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PubMed1985

Hypokalemic paralysis in Sjögren's syndrome secondary to renal tubular acidosis.

A 62-year-old woman with Sjögren's syndrome, distal renal tubular acidosis and hypokalemic muscle paralysis is described. The sicca syndrome was nearly subclinical and went unrecognized for several years. The main and first manifestation to be expressed was that of hypokalemic muscle paralysis secondary to renal tubular acidosis. In the last decade several reports have appeared indicating that renal tubular acidosis is associated with Sjögren's syndrome. The data in this report support the view that adult onset distal renal tubular acidosis is often a disorder of an autoimmune disease, frequently that of Sjögren's syndrome. The complications to renal tubular acidosis such as hypokalemic muscle paralysis or chronic muscle weakness, nephrolithiasis, and osteomalacia can be avoided if the diagnosis of renal tubular acidosis is made and corrective alkali therapy is maintained.

Acidosis, Renal Tubular↗
PubMed2001

Metabolic and endocrine effects of metabolic acidosis in humans.

Metabolic acidosis is an important acid-base disturbance in humans. It is characterised by a primary decrease in body bicarbonate stores and is known to induce multiple endocrine and metabolic alterations. Metabolic acidosis induces nitrogen wasting and, in humans, depresses protein metabolism. The acidosis-induced alterations in various endocrine systems include decreases in IGF-1 levels due to peripheral growth hormone insensitivity, a mild form of primary hypothyroidism and hyperglucocorticoidism. Metabolic acidosis induces a negative calcium balance (resorption from bone) with hypercalciuria and a propensity to develop kidney stones. Metabolic acidosis also results in hypophosphataemia due to renal phosphate wasting. Negative calcium balance and phosphate depletion combine to induce a metabolic bone disease that exhibits features of both osteoporosis and osteomalacia. In humans at least, 1,25-(OH)2 vitamin D levels increase, probably through phosphate depletion-induced stimulation of 1-alpha hydroxylase. The production rate of 1,25-(OH)2 vitamin D is thus stimulated, and parathyroid hormone decreases secondarily. There is experimental evidence to support the notion that even mild degrees of acidosis, such as that occurring by ingestion of a high animal protein diet, induces some of these metabolic and endocrine effects. The possible role of diet-induced acid loads in nephrolithiasis, age-related loss of lean body mass and osteoporosis is discussed.

Acidosis↗
PubMed1998

[Decompensated diabetes mellitus and hyperchloremic metabolic acidosis: a case with both pathologies].

Diabetic ketoacidosis is manifested by elevated blood glucose levels, ketosis and metabolic acidosis with increased anion gap. A transitory hyperchloremic acidosis, with normal anion gap, can appear. We report a 21 years old female with a type 2 diabetes mellitus, admitted to the emergency room of a general hospital with hyperglycemia, absence of ketonemia, severe hypokalemia and hyperchloremic metabolic acidosis. Initially, she was diagnosed and treated as a severe diabetic ketoacidosis. Normal blood glucose levels were rapidly achieved but electrolyte and acid base alterations persisted, leading to the suspicion that another associated condition was causing the acidosis and hypokalemia. Urinary pH and anion gap measurement, the study of renal acidification and a bicarbonate overload test lead to the diagnosis of a distal renal tubular acidosis, secondary to a Sjögren syndrome, that was confirmed with a Schirmer test and positive anti Ro antibodies. In this diabetic patient, the acute hyperglycemia intensified the hypokalemia of her distal renal tubular acidosis and unchained the acute metabolic condition.

Acidosis, Renal Tubular↗
PubMed2001

Respiratory acidosis.

