sodium-bicarbonate and Hypokalemia

Distal renal tubular acidosis is a relatively infrequent condition with complex pathophysiology that can present with life-threatening electrolyte abnormalities.. We describe a case of a 57-year-old Caucasian woman with previous episodes of hypokalemia, severe muscle weakness, and fatigue. Upon further questioning, symptoms of dry eye and dry mouth became evident. Initial evaluation revealed hyperchloremic metabolic acidosis, severe hypokalemia, persistent alkaline urine, and a positive urinary anion gap, suggestive of distal renal tubular acidosis. Additional laboratory workup and renal biopsy led to the diagnosis of primary Sjögren's syndrome with associated acute tubulointerstitial nephritis. After potassium and bicarbonate supplementation, immunomodulatory therapy with hydroxychloroquine, azathioprine, and prednisone was started. Nonetheless, her renal function failed to improve and remained steady with an estimated glomerular filtration rate of 42 ml/min/1.73 m. Cases of renal tubular acidosis should be carefully evaluated to prevent adverse complications, uncover a potentially treatable condition, and prevent the progression to chronic kidney disease. Repeated episodes of unexplained hypokalemia could be an important clue for diagnosis.

Topics: Acid-Base Equilibrium; Acidosis, Renal Tubular; Disease Progression; Female; Glomerular Filtration Rate; Humans; Hypokalemia; Immunomodulation; Middle Aged; Potassium; Sjogren's Syndrome; Sodium Bicarbonate; Trace Elements; Treatment Outcome

Topics: Animals; Antidepressive Agents, Tricyclic; Antidotes; Aspirin; Heart Failure; Humans; Hypokalemia; Injections, Intravenous; Sodium Bicarbonate; Tachycardia, Ventricular

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Topics: Acidosis; Clinical Trials as Topic; Disease Progression; Glomerular Filtration Rate; Humans; Hypercapnia; Hypocalcemia; Hypokalemia; Renal Dialysis; Renal Insufficiency, Chronic; Sodium Bicarbonate

Topics: Adrenergic beta-Agonists; Aldosterone; Diagnosis, Differential; Gluconates; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney Tubules; Potassium; Renal Dialysis; Sodium Bicarbonate

The objective of this teaching session with Professor McCance is to develop an approach to the management of patients with a very low plasma potassium (K(+)) concentration (P(K)). The session begins with a quiz based on six recent medical consultations for a P(K) < 2 mmol/l. Professor McCance outlined how he would proceed with his diagnosis and therapy, using the synopsis that described each patient. This approach was then applied to a new patient, a 69-year-old woman who had a large volume of dependent oedema and developed a severe degree of weakness and hypokalaemia during more aggressive diuretic therapy that included a K(+)-sparing diuretic. The initial challenge for Professor McCance was to deduce why the K(+)-sparing diuretic was not effective in this patient. He also needed to explain why the P(K) was so low on admission.

Topics: Acidosis; Adult; Aged; Alkalosis; Cell Physiological Phenomena; Creatinine; Diuretics; Female; Humans; Hypokalemia; Kidney; Male; Middle Aged; Paralysis; Potassium; Sodium Bicarbonate

Topics: Acidosis, Renal Tubular; Diagnosis, Differential; Humans; Hypokalemia; Neurons, Afferent; Peripheral Nervous System Diseases; Prognosis; Sodium Bicarbonate

Topics: Calcium Gluconate; Glucose; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney; Polystyrenes; Potassium; Sodium Bicarbonate

Tubular acidosis is diagnosed when hyperchloremic acidosis is associated with inappropriate NH4 excretion (less than or equal to 40 mmol/24 hours). Urinary pH is variable because it depends on the secretion of H+ into the collecting duct and is inversely correlated with the amount of ammonia available in the urine. Administration of NaHCO3 for diagnostic purpose allows to eliminate proximal tubular acidosis and to measure the elevation of urinary PCO2 reflecting the secretion of H+ in the collecting duct. Hypokalemia points towards distal tubular acidosis, either by defect of H(+)-ATPases pumps, or by the incapacity to create a normal gradient of H+. In contrast hyperkalemia suggests distal tubular acidosis associated either with hypoaldosteronism or with diminution of trans-epithelial voltage or with pseudohypoaldosteronism. The incidence of distal tubular acidosis with hyperkalemia is increasing whereas distal tubular acidosis with hypokalemia remain rare.

