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PubMed1990

Rhabdomyolysis associated with hypokalaemic periodic paralysis of renal tubular acidosis.

Two cases of hypokalaemia with serum potassium levels of 1.4 mmol/L and 1.9 mmol/L causing severe periodic paralysis since childhood are presented. There were associated with muscular aches and markedly raised muscle enzymes suggesting massive rhabdomyolysis. These abnormalities were due to renal tubular acidosis with markedly acidic arterial pH. The hypokalaemia and rhabdomyolysis responded to potassium and bicarbonate replacement. We postulate these patients had sporadic distal type of renal tubular acidosis and that the hypokalaemia and acidosis had caused the rhabdomyolysis.

Acidosis, Renal Tubular↗
PubMed1990

Endemic primary distal renal tubular acidosis in Thailand.

Within a period of 3 years, 103 patients with primary type I distal renal tubular acidosis were reported from two hospitals in the northeast of Thailand, with cases peaking in the summer. The patients' age ranged from 18 to 76 with a mean and mode of 39 and 47 years, respectively. The female to male ratio was 3.3:1. All patients presented with generalized muscle weakness and bone pain and nocturia were frequent manifestations. Hypokalaemia and hyperchloraemic metabolic acidosis were constant findings and were more pronounced in patients with roentgenographic evidence of nephrocalcinosis and osteomalacia. Urinary citrate was extremely low in most of the patients. Nephrocalcinosis and/or renal stones were present in 27.2% of the patients and osteomalacia was found in 23.3%. All patients were Lao-Thai. This is the first report of a large group of patients with distal renal tubular acidosis, endemic within a particular geographical region.

Acidosis, Renal Tubular↗
PubMed1975

[Danger of fetal acidosis in vaginal delivery from breech presentation (author's transl)].

On the basis of our own experience and the literature the risk of acidosis, which corresponds to the risk of asphyxia, during vaginal delivery of breech presentations is examined. Compared with delivery of vertex presentation it is 3-10 times greater. The risk of acidosis does not depend on the duration of pregnancy and only a little on the parity of the mother. Even with carefully selective indication for primary Caesarean section it cannot be reduced below the high level. Typically there is acute compression of the cord at the end of the first or later stages of labor. Even with intensive intra-partum care it cannot safely be predicted with sufficient certainty. As a criterion of the efficiency of modern obstetrics the impact of acidosis in umbilical blood and its increase in breech presentation is discussed. Only systematic Caesaren section before or early in labor will lower the risk to that of vertex presentation. This is done and recommended by the authors. Links between acdosis in umbilical blood and permanent cerebral damage are probable but by no means certain and their importance in unknown. Selective indication for Caesarean section which has to be made generously, represents an acceptable alternative.

Acidosis↗
PubMed1990

[Lactic acidosis associated with metformin].

Lactic acidosis is an extremely rare but serious complication of treatment with metformin. In order to avoid lactate acidosis, it is important to select patients correctly and to ensure that contraindications such as cases of renal involvement, advanced age and chronic alcoholism are observed prior to treatment with metformin. In addition, it is necessary to carry out meticulous follow-up control of the patients with annual investigations of renal and hepatic functions and clinical assessment approximately four times per annum with the object of revealing commencing symptoms of diabetes and ischaemic conditions. In this manner, the majority of cases of lactate acidosis can be avoided.

Acidosis, Lactic↗
PubMed1989

Hemodialysis in the treatment of lactic acidosis in diabetics treated by metformin: a study of metformin elimination.

The aim of this study was to determine the characteristics of metformin elimination by dialysis. For this purpose we report the kinetic parameters during dialysis and the metformin clearance (i.e. dialysance) in four patients presenting with lactic acidosis which occurred on metformin therapy. We also studied metformin elimination in two chronically hemodialyzed diabetic patients inadvertently maintained on metformin therapy and in two chronically hemodialyzed non-diabetic patients who took a single dose of metformin before a dialysis session. Analysis of plasma concentration-time curves showed a biphasic pattern of metformin - elimination, according to a two-compartment model. We demonstrate that metformin may be removed even after reaching an equilibrium between blood and dialysate levels in a recirculating system, suggesting a storage of metformin in a deep compartment with a gradient of concentration between this compartment and the blood. Lastly, metformin dialysance appears satisfactory (68 ml/min) even in the case of relatively low blood flow; this value reached 170 ml/min under good hemodynamic conditions. In conclusion, hemodialysis efficiently removes metformin and corrects metabolic acidosis in patients with metformin-induced lactic acidosis.