Respiratory acidosis, or primary hypercapnia, is the acid-base disorder that results from an increase in arterial partial pressure of carbon dioxide. Acute respiratory acidosis occurs with acute (Type II) respiratory failure, which can result from any sudden respiratory parenchymal (eg, pulmonary edema), airways (eg, chronic obstructive pulmonary disease or asthma), pleural, chest wall, neuromuscular (eg, spinal cord injury), or central nervous system event (eg, drug overdose). Chronic respiratory acidosis can result from numerous processes and is typified by a sustained increase in arterial partial pressure of carbon dioxide, resulting in renal adaptation, and a more marked increase in plasma bicarbonate. Mechanisms of respiratory acidosis include increased carbon dioxide production, alveolar hypoventilation, abnormal respiratory drive, abnormalities of the chest wall and respiratory muscles, and increased dead space. Although the symptoms, signs, and physiologic consequences of respiratory acidosis are numerous, the principal effects are on the central nervous and cardiovascular systems. Treatment for respiratory acidosis may include invasive or noninvasive ventilatory support and specific medical therapies directed at the underlying pathophysiology.

Acidosis, Respiratory↗
PubMed1975

Phenformin-associated lactic acidosis; a review.

A case of lactic acidosis associated with phenformin therapy for diabetes mellitus is reported, and 34 previously reported cases of lactic acidosis associated with phenformin therapy are reviewed to determine if any predisposing factors to lactic acidosis were apparent. Observations of sex, age, duration of diabetes, pathologic conditions, dosage, duration of phenformin therapy and the onset of symptoms preceding lactic acidosis were made. Renal impairment, urinary tract infections, hepatic impairment, ethanol ingestion and poorly controlled congestive heart failure were found to be predisposing factors to lactic acidosis. The appearance of a syndrome of impending lactic acidosis consisted of anorexia, nausea, vomiting with abdominal pain or lethargy.

Acidosis↗
PubMed2001

Riboflavin treatment of antiretroviral induced lactic acidosis and hepatic steatosis.

BACKGROUND: Antiretroviral induced lactic acidosis and hepatic steatosis is a rare syndrome caused by inhibition of deoxyribonucleic acid (DNA) polymerase gamma by the Nucleoside Reverse Transcriptase Inhibitor (NRTI) class of antiretrovirals. There have been recent reports of NRTI-induced lactic acidosis treated with high-dose riboflavin. INTERVENTION AND RESULTS: We report a case of NRTI lactic acidosis reversed with high-dose riboflavin. Treatment with 50 mg of riboflavin per day was initiated on hospital day 10 after the patient developed respiratory failure. Arterial lactate decreased from 11.9 mmol/dL to 2.1 mmol/dL. Despite lactic acidosis reversal the patient developed acute respiratory distress syndrome (ARDS) and expired. Autopsy confirmed extensive hepatic steatosis with no infectious agents identified. CONCLUSION: Nucleoside Reverse Transcriptase Inhibitor lactic acidosis will likely become more prevalent with the trend toward aggressive antiretroviral treatment. This report provides additional support for the efficacy of riboflavin treatment to reverse this serious complication of antiretroviral therapy. Clinicians should have a high index of suspicion for lactic acidosis in a patient on NRTIs and the medications should be stopped at the earliest sign of toxicity.

Acidosis, Lactic↗
PubMed1993

Haemodynamic changes associated with thermodilution cardiac output determination during metabolic acidosis or hypoxic hypoxia in dogs.

Haemodynamic alterations elicited by iced injectate during thermodilution cardiac output measurements were evaluated in the presence of metabolic acidosis or hypoxic hypoxia in 14 instrumented anaesthetized dogs. The alterations in some haemodynamic variables during slowing of the heart rate following injection of 3 ml iced injectate were slightly greater in metabolic acidosis and hypoxic hypoxia as compared to animals without metabolic acidosis or hypoxic hypoxia (P < 0.05), but the changes were clinically insignificant. No serious haemodynamic changes were found during any cardiac output measurement by thermodilution in the presence of metabolic acidosis or hypoxic hypoxia. The values of cardiac output measured by thermodilution correlated closely with those of pulmonary blood flow measured by an electromagnetic flowmeter in the metabolic acidosis and hypoxic hypoxia groups (r > 0.9). It is concluded that thermodilution using iced injectate will estimate right ventricular output accurately in conditions of metabolic acidosis and hypoxic hypoxia.