Topics: Acidosis, Renal Tubular; Bicarbonates; Humans; Hyperkalemia; Hypokalemia; Sodium; Sodium Bicarbonate

Mechanisms of renal potassium excretion and internal potassium balance as the main determinants of serum and/or total body potassium are discussed. Renal handling of potassium is reviewed, with particular attention to the effects of diuretics, acid-base disturbances and aldosterone-deficient states. Among the regulatory processes of internal potassium balance, the importance of adrenergic stimuli/drugs, of acid-base balance, and of magnesium and insulin is stressed. Physiologic and pathophysiologic evidence provides the basis for discussion of relevant clinical implications.

Topics: Acid-Base Equilibrium; Adult; Aged; Alkalosis; Bicarbonates; Biological Transport; Catecholamines; Chlorides; Diuretics; Female; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney; Kidney Tubules; Magnesium Deficiency; Male; Middle Aged; Potassium; Renin-Angiotensin System; Sodium; Sodium Bicarbonate; Stress, Physiological

Topics: Bicarbonates; Diabetic Ketoacidosis; Diphosphoglyceric Acids; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Hypokalemia; Infusions, Parenteral; Insulin; Magnesium Deficiency; Magnesium Sulfate; Phosphates; Sodium Bicarbonate; Time Factors

Ninety four children aged less than 5 years with diarrhoeal dehydration and acidosis were treated randomly with either World Health Organisation (WHO) oral rehydration solution containing sodium chloride, potassium chloride, sodium bicarbonate and glucose or an oral solution with tripotassium citrate monohydrate replacing the sodium bicarbonate and potassium chloride in the WHO solution. Fifty five children (58%) were hypokalaemic (potassium less than 3.5 mmol/l) on admission. All but two in the citrate group were successfully treated. There were no significant differences in rehydration solution intake, stool output, gain in body weight, and fall in plasma specific gravity and haematocrit between the two treatment groups after 48 hours' treatment. Significant improvement in the serum potassium concentration was observed in the hypokalaemic children receiving potassium citrate solution compared with children receiving WHO solution after 24 and 48 hours' treatment. None developed hyperkalaemia. Although children receiving potassium citrate solution corrected their acidosis at a slower rate than the WHO solution group during the first 24 hours, by 48 hours satisfactory correction was observed in all. Tripotassium citrate can safely replace sodium bicarbonate and potassium chloride and may be the most useful and beneficial treatment for diarrhoea and associated hypokalaemia.

Topics: Acidosis; Bicarbonates; Child, Preschool; Citrates; Citric Acid; Clinical Trials as Topic; Diarrhea; Double-Blind Method; Feces; Fluid Therapy; Humans; Hypokalemia; Infant; Infant, Newborn; Potassium Chloride; Sodium; Sodium Bicarbonate

Sodium bicarbonate, in the form of baking soda, is widely used as a home remedy, and as an additive for personal and household cleaning products. Its toxicity has previously been reported following oral ingestion in the setting of dyspepsia. However, its use as a non-ingested agent, like a toothpaste additive, has not been reported as a potential cause of toxicity.. We are reporting a case of an 80-year-old woman who presented with chronic metabolic alkalosis and hypokalemia secondary to exogenous alkali exposure from baking soda as a toothpaste additive, which might have represented an underreported ingestion of the substance.. Considering that one teaspoon of baking soda provides approximately 59 m-equivalents (mEq) of bicarbonate, specific questioning on its general use should be pursued in similar cases of chloride resistant metabolic alkalosis.

