The most severe metabolic alkalosis in a patient with chronic renal failure due to soda ingestion and vomiting

International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 14 The Most Severe Metabolic Alkalosis in a Patient With Chronic Renal Failure Due to Soda Ingestion and vomiting Authors Irini M. Kalogiannidou (MD) Nephrologist, Consultant Renal Unit «Dimokrition», Komotini, Thrace, Greece Antoniou Rossidi 11, 69132, Komotini, Thrace, Greece  (+30) 69777 88470 ✉ [email protected] ORCID: 0000-0001-5492-4151 Konstantinos S. Mavromatidis (MD) Nephrologist, Director Renal Unit «Dimokrition», Komotini, Thrace, Greece Antoniou Rossidi 11, 69132, Komotini, Thrace, Greece  (+30) 69722 70092 ✉ [email protected] ORCID: 0000-0002-1601-5341 Affiliaon (for all authors) Renal Unit «Dimokrition», Komotini, Thrace, Greece Corresponding Author Konstantinos S. Mavromatidis (MD) Nephrologist, Director of Renal Unit «Dimokrition» Komotini, Thrace, Greece Tel/Fax: (+30) 25310 30706 Mobile: (+30) 69722 70092 E-mail: [email protected] Internaonal Journal of Pharmaceucal Science and Health Care Available online on h'p://www.rspublicaon.com/ijphc/index.html ISSN 2249 – 5738 International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 15 ARTICLE INFO ABSTRACT ©2025 RS Publicaon Paper ID: IJPHC690C7FB06083D Received: 2025-10-08 Published: 2025-11-07 DOI: https://dx.doi.org /10.5281/zenodo.17 553019 Page No: 14-24 Indigestion and epigastric pain are common manifestations of several disorders of the upper digestive system. The use of over-the-counter different preparations that relieve these symptoms may pose a lot of problems. This is because drugs such as soda and other are advertised by the media as appropriate for these conditions, without however, considering their possible abuse, as well as the situation of each patient. The patient who was presented in the emergency department had indigestion and epigastric pain, for which he had been taking for many years a significant amount of baking soda. He presented findings and symptoms of very severe metabolic alkalosis from soda (with the highest level of pH in the literature) and accompanying also severe hypokalemia, hypochloremia and hypocalcemia. From the investigation it was revealed that he also had significant pyloric stenosis. The above was treated conservatively with administration of NaCI 0,9%, KCI, calcium gluconate and acetazolamide. After three days all the symptoms were released except chronic renal failure and pyloric stenosis. The case and its severity are discussed. Key words: Acetazolamide, baking soda, chronic renal failure, ypocalcemia, hypochloremia, metabolic alkalosis, pyloric stenosis Introduction Metabolic alkalosis is a very common acid-base disorder that occurs in cases of acid loss or addition of new bicarbonate molecules (HCO 3- ) to the body and is maintained by factors that prevent the loss of bicarbonates through the kidneys, such as chronic renal failure (CRF), hypovolemia, hypochloremia, and hypokalemia. However, severe metabolic alkalosis is a very rare acid-base disorder in patients visiting the emergency department (ED). Patients suspected of increased exogenous bicarbonate intake include alcoholics, those with gastrointestinal disorders (dyspepsia) and CRF. 1,2 For oral administration of bicarbonates, the corresponding preparation, which is a food additive (baking soda), is used in many countries. Of course, baking soda is also used in toothpastes and/or as an antacid (usual doses 1-2 gr/4 hours). There is also a significant number of cases of oral administration of soda in excessive quantities Cite This Paper: Konstantinos S. Mavromatidis and Irini M. Kalogiannidou (2025). "The most severe metabolic alkalosis in a patient with chronic renal failure due to soda ingestion and vomiting’s". INTERNATIONAL JOURNAL PHARMACEUTICAL SCIENCE AND HEALTH CARE (IJPHC), vol. 15, no. 6, 2025, pp. 14-24. DOI: https://dx.doi.org/10.5281/zenodo.17553019 International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 16 (4-40 gr/24 hours) 1 , where this overdose leads to metabolic alkalosis, sometimes of varying severity, often life-threatening. The kidneys have the ability to excrete large amounts of bicarbonate in the urine, however, in conditions of decreased glomerular filtration rate or increased renal reabsorption, high amounts of bicarbonate return to the blood, resulting in metabolic alkalosis. Gastric loss of H + , Cl - and the subsequent decrease in K + and volume contribute both to the onset and maintenance of metabolic alkalosis (hypovolemia, hypokalemia, and hypochloremia). The combination of metabolic alkalosis and renal failure is rare. It can be seen in patients with hypovolemia and increased reabsorption of endogenous bicarbonate or in the inability to remove exogenously administered excessive amounts (baking soda, preparations for gastric discomfort such as Gaviscon). 1,3,4 Thus, it can occur in patients with renal failure who take antacids containing the carbonate radical (such as CaCO 3 ) or salts of hydroxyl with magnesium or aluminum [Al(OH) 3 , Mg(OH) 2 ], which neutralize H + in the stomach, while the bicarbonates of pancreatic secretions remain unaffected, as a result of which they can be reabsorbed later. In patients with renal failure who take large amounts of soda, such as in the form of baking soda, it can also cause severe metabolic alkalosis. 5,6,7 Case presentation This is a 64-year-old patient who presented to the ED with severe weakness, tremor of the upper arms (mainly the hands) and the below jaw, as well as numbness of the lips, perioral area and upper arms. Clinically, no significant findings were noted except for impaired level of consciousness, severe weakness, dizziness, slowwittedness, tremulous speech, tremor and spasms of the arms, spasms of the face and chewing teeth and abrasions on the face, which he attributed to two fainting episodes that he had on the day he visited the hospital. Οf the vital signs he had, blood pressure was 70/40 mmHg, pulses 86/min and breaths 20/min. Arterial blood gases revealed severe alkalemia (pH>7.80, PaCO 2 47 mmHg, PaO 2 69 mmHg, HCO 3- >70 mmol/L), due to both severe metabolic alkalosis and insufficient compensatory respiratory acidosis (expected PaCO 2 60 mmHg), severe hypokalemia (K + 2.6 mmol/L), hypochloremia (CI - 60 mmol/L) and hypocalcemia (total serum calcium 1.87 mmol/L and ionized calcium 0.66 mmol/L). Other laboratory findings included renal failure (serum creatinine 327.2 mmol/L and urea 22.31 mmol/L). His overall laboratory picture is shown in Table 1. International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 17 Day 1st 2nd 3rd 4th 5th 6th 7th Time 6:30 8:44 11:00 19:47 9:55 20:02 7:41 20:48 8:50 9:33 7:55 7:55 pH >7.80 7.639 7.601 7.542 7.514 7.467 7.459 7.433 7.407 7.450 7.442 PaCO2 (mmHg) 47 55.7 62.2 62.3 57.3 53.9 52.0 38.8 46.6 35.3 33.5 PaO2 (mmHg) 69 63 55.1 51 57.5 66.4 67.9 77 77.5 84.8 80.9 HCO3- (mmol/L) >70 58.5 59.8 52.3 45.1 38.1 36.1 25.3 28.7 24.0 22.3 SaO2 (%) - 95 91.9 88.8 91.7 93.8 94.1 95.8 95.4 96.8 96.4 Biochemical test Glucose (mmol/L) 6.66 3.21 6.44 6.16 5.22 4.77 Urea (mmol/L) 22.31 25.47 28.80 19.64 21.48 19.98 17.48 Creatinine (mmol/L) 327.2 309.5 291.8 274.1 256.4 247.6 194.5 Sodium (mmol/L) 134 133 136 149 141 140 147 Potassium (mmol/L) 2.60 2.42 3.87 4.0 4.27 4.24 4.39 Calcium (mmo/L) 1.87 2.5 2.3 2.05 2.17 2.27 - Phosphate (mmol/L) 1.97 1.81 1.07 0.77 0.74 0.94 - Chloride (mmol/L) 60 75 102 103 105 - Serum osmotic pressure (mOsm/kg) 298 Blood tests Hct (%) 37.9 37.1 37.8 36.3 36.4 37.3 41.0 Hb (gr/dl) 13.0 12.3 12.3 11.3 11.8 12.1 13.7 Platelets (cells/μL) 224000 220000 196000 198000 230000 260000 284000 Leukocytes (cells/μL) 11430 14440 1040.6 8900 8100 8140 7810 ESR (1st hour) 40 43 Urine (random sample) Chloride (mmol/L) 21.8 Sodium (mmol/L) 