Acidosis↗
PubMed2000

[Expression of citrate transporter mRNA in the kidneys of rats with metabolic acidosis].

The purpose of the present study was to examine whether metabolic acidosis affects the expression of rat renal Na(+)/citrate cotransporter. Female Wistar rats were pair-fed with normal rat chow and drinking water (control) or water with 0.28 mol/L NH4Cl (metabolic acidosis). The mRNA of two renal Na(+)/citrate cotransporters, which were respectively expressed on apical and basolateral membrane, were measured by Northern blot with two probes, SDCT1 and SDCT2. Animals were sacrificed on day 1,3 and 7. On the 1st day, the blood plasma HCO(-)3 of acidosis group decreased significantly (P<0.01), but the mRNA abundance did not change. On the 3rd day in the acidosis group, the blood plasma HCO(-)3 increased slightly more than that on the 1st day, but was still significantly lower than that of the control group (P<0.01). Both the probes detected some increase in mRNA of brush border and basolateral Na(+)/citrate cotransporter. On the 7th day, the blood plasma HCO(-)3 of the acidosis group continuously increased and there was no significant difference between the two groups. The abundance of brush border and basolateral Na(+)/citrate cotransporter mRNA increased, but there was no difference between those of the 3rd day and the 7th day. It is concluded that metabolic acidosis can induce increase of Na(+)/citrate cotransporter mRNA, which may be responsible for hypocitraturia.

Acidosis↗
PubMedDate not supplied

Metformin-associated lactic acidosis: case reports and literature review.

BACKGROUND: Lactic acidosis is a widely recognized, though rare, side effect of metformin. This paper describes five patients admitted to Chang Gung Memorial Hospital from 1 September 1998 to 31 May 2001 suffering severe lactic acidosis caused by metformin, and reviews the literature. PATIENTS: Five cases diagnosed as having meftormin-associated lactic acidosis (MALA) were discovered during the study period. Three had normal renal function before the onset of MALA and two had attempted suicide bytaking large amounts of metformin. One patient with end-stage renal disease developed MALA despite regularhemodialysis three times a week. One of the patients who had taken metformin to attempt suicide was not diabetic. RESULTS: All patients suffered severe metabolic acidosis with a high anion gap and blood lactate level. Four developed profound hypotension, and three of these also suffered acute respiratory failure. Three patients received conventional hemodialysis and two continuous renal replacement therapy. A young non-diabetic female who had taken a large dose of metformin to commit suicide died from multiple organ failure despite aggressive treatment. CONCLUSIONS: Lactic acidosis is a serious reaction to metformin, and hemodialysis (the treatment of choice) should be done urgently to prevent serious complications. MALA should be suspected in patients presenting with wide anion gap metabolic acidosis and high blood lactate, even when they are non-diabetic.

Acidosis, Lactic↗
PubMed1992

Combined acute hypoxemia and hypercapnic acidosis increases atrial natriuretic polypeptide in conscious dogs.

To evaluate the changes in atrial natriuretic polypeptide during acute hypoxemia and acute hypercapnic acidosis, conscious mongrel dogs with controlled sodium intake were evaluated in four protocols: (1) 80 min of acute hypoxemia (PaO2 = 34 +/- 1 mm Hg) followed by 40 min of combined hypoxemia and hypercapnic acidosis (PaO2 = 38 +/- 1 mm Hg, PaCO2 = 60 +/- 3 mm Hg, pH = 7.15 +/- 0.03) (n = 7); (2) 40 min of combined acute hypoxemia and hypercapnic acidosis (PaO2 = 36 +/- 1 mm Hg, PaCO2 = 56 +/- 2 mm Hg, pH = 7.20 +/- 0.03) induced immediately following control measurements (n = 5); (3) 120 min of acute hypercapnic acidosis (PaCO2 = 58 +/- 1 mm Hg, pH = 7.20 +/- 0.01) (n = 5), and (4) 120 min of normoxemia and normocapnia (n = 7). These studies did not observe any association between urinary sodium excretion and circulating atrial natriuretic polypeptide during acute blood gas derangements in conscious dogs. The natriuresis with acute hypoxemia or acute hypercapnic acidosis was unaccompanied by change in plasma atrial natriuretic polypeptide concentrations. Conversely, the rise in circulating atrial natriuretic polypeptide during combined acute hypoxemia and hypercapnic acidosis was not associated with an increase in urinary sodium excretion. These observations do not exclude a role for atrial natriuretic polypeptide in altering sodium excretion during acute blood gas derangements, since the effects of this autacoid on renal sodium excretion may have been offset by other counterregulatory mechanisms of sodium excretion activated during the acute blood gas derangement.