Topics: Aged, 80 and over; Alkalosis; Chlorides; Female; Humans; Hypokalemia; Renal Insufficiency, Chronic; Sodium Bicarbonate; Toothpastes

A 61-year-old woman was admitted to our hospital because of muscle paralysis and was found to have severe hypokalemia. A gallium-67 scintigram revealed a positive accumulation in the bilateral salivary glands, and a labial minor salivary gland biopsy demonstrated a massive lymphocyte infiltrate around the salivary ducts. She was diagnosed with Sjögren's syndrome (SS) associated with renal tubular acidosis. Renal biopsy revealed tubulointerstitial nephritis with a mild focal infiltration of lymphocytes and plasma cells. These pathological features were compatible with SS with renal involvement. Acidosis and hypokalemia were corrected with sodium bicarbonate and potassium chloride, which relieved the patient's symptoms. Although steroid therapy has been reported to be effective in SS-associated tubulointerstitial nephritis, the patient's serum potassium level could be controlled without administering steroids during the first admission. Five years later, she was admitted again because of severe liver dysfunction attributed to autoimmune hepatitis. Oral administration of prednisolone resulted in the normalization of her transaminase levels, and the control of her serum potassium level became easier. It has been reported that patients with SS with salivary gland involvement tend to have hepatic complications, and those with hepatic complications tend to have renal involvement. Physicians should be aware of hepatic involvement, even if there is no liver dysfunction at the initial diagnosis of SS with salivary gland and renal involvement. It remains uncertain whether the administration of a low dose of steroids before the onset of autoimmune hepatitis might have prevented the development of liver dysfunction in our patient.

Topics: Acidosis, Renal Tubular; Administration, Oral; Female; Hepatitis, Autoimmune; Humans; Hypokalemia; Kidney; Lymphocytes; Middle Aged; Nephritis, Interstitial; Plasma Cells; Potassium Chloride; Prednisolone; Severity of Illness Index; Sjogren's Syndrome; Sodium Bicarbonate

Topics: Acidosis; Adolescent; Antidepressive Agents, Tricyclic; Drug Overdose; Female; Humans; Hypokalemia; Hypotension; Pneumonia; Respiration, Artificial; Respiratory Distress Syndrome; Sodium Acetate; Sodium Bicarbonate; Suicide, Attempted; Vasoconstrictor Agents

Baking soda (sodium bicarbonate) is a common household item that has gained popularity as an alternative cancer treatment. Some have speculated that alkali therapy neutralizes the extracellular acidity of tumor cells that promotes metastases. Internet blogs have touted alkali as a safe and natural alternative to chemotherapy that targets cancer cells without systemic effects. Sodium bicarbonate overdose is uncommon, with few reports of toxic effects in humans. The case described here is the first reported case of severe metabolic alkalosis related to topical use of sodium bicarbonate as a treatment for cancer. This case highlights how a seemingly benign and readily available product can have potentially lethal consequences.

Topics: Administration, Topical; Aged; Alkalies; Alkalosis; Female; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Hypokalemia; Neoplasms; Sodium Bicarbonate; Treatment Outcome

This case report describes the possible benefit of intravenous lipid emulsion in two patients surviving a severe intoxication with hydroxychloroquine in a dose that was previously considered to be lethal. The first case involves a 25-year-old female who ingested 17.5 grams of hydroxychloroquine, approximately one hour before presentation. An ECG showed QRS widening and the lab results showed hypokalaemia. She became unconscious, and developed hypotension and eventually apnoea. After intubation, supportive care consisted of norepinephrine and supplementation of potassium. Moreover, sodium bicarbonate and intravenous lipid emulsion were started to prevent cardiac toxicity. After these interventions, haemodynamic stability was established within a few hours. Although cardiomyopathy was confirmed, the patient recovered after two weeks. The second case concerns a 25-year-old male who took 5 grams of hydroxychloroquine. At presentation, two hours after intake, he showed QTc prolongation and hypokalaemia. The patient was treated with the usual supportive care and, although presentation to hospital was later, with intravenous lipid emulsion. Also this patient recovered. In conclusion, these cases show the benefit of supplemental intravenous lipid emulsion to prevent cardiac toxicity after a severe intoxication with hydroxychloroquine.