Acidosis, Lactic↗
PubMed1989

Metabolic acidosis.

This article reviews acid-base homeostasis and discusses the approach to the acidotic patient, with special reference to problems commonly encountered in emergency practice. General principles of therapy are presented, and their application to specific types of life-threatening metabolic acidosis addressed. By extension, recommendations are made concerning the treatment of the acidosis associated with cardiac arrest. Finally, preliminary information is presented on promising new approaches to the treatment of metabolic acidosis that are currently under investigation.

Acid-Base Equilibrium↗
PubMed1989

[Metabolic acidosis and hypoglycemia during calcium hopantenate administration--report on 5 patients].

Calcium hopantenate (HOPA) has been widely used as an activator of cerebral metabolism in Japan. However, several cases of acute encephalopathy during HOPA administration were recently reported, which were characterized by marked metabolic acidosis and hypoglycemia. The encephalopathy in these patients was named Reye-like syndrome because of the similarity to Reye's syndrome in children. The purposes of this presentation are to report on 5 patients with acute encephalopathy developing during HOPA administration, to summarize their symptoms and clinical courses, and to discuss the pathogenesis of metabolic acidosis and hypoglycemia. Initial characteristics of the clinical course in all patients were loss of appetite, nausea and vomiting, followed by unconsciousness. Laboratory examinations revealed marked metabolic acidosis, severe hypoglycemia, hyperlactacidemia, leukocytosis, ketonuria, and increased Ht and BUN. A few days after development of the initial symptoms, mild renal and liver dysfunction, and elevation of serum amylase were observed in all patients. Hyperlactacidemia was present in 4 in the initial period. Blood concentration of HOPA was 2.131 micrograms/ml in patient 1 (8-10 hours after final administration), and 10.7 micrograms/ml in patient 5 (24 hours after final administration). These values are extremely high, because usually HOPA concentration is almost negligible 7 hours after the drug is taken. As the pathogenesis of acute encephalopathy due to HOPA administration, the failure of fatty acid beta-oxidation has been proposed by some investigators. However, the serum concentrations of CoA, pantothenic acid and carnitine during the initial stage were not reduced in our patients. Furthermore, it is very difficult to explain the severe hypoglycemia in terms of the beta-oxidation theory.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Lactic↗
PubMed1989

Protein and amino acid metabolism in uremia: influence of metabolic acidosis.

Loss of lean body mass occurs frequently in patients with acute or chronic renal failure, but the mechanism(s) causing this abnormality are unknown. Using animal models of experimental uremia, it was found that excess lactate formation in muscle is directly related to the rate of protein breakdown. This suggests that abnormal energy metabolism may be one mechanism for protein wasting. A second mechanism involves metabolic acidosis. Metabolic acidosis activates the catabolism of protein and amino acids in muscle of uremic rats independently of azotemia. Defects in sodium transport by Na,K-ATPase and the Na/K/Cl cotransport system suggest that intracellular ions including hydrogen may be abnormal. If this were the case, uremia would increase the susceptibility to the catabolic effect of metabolic acidosis.

Acidosis↗
PubMed1989

Umbilical artery Doppler velocimetry as a predictor of fetal hypoxia and acidosis at birth.

We studied the relationship between preoperative umbilical artery Doppler waveforms and umbilical vein pO2 and pH at elective cesarean section. An absence of end-diastolic velocities had a strong statistical association with hypoxia and acidosis, and was an accurate clinical test for hypoxia (sensitivity 78%, specificity 98%, positive predictive value 88%, and negative predictive value 98%) and acidosis (sensitivity 90%, specificity 92%, positive predictive value 53%, and negative predictive value 100%). It was also a clinically sensitive indicator of perinatal morbidity and mortality. Most fetuses with no end-diastolic velocities were growth-retarded, but the reverse was not true. The absence of end-diastolic velocities also divided both mature and immature fetuses into high- and low-risk groups for hypoxia and acidosis. In the presence of end-diastolic velocities, only very high S/D ratios (above 4.5) have any association with hypoxia. As a noninvasive test of fetal umbilical vein pO2 and pH, umbilical artery Doppler performs well.

Acidosis↗
PubMed1989

[Dose dependent effects of dichloroacetate on lactic acidosis in dogs].