Acidosis↗
PubMed1992

Severity of chronic metabolic acidosis and growth of rats with chronic uremia.

To determine what levels of chronic metabolic acidosis affect growth in uremia, we compared two groups of uremic rats receiving a 30% protein diet. This diet induced acidosis in A rats (n = 52; pH: 6.9-7.35) which was prevented by the addition of NaHCO3 in the diet of B rats (n = 52; pH: 7.38-7.46). A rats were separated into five groups by increasing severity of acidosis and were matched with B rats of similar renal function. Comparison between A and B rats showed: (1) no difference in food intake; (2) a reduction of weight gain only for severe acidosis with pH around 7.20 or less; (3) a reduction of length gain which was observed for less severe acidosis than reduction of weight gain, but which did not exist for marginal acidosis (pH > 7.25).

Acidosis↗
PubMed2005

Hypophosphatemia and metabolic acidosis.

The aim of the paper was to describe an unusual case of non lactic metabolic acidosis connected to hypophosphatemia and refractory to infusion of bicarbonate. A 37 year old man was admitted to Intensive Care Unit with a severe metabolic acidosis. On admission the arterial gas analysis showed non lactic metabolic acidosis (pH 7.17; base excess [BE] -20.3; lactic acid 0.8 mMol/L), with hypoxemia and critical hypocapnia. Despite therapy with bicarbonate the acidosis persisted. After 4 hours glucose phosphate was administered, although the phosphoremia was unknown. After phosphate supplementation an improvement of acidosis was observed. Our hypothesis is that in the kidney phosphate depletion caused impaired tubular reabsorption of bicarbonate, which led to a non lactic metabolic acidosis.

Acidosis↗
PubMedDate not supplied

Sodium bicarbonate versus THAM in ICU patients with mild metabolic acidosis.

BACKGROUND: Sodium bicarbonate is despite its side effects, considered the standard alkali therapy in metabolic acidosis. THAM is an alternative alkalizing agent; however, there are limited data on the use of THAM in metabolic acidosis. The aim of this study was to compare the efficacy and adverse effects of a single dose of sodium bicarbonate and THAM in intensive care unit (ICU) patients with mild metabolic acidosis. METHODS: 18 adult ICU patients with mild metabolic acidosis (serum bicarbonate < 20 mmol/L) were randomized to a single dose of either sodium bicarbonate or THAM, administered over a 1-hour period, and titrated to buffer the excess of acid load. RESULTS: Sodium bicarbonate and THAM had equivalent alkalinizing effect during the infusion period. This was still present 4 hours after start of infusion of sodium bicarbonate, and until 3 hours after start of infusion of THAM. Serum potassium levels decreased after sodium bicarbonate infusion, and remained unchanged after THAM. After sodium bicarbonate, sodium increased, and after THAM, serum sodium decreased. CONCLUSIONS: Sodium bicarbonate and THAM had a similar alkalinizing effect in patients with mild metabolic acidosis; however, the effect of sodium bicarbonate was longer lasting. Sodium bicarbonate did decrease serum potassium, and THAM did not; THAM is therefore not recommended in patient with hyperkalemia. As sodium bicarbonate leads to an increase of serum sodium and THAM to a decrease, THAM may be the alkalinizing agent of choice in patients with hypernatremia. Similarly, because sodium bicarbonate increases PaCO2 and THAM may even decrease PaCO2, sodium bicarbonate is contraindicated and THAM preferred in patients with mixed acidosis with high PaCO2 levels.