Topics: Adult; Arrhythmias, Cardiac; Chromatography, Liquid; Drug Overdose; Electrocardiography; Fat Emulsions, Intravenous; Female; Humans; Hydroxychloroquine; Hypokalemia; Hypotension; Male; Norepinephrine; Potassium Chloride; Sodium Bicarbonate; Suicide, Attempted; Tandem Mass Spectrometry; Vasoconstrictor Agents

Topics: Acidosis; Animals; Atrial Fibrillation; Boric Acids; Crystalloid Solutions; Electrocardiography; Female; Horse Diseases; Horses; Hypokalemia; Isotonic Solutions; Potassium Chloride; Sodium Bicarbonate

Pica is a commonly underappreciated disorder in pregnancy that can lead to several complications, including severe metabolic derangements and other adverse outcomes. We report a case of baking soda pica in pregnancy associated with both rhabdomyolysis and cardiomyopathy.. A multigravid woman at 37 weeks of gestation presented with weakness and severe hypokalemia. She subsequently had development of rhabdomyolysis and presumed peripartum cardiomyopathy. After delivery, it was discovered that the patient had a long history of consumption of large quantities of baking soda. Her condition improved with cessation of the pica.. Clinicians must have a high index of suspicion for pica in pregnancy because it can lead to complex diagnostic challenges and pregnancy complications. The diagnosis should be considered in a patient with unexplained metabolic abnormalities.

Topics: Adult; Cardiomyopathies; Female; Humans; Hypokalemia; Muscle Weakness; Pica; Pregnancy; Pregnancy Complications, Cardiovascular; Rhabdomyolysis; Sodium Bicarbonate

Underlying causes of metabolic alkalosis may be evident from history, evaluation of effective circulatory volume, and measurement of urine chloride concentration. However, identification of causes may be difficult for certain conditions associated with clandestine behaviors, such as surreptitious vomiting, use of drugs or herbal supplements with mineralocorticoid activity, abuse of laxatives or diuretics, and long-term use of alkalis. In these circumstances, clinicians often are bewildered by unexplained metabolic alkalosis from an incomplete history or persistent deception by the patient, leading to misdiagnosis and poor outcome. We present a case of severe metabolic alkalosis and hypokalemia with a borderline urine chloride concentration in an alcoholic patient treated with a thiazide. The cause of the patient's metabolic alkalosis eventually was linked to surreptitious ingestion of baking soda. This case highlights the necessity of a high index of suspicion for the diverse clandestine behaviors that can cause metabolic alkalosis and the usefulness of urine pH and anion gap in its differential diagnosis.

Topics: Acid-Base Equilibrium; Aged; Alcoholism; Alkalosis; Chlorides; Comorbidity; Eating; Humans; Hydrogen-Ion Concentration; Hypokalemia; Male; Sodium Bicarbonate; Thiazides; Urine

We report a unique case of diabetic ketoacidosis in which a relatively low potassium level on admission was associated with consequent life-threatening and refractory arrhythmia secondary to inappropriate use of intravenous insulin and bicarbonate therapy. The latter was reversed by rapid bolus potassium injection. Although we do not advocate this approach in every case, we emphasise that a bolus injection of potassium may be life saving in such cases. The lessons from this case have led to multidisciplinary meetings and modification of the institute's diabetic ketoacidosis clinical pathway.

Topics: Adult; Diabetic Ketoacidosis; Female; Heart Arrest; Humans; Hypoglycemic Agents; Hypokalemia; Insulin; Potassium Chloride; Sodium Bicarbonate; Young Adult

Our objective was to study the risk factors and mechanisms of hypernatraemia in critically ill patients, a common and potentially serious problem.. In 2005, all patients admitted to the medical, surgical or neurological intensive care unit (ICU) of a university hospital were reviewed. A 1:2 matched case-control study was performed, defining cases as patients who developed a serum sodium >/=150 mmol/l in the ICU.. One hundred and thirty cases with ICU-acquired hypernatraemia (141 +/- 3 to 156 +/- 6 mmol/l) were compared to 260 controls. Sepsis (9% versus 2%), hypokalaemia (53% versus 34%), renal dysfunction (53% versus 13%), hypoalbuminaemia (91% versus 55%), the use of mannitol (10% versus 1%) and use of sodium bicarbonate (23% versus 0.4%) were more common in cases (P < 0.05 for all) and were independently associated with hypernatraemia. During the development of hypernatraemia, fluid balance was negative in 80 cases (-31 +/- 2 ml/kg/day), but positive in 50 cases (72 +/- 3 ml/kg/day). Cases with a positive fluid balance received more sodium plus potassium (148 +/- 2 versus 133 +/- 3 mmol/l, P < 0.001). On average, cases were polyuric (40 +/- 5 ml/kg). Mortality was higher in cases (48% versus 10%, P < 0.001), for which hypernatraemia was an independent predictor (odds ratio 4.3, 95% confidence interval 2.5 to 7.2).. Hypernatraemia seems to develop in the ICU because various factors promote renal water loss, which is then corrected with too little water or overcorrected with relatively hypertonic fluids. Therapy should therefore rely on adding electrolyte-free water and/or creating a negative sodium balance. Adjustments in intravenous fluid regimens may prevent hypernatraemia.

