Base Equilibrium↗
PubMed1978

Balance of net base in the rat. IV. Effects of oral calcium and phosphate loading.

Mineral and net base balances were studied in groups of male weanling Wistar rats given oral loads of calcium chloride, monocalcium phosphate plus monosodium phosphate, and disodium phosphate plus monopotassium phosphate, respectively. A group of adult nongrowing rats loaded with calcium chloride was included for comparison. In response to CaCl2 loading, gastrointestinal net base absorption was inhibited due, largely, to luminal precipitation of tertiary phosphates of calcium and magnesium. In the weanling animal, however, a rise in the rate of renal net acid excretion matched the concomitant decrement in the rate of net base absorption, permitting of continued skeletal net base storage. Similarly, in the adult animals augmented renal net acid excretion offset a positive rate of gastrointestinal net acid absorption with a resultant (normal) zero net base balance. Loading with monocalcium phosphate and disodium phosphate at a constant oral net base intake did not influence the overall net base balance, but disodium phosphate loading caused significant sodium retention.

Acid-Base Equilibrium↗
PubMed1977

Physiological viewpoints on clinical acid-base diagnostics.

Acid-base physiology is concerned with sources, extent, and control of hydrogen ion donation in the body, at the organ-physiological as well as the molecular level of study. With the introduction of Van Slyke's methods for quantitative carbon dioxide measurements in biological fluids, one important source of hydrogen ion donation became identifiable; and these and derived methods have permitted of fairly precise quantitative descriptions of transport and pulmonary elimination of carbon dioxide. However, the inevitable operational concept of non-carbonic (non-volatile) contributions to the titratable acidity of the body fluids has been a cause of considerable methodological and conceptual difficulties; and whereas it is now possible by means of the micro-equilibration technique to make accurate assessments of the concentration of non-volatile titratable acid (base) in blood, the question of the physiological relevance of the concept of 'base excess' remains open. In particular, the concept of non-carbonic acid does not possess a specific relevance with respect to the acid-base physiology of kidney, bone, and gastro-intestinal tract comparable to the 'substrate-specificity of carbon dioxide with respect to the lung. Our studies indicate that a subdivision of the titratable non-carbonic acid of any biological medium in two subcomponents will provide an improvement of specificity, adequate for a system physiological approach at the organ level. Thus, a distinction should be made between (1) processes of hydrogen ion donation, reversible by endogenous metabolic means (quantitated in terms of the component MA = metabolizable non-carbonic acid) and (2) processes of hydrogen ion donation associated with gastro-intestinal, skeletal, and renal transport, storage, and control of non-metabolizable non-carbonic acid (NA). Some implications of this distinction for acid-base physiology and acid-base diagnostics are discussed.

Acid-Base Equilibrium↗