Acidosis↗
PubMedDate not supplied

Metabolic and clinical consequences of metabolic acidosis.

Acid-base balance is precisely regulated by pulmonary and renal responses while body buffers help to control pH. When its regulation becomes abnormal, accumulation of hydrogen ions cause metabolic acidosis and several responses are activated. These responses interfere with the metabolism of bones and muscle. Metabolic acidosis induces abnormalities in the release and function of several hormones including defects in growth hormone, IGF-1, insulin, glucocorticoids, thyroid hormone, parathyroid hormone and vitamin D. Clinical consequences of these abnormal metabolic responses include impaired growth of infants and children and loss of bone and muscle mass in adults. Notably, abnormalities in bone and muscle metabolism can be present even when there is little or no decrease in the plasma bicarbonate concentration. The abnormalities can be corrected by treatment with NaHCO 3 . In patients with chronic kidney disease, many abnormalities in bone and muscle metabolism can be directly linked to the presence of metabolic acidosis and these abnormalities can be largely corrected by treating acidosis with NaHCO3. Recent insights indicate that several consequences of metabolic acidosis including the development of insulin resistance can stimulate muscle protein degradation by activating proteolytic mechanisms. To avoid abnormalities in metabolism and the loss of bone and muscle, metabolic acidosis must be corrected in normal adults and in patients with kidney disease.

Acid-Base Equilibrium↗
PubMedDate not supplied

[A clinical case of development of lactic acid acidosis in a diabetic patient taking metformin].

Metformin is a biguanide. Due to its effects in suppressing the hepatic production of endogenous glucose and in increasing insulin sensitivity in adipose tissue and skeletal muscle, the agent is used particularly in type 2 diabetes mellitus and metabolic syndrome, in which insulin resistance is especially pronounced. Lactic acidosis is one of the most important side effects of metformin. A male patient, born in 1923, was admitted to the emergency unit of our hospital for sudden vertigo, weakness, dyspnea, cyanosis, and lethargy. His history data showed that the patient had been suffering from type 2 diabetes mellitus for 10 years and taking Glargin (insulin), 12 U/kg, once daily and Glucophage (metformin), 850 mg thrice daily. The patient's general condition was fair; stupor, time and spatial orientation were absent. Analysis of arterial blood gases showed the presence of metabolic acidosis, hypokalemia, hypoxemia, and hypercapnia. Thereafter the patient was transferred to the intensive care unit of the hospital; intubated and connected to a T-bird ventilation apparatus. On the following day, an analysis of arterial blood gases indicated the proximity of the results to their physiological parameters. Ventilation was stopped; and monitoring of the patient continued by following the T-shape type of ventilation discontinuation. There were no X-ray signs of pneumonia or pulmonary edema. On the same day, the patient was extubated and oxygen inhalation in a dose of L/min was continued through a mask. On day 4 since therapy was initiated, the patient's vital signs, serum sugar and lactate levels became normal. By determining a new treatment regimen, the patient was discharged from the intensive care unit. Dyspnea, acidosis, and hypoxia developed in the patient resulted from lactic acidosis caused by the use of metformin. It should be remembered that dyspnea, acidosis, and hypoxia, which suddenly developed in metformin-treated patients with type 2 diabetes mellitus, may be caused by lactic acidosis.

Acidosis, Lactic↗
PubMedDate not supplied

[Gastric emptying and metabolic acidosis. I. Study of an experimental model in rats, using an ammonium chloride solution administered through the orogastric route].