Topics: Adult; Aged; Case-Control Studies; Critical Illness; Female; Fluid Therapy; Humans; Hypernatremia; Hypoalbuminemia; Hypokalemia; Intensive Care Units; Kidney Diseases; Male; Mannitol; Middle Aged; Risk Factors; Sepsis; Sodium Bicarbonate; Water-Electrolyte Balance

Topics: Acidosis; Adult; Humans; Hypokalemia; Infusions, Intravenous; Male; Sodium Bicarbonate; Tachycardia, Ventricular

Uncommon metabolic abnormalities in the emergency department could be a result of drug overdose due to uncommon agents.. A 35-year-old male presented to the emergency department with a Glasgow Coma Scale (GCS) of 3/15 and a normal pulse rate and blood pressure. Subsequent questioning after recovery revealed he had ingested 2 L of Gaviscon over the preceding 48 hours. He had normal haematology, liver, and renal function during admission. The electrocardiogram showed T wave inversion in the inferior leads on admission. Arterial blood gas on air was: pH 7.54, HCO3 50 mmol/L (50 meq/L), Chloride 66 mmol/L, anion gap was 19, pO2 11 kPa (82.5 mmHg), and pCO2 8 kPa (60 mmHg). Serum sodium was 127 mmol/L and serum potassium was 1.6 mmol/L. His GCS improved within one hour of admission with supportive care, and his serum potassium and bicarbonate improved within 24 hours. He subsequently made a full recovery. Discussion. Bicarbonate ingestion in the form of Gaviscon(R) and vomiting made this patient alkalotic, and simple supportive care provided effective management with a complete recovery.. This case illustrates how a severe metabolic alkalosis can result from a significant ingestion of Gaviscon, and that such presentations can give rise to diagnostic dilemma.

Topics: Adult; Alginates; Alkalosis; Aluminum Hydroxide; Antacids; Drug Combinations; Humans; Hypokalemia; Male; Severity of Illness Index; Silicic Acid; Sodium Bicarbonate; Treatment Outcome

We report a case of baking soda pica in a woman at 31 weeks of pregnancy causing severe hypokalemic metabolic alkalosis and rhabdomyolysis.. A multigravida at 31 weeks of gestation presented with weakness and muscle pain. She was found to have severe hypokalemic metabolic alkalosis and rhabdomyolysis, with elevation in serum transaminases and hypertension. We initially thought the patient had an atypical presentation of preeclampsia until it was realized that she was ingesting 1 full box of baking soda (454 g sodium bicarbonate) per day. Symptoms and abnormal laboratory findings resolved with discontinuation of the patient's pica practices.. Pica is a common but often overlooked practice that can potentially lead to life-threatening disorders. A thorough evaluation of a patient's dietary intake is extremely important, especially in the setting of atypical presentations of disease in pregnancy.

Topics: Adult; Alkalosis; Female; Humans; Hypokalemia; Pica; Pregnancy; Pregnancy Complications; Rhabdomyolysis; Sodium Bicarbonate

Topics: Anti-Inflammatory Agents, Non-Steroidal; Female; Humans; Hypokalemia; Ibuprofen; Middle Aged; Nonprescription Drugs; Potassium; Sodium Bicarbonate; Treatment Outcome

Topics: Alum Compounds; Calcium Sulfate; Causality; Diagnosis, Differential; Electrolytes; Female; Humans; Hyperkalemia; Hypokalemia; Kidney Failure, Chronic; Middle Aged; Pica; Renal Dialysis; Sodium Bicarbonate; Starch

A patient with a history of cerebrovascular disease, hypertension, and previous gastrectomy developed metabolic alkalosis and myoclonus. His medications included the anti-hypertensive agents nicardipine hydrochloride, delapril, prazosin; dihydroergotoxin and ticlopidine for cerebral infarction; estazolam for insomnia; azuren-L-glutamine compound and S-M powder. In addition, he had taken 12 grams per day of Ohta's Isan antacid, which contained 625 mg sodium bicarbonate per 1.3 g of antacid powder over a 6-month period. This antacid is commonly used in Japan. This is the first report of a case of metabolic alkalosis and myoclonus secondary to ingestion of a commercially available antacid in Japan.