Dose dependent effects of DCA (dichloroacetate) on lactic acidosis were studied in 30 mongrel dogs under pentobarbital anesthesia. Lactic acidosis was induced by infusion of either lactate (n = 15) or pyruvate (n = 15) for 20 min. In each dog, saline or DCA (100 mg.kg-1 or 300 mg.kg-1) was given for ten min iv. at ten min after the beginning of lactate or pyruvate infusions. Reduction in serum pyruvate levels was more prominent than that in lactate levels in both the lactate and pyruvate infusion groups. DCA in a dose of 100 mg.kg-1 was more effective to reduce serum pyruvate levels and arterial pH than 300 mg.kg-1 of DCA. There were no differences between saline and DCA (100 mg.kg-1 or 300 mg.kg-1) administrations in mean arterial pressure and cardiac index. This study confirmed the hypothesis that DCA reduces serum lactate levels via acceleration of pyruvate metabolism. It was concluded that the ability of DCA to reduce serum lactate levels is dose-dependent and a large dose of DCA (300 mg.kg-1) would not be necessary for lactic acidosis.

Acetates↗
PubMed1988

Severe metabolic acidosis induced in a patient during fasting by KCl administration.

The purpose of this study was to determine the cause of an acute metabolic acidosis of the normal anion gap type which developed during a 3 day period when 64 mmol of KCl was administered daily to an obese but otherwise healthy subject fasted for 2 weeks (called the index case). She had typical ketoacidosis of fasting for the first 13 days of fasting; since the plasma [K] was 3.6 mmol/l, she was given 64 mmol of KCl daily for 3 days. On day 3 of KCl treatment, the plasma [HCO3] was 13 mmol/l with no change in the plasma anion gap or 3-hydroxybutyrate concentration; the plasma [K] had risen to 4.3 mmol/l. The cause of the acidosis was a reduction of urine ammonium excretion by 42 mmol/day without a parallel fall in the rate of 3-hydroxybutyrate excretion. Since renal ammonium production can be inhibited by K administration, 5 other obese subjects were studied in a similar fashion to gain insight into the problem. They had a similar reduction in the daily rate of ammonium excretion (41 mmol) after KCl; however, their daily 3-hydroxybutyrate excretions declined by a similar amount (47 mmol) and thus metabolic acidosis did not develop.

3-Hydroxybutyric Acid↗
PubMed1986

[Lactic acidosis].

Lactic acidosis is a metabolic disturbance characterized by an increase of the production/clearance ratio of lactate. Lactate is a catabolite of glycolysis when this takes place under anaerobic conditions. Clinically LA is characterized by: signs of acidosis, venous blood lactate greater than 5 mMol/l, arterial pH less than 7.25. LA is classified in type A, due to shock, and type B which, in turn, can be divided according to its pathogenesis in B1 correlated to particular pathologies, B2 due to exogenous substances and B3 caused by congenital metabolic diseases. LA is of particular interest in type II diabetes mellitus treated by phenformin. Current therapeutic directions, although suboptimal, are: to eliminate the causes of lactate hyperproduction by maintaining a sufficient efficiency of the cardio-vascular apparatus, to correct acidosis by using alkalinizing solutions, to remove pharmacologically or by dialysis the excess of lactate.

Acidosis↗
PubMed1986

Metabolic acidosis.

Metabolic acidosis is the most frequent acid-base abnormality observed in the critically ill. Although there are many different causes, in the absence of ketosis and renal failure lactic acidosis is the most likely underlying disturbance. Controversy continues to surround the relative roles of the liver and the kidneys in the control of acid-base balance. There is no consensus concerning the use of bicarbonate in the treatment of a life-threatening metabolic acidosis.

Acidosis↗
PubMedDate not supplied

[Changes in the levels of various substrates of nitrogen metabolism and tricarboxylic acid cycle during experimental acidosis in calves].

The effect of experimental metabolic acidosis and its correction for nitrogen and energy metabolism was studied in new-born calves. It was discovered that a change in the acid-base balance towards acidosis causes a sharp increase in "ammoniogenesis", urea formation and inhibition of the tricarboxylic acid cycle, which is also observed in calves suffering from dyspepsia with symptoms of acute diarrhea. Alongside with the use of therapeutic measures for treating dyspepsia of new-born calves, it is necessary to control the acid-base balance of blood in the calves and in case of revealing the acidosis state to use means of its correction.

Acid-Base Equilibrium↗
PubMed1978

Correction of metabolic acidosis by the kidney during isometric expansion of extracellular fluid volume.