The goal of the study was get an experimental model of metabolic acidosis which was appropriated in future gastric emptying studies. For this proposal were utilized 141 female Wistar rats in three stages: in the first (n = 27) was defined the installation, manutention and spontaneous recuperation of the metabolic acidosis produced by the orogastric infusion of a two ml by 100 g of an 0.5 M ammonium chloride solution; in the second (n = 60), it was studied the gastric emptying of the same solution utilized in the first stage and in the last stage (n = 54) it was determined the gastric emptying of the water, for excluding the possibility that the acidificant solution had caused any lesion in the gastric mucosa. As control group were utilized animals fed as a sodium chloride solution in the same concentration and volume that the acidificant solution. The results showed that 6 hours after the infusion, the gastric emptying of two above mentioned meals was complete and there was still a moderate metabolic acidosis in the group with infusion of ammonium chloride solution. Further more, the metabolic acidosis persisted in moderate values until 8 hours after the infusion. Based on these data the interval between 6 and 8 hours after the infusion of the these solutions was considered the best to the further studies about metabolic acidosis and gastric emptying. Finally, the gastric emptying of water, studied in rats with acidosis and controls demonstrated no differences between them. This was interpreted as a clue that the ammonium chloride solution did not modificate the integrity of the gastric mucosa.

Acidosis↗
PubMedDate not supplied

Renal tubular acidosis in childhood.

Nineteen children with clinical diagnoses of renal tubular acidosis were followed for periods ranging from 3 months to 20 years. Twelve patients had Type 1 renal tubular acidosis, five had Type 2, and two had Type 4. No sex predilection was found for any one of the types. Most patients had been diagnosed before 18 months of age, with failure to thrive the most common presentation. Tachypnea, polydipsia, polyuria, and vomiting were frequent symptoms. Some of these children had associated renal hypoplasia, vesicoureteral reflux, unilateral renal agenesis, glomerulocystic disease, adult polycystic kidney disease, and cyanotic congenital heart disease. Urinary anion gap may be useful for differential diagnosis of altered distal urinary acidification from other hyperchloremic metabolic acidosis. Furosemide test may need further investigation. Inability to raise urine to blood pCO2 gradient is helpful for diagnosis of Type 1 renal tubular acidosis. Hypokalemia, hypocalcemia, hypophosphatemia, decreased tubular reabsorption of phosphate, and hypercalciuria occurred in some patients. Complications included rickets in two, nephrocalcinosis in one, and episodic hematuria in one. There was relative bicarbonate wasting in children with Type 1 renal tubular acidosis, with a mean therapeutic bicarbonate requirement of 4.4 +/- 2.6 meq/kg/day. The mean bicarbonate dose for patients with Type 2 renal tubular acidosis was 8.3 +/- 2.6 meq/kg/day. Most children had good response to treatment with complete catch-up linear growth in 13, improved growth in 4, and continuing poor growth in 2. Two patients died during follow-up. Two other patients maintained normal growth without medication.

Acidosis, Renal Tubular↗
PubMed1986

Therapeutic benefit of dichloroacetate in experimentally induced hypoxic lactic acidosis.

Although dichloroacetate (DCA) ameliorates type B lactic acidosis, its effectiveness in type A hypoxic lactic acidosis is uncertain on both theoretical and experimental grounds. Because this drug was reported recently to successfully ameliorate lactic acidosis in patients with type A lactic acidosis, we tested its effect on pure hypoxia-induced lactic acidosis in rats. Anesthetized, mechanically ventilated rats were subjected to a decrease in FiO2, from 21% to 7.5% over a 20-minute period, and maintenance of hypoxia for an additional hour. Either DCA (300 mg/kg) or equal volumes of normal saline solution or hypertonic saline solution was infused during the induction period. DCA significantly attenuated the rise in blood lactate levels in comparison with both control groups, and also resulted in maintenance of a higher blood pH and bicarbonate level. Systolic blood pressure was also maintained at a higher, although significantly subnormal level, in the DCA group. DCA increased urine flow rate and sodium excretion, and additional studies with the isolated perfused rat kidney suggested that this resulted in part from a direct drug-mediated effect on renal sodium handling. Although these results do not delineate the underlying mechanisms, they clearly demonstrate that DCA is an effective form of therapy for type A lactic acidosis.

Acetates↗