Topics: Aged; Alkalosis; Antacids; Cardiovascular Agents; Cerebral Infarction; Dyspepsia; Gastrectomy; Humans; Hypertension; Hypnotics and Sedatives; Hypokalemia; Male; Myoclonus; Sleep Initiation and Maintenance Disorders; Sodium Bicarbonate

Severe hypokalemia is an uncommon cause of rhabdomyolysis. We describe a patient, 28-year-old woman, with distal renal tubular acidosis (DRTA) who developed severe hypokalemia and rhabdomyolysis. Muscle biopsy shows focal muscular necrosis mainly in type II muscle fibers and mild macrophagic reaction. After correcting the acidosis with oral administration of alkalinizing salts, clinical and laboratory improvement was seen. This clearly establish a causal relationship between the positive acid balance, hypokalemia and the muscular manifestation in DRTA.

Topics: Acidosis, Renal Tubular; Adult; Diagnosis, Differential; Female; Humans; Hypokalemia; Potassium Chloride; Rhabdomyolysis; Sodium Bicarbonate

Sodium bicarbonate is an extremely well-known agent that historically has been used for a variety of medical conditions. Despite the widespread use of oral bicarbonate, little documented toxicity has occurred, and the emergency medicine literature contains no reports of toxicity caused by the ingestion of baking soda. Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The case of a patient with three hospital admissions in 4 months, all the result of excessive oral intake of bicarbonate for symptomatic relief of dyspepsia is reported. Evaluation and treatment of patients with acute bicarbonate ingestion is discussed.

Topics: Acute Disease; Alkalosis; Humans; Hypokalemia; Male; Middle Aged; Poisoning; Sodium Bicarbonate

The pathogenesis of renal potassium wasting and hypokalemia in classic renal tubular acidosis (type 1 RTA) remains uncertain. The prevailing theory is that K(+)-Na+ exchange is stimulated due to an inability of the distal tubule to establish a normal steep lumen-peritubular H+ gradient. We encountered a 42-year-old woman with type 1 RTA associated with Sjögren's syndrome, in whom renal potassium wasting and hypokalemia persisted despite sustained correction of systemic acidosis with alkali therapy and increased intake of potassium. In addition, plasma renin activity was markedly increased and the serum aldosterone level was upper-normal despite the hypokalemia. Increased intake of sodium resulted in suppression on the serum aldosterone and correction of renal potassium wasting and hypokalemia. This case shows that secondary hyperaldosteronism, possibly due to an impairment of sodium conservation in the distal tubule, may contribute to the loss of potassium from the distal tubule even after the correction of acidosis.

Topics: Acidosis, Renal Tubular; Adult; Aldosterone; Ammonium Chloride; Bicarbonates; Blood Gas Analysis; Female; Humans; Hydrogen-Ion Concentration; Hyperaldosteronism; Hypokalemia; Kidney; Potassium; Potassium, Dietary; Sjogren's Syndrome; Sodium; Sodium Bicarbonate; Sodium, Dietary; Urine; Water-Electrolyte Balance

Topics: Bicarbonates; Calcium Gluconate; Humans; Hyperkalemia; Hypokalemia; Polystyrenes; Potassium; Sodium; Sodium Bicarbonate

Sodium bicarbonate abuse is unusual, and rarely reported. A patient was extensively investigated at several hospitals for a recurrent hypokalaemic metabolic alkalosis; it transpired that she had been abusing sodium bicarbonate for 8 years and had gained hospital admission at will by taking large amounts. She also showed features of the Munchausen syndrome.

Topics: Adult; Alkalosis; Bicarbonates; Female; Humans; Hypokalemia; Munchausen Syndrome; Sodium; Sodium Bicarbonate; Substance-Related Disorders

Topics: Alkalosis; Humans; Hypokalemia; Ketone Bodies; Nausea; Paralysis; Potassium; Sodium Bicarbonate; Vomiting