In dogs with chronic hypochloremic metabolic alkalosis associated with ECFV contraction, plasma [HCO-3] ([HCO-3]p) normalizes during expansion of ECFV with a solution containing Cl- and HCO-3 in concentrations duplicating those in the plasma before expansion (isometric expansion). The kidney selectively rejects administered HCO-3 and retains Cl-. If this preferential Cl- less than HCO-3 reabsorptive selectivity were a characteristic renal response to ECFV expansion, isometric expansion during hyperchloremic acidosis would exacerbate the acid-base disturbance rather than correct it as it does in alkalosis. We examined the effect of isometric expansion in dogs with chronic hyperchloremic metabolic acidosis induced by HCl feeding or mineralocorticoid hormone deficiency. During expansion, as the expected decrease occurred in the fractional reabsorption of Na+, a lesser decrease occurred in fractional reabsorption of HCO-3, whereas a greater decrease occurred in fractional reabsorption of Cl-. The kidney selectively retained administered HCO3 and rejected Cl-. [HCO-3]p normalized. The shift to bicarbonate-selective from chloride-selective anion reabsorption during ECFV expansion in metabolic acidosis vs. metabolic alkalosis indicates that in response to ECFV expansion- the kidney selectively alters the ratio of bicarbonate to chloride concentration in the tubular reabsorbate in the direction that tends to normalize plasma acid-base composition, irrespective of the direction of deviation of the initial plasma bicarbonate concentration. The signal that initiates the shift in anion reabsorptive selectivity remains to be identified.

Acidosis↗
PubMedDate not supplied

Type I primary hyperoxaluria associated with type I renal tubular acidosis.

An 8-year-old boy who had suffered from recurrent stone formation since the age of 4 years, was admitted as an emergency due to anuria for a half day on November 20, 1986. Kidney-ureter-bladder film showed that the urethra was obstructed by a stone, and emergent cystoscopy was performed to remove it. He is the product of consanguinous marriage, his parents being first cousins. There was no family history of renal stone. Laboratory investigations showed hypokalemic, hyperchloremic metabolic acidosis. The ammonium chloride loading test revealed inability to acidify the urine and a markedly decreased excretion of titrable hydrogen ion and ammonium ion in the urine. These results indicate that this is a case of Type I renal tubular acidosis. His 24-hour urinary excretion of oxalate and glyoxylate were also markedly increased. There were no underlying causes leading to the development of secondary hyperoxaluria. These results also establish the diagnosis of Type I primary hyperoxaluria. The patient then received regimens of Polycitra 1ml/kg/day and Vitamin B6 50mg/day for 4 months. However, urinary stone developed again in this patient 4 months later. To our knowledge, Type I primary hyperoxaluria in association with Type I renal tubular acidosis has not been previously reported.

Acidosis, Renal Tubular↗
PubMed1986

Hyperchloremic metabolic acidosis with high serum potassium in renal transplant recipients: a cyclosporine A associated side effect.

In four out of 23 renal transplant recipients treated with cyclosporine A (CyA) and prednisone, hyperchloremic metabolic acidosis with high serum potassium was detected. The patients with metabolic acidosis had a normal anion gap and they all had a urine pH less than 6.0. Plasma renin activity (PRA) was in the low normal range and serum aldosterone in the normal range. Following reduction of the CyA dose, serum bicarbonate increased, serum chloride and serum potassium fell. None of these parameters, however, became normal. Because of morphological changes and sustained reduced renal function, two patients were switched from CyA to azathioprine plus prednisone. Within two weeks after switching, serum bicarbonate, serum chloride, and serum potassium normalized. These data suggest, that CyA induces dose dependent hyperchloremic metabolic acidosis with high serum potassium in renal transplant recipients.

Acidosis↗
PubMed1987

Effect of metabolic acidosis on fetal renal haemodynamics.

The effects of metabolic acidosis on renal haemodynamics and intrarenal blood flow distribution was studied in two groups of chronically-catheterized fetal sheep between 122 and 130 days of gestation. One group (experimental group) was studied before and during infusion of 1.1 M lactic acid, whereas the second group received on infusion of dextrose 5% (w/v) in water and served as a time-control group. Infusion of lactic acid for 2 h decreased fetal arterial pH from 7.37 +/- 0.01 to 6.95 +/- 0.02, did not change arterial blood pressure, but produced a significant decrease in renal blood flow (41 +/- 3 to 33 +/- 7 ml/min, P less than 0.05) and a significant increase in renal vascular resistance (1.42 +/- 0.13 to 1.86 +/- 0.18 mmHg/ml/min, P less than 0.05). Moreover, a significant decline in cortical blood flow was also observed in the outer portion of the renal cortex during lactic acidosis. Taken together, these results suggest that metabolic acidosis produces significant changes in fetal renal haemodynamics not associated with changes in arterial blood pressure.

Acidosis↗