59.8 Potassium (mmol/L) 7.8 7.52 pH 7.80 Osmotic pressure (mOsm/kg) 415 Bicarbonates (mmol/L) >60 22 24 hours urine Sodium (mmol/L) 112 Potassium (mmol/L) 13.8 Chloride (mmol/L) 40.6 Table 1: It includes the patient's blood gases and the laboratory findings from admission to the hospital until recovery (ESR=erythrocyte sedimentation rate) International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 18 The patient initially stated that he had vomited 2-3 times/24h for a month (induced to relieve the indigestion he had and which were of large amount), then when asked he added that he had also been taking large amounts of soda for many years (since the age of 20). As he stated characteristically, he drank 5-8 glasses of water daily, in each of which he was putting a teaspoon of soda (25-40 gr NaHCO 3 /24h or 300-480 mmol HCO 3- /24h), as well as taking 1 teaspoon of soda before each meal (again due to the indigestion he had). In fact, he stated characteristically that in his life he did not remember ever drinking water after the age of 20, without putting baking soda in it. From his history, it was found that he was unaware of the existence of CRF that he had (eGFR 18 ml/min, MDRD) and which was confirmed by ultrasound (kidneys with increased echogenicity and fuzziness of corticomedullary area). From the rest of the renal function test, albuminuria was found (1.1 gr/24h), while from the stomach, gastroscopy revealed a significant stenosis of the pylorus, where a prepyloric ulcer was also found in the lesser curvature, with a crater of 2 cm in diameter and gastritis with evidence of atrophy. Biopsies taken from the site were negative for malignancy. From the electrocardiogram, a prolongation of the QT interval (0.44 sec) was found. The results of the biochemical and hematological tests, as well as the urine tests, are shown in Table 1. He was treated with rapid administration of 0.9% NaCl, simultaneous administration of KCl and calcium gluconate, as well as with acetazolamide tablets (250 mg × 3/24h for 3 days) (Figure 1). Progressively, all electrolyte and acid-base disturbances were restored and the patient showed progressive clinical improvement (spastic movements of the upper limbs, numbness were stopped and contact with the environment was restored) already from the first day of treatment (slow-wittedness calm after 3 days). On the third day, the pH (7.433), the CI - (103 mmol/L), the K + (4 mmol/L) and the total calcium (2.3 mmol/L) were completely restored. The exact composition of the sera administered and their composition, as well as the changes in bicarbonate and chloride during the first 5 days, are shown in Figure 1. International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 19 Figure 1: Shows the changes in bicarbonate and chloride during the patient's first 5 days of hospitalization, as well as the administration of fluids and electrolytes during these days Discussion Normally, 180 L of filtrate are filtered daily in the kidneys, which contain approximately 24 mmol/L of bicarbonates, i.e. 4,320 mmol of HCO 3are filtered. This amount is reabsorbed by 85-90% in the proximal tubules with the help of carbonic anhydrase and the remaining amount is reabsorbed in the distal tubules by the αintercalated cells with the help of the CI - -HCO 3- -countertransporter). Four factors regulate the reabsorption of bicarbonates: a) their concentration in the filtrate, b) the flow of the filtrate, c) the PaCO 2 and d) the levels of angiotensin-II (an increase in any of these factors increases their reabsorption). It is worth noting here that the reduction in parathyroid hormone (PTH) levels is also associated with an increase in bicarbonate reabsorption. Alkalemia from exogenous alkali administration is rare and unlikely, unless the bicarbonate load is excessive or there is some degree of renal failure, due to a decrease in their filtered load. 8,9 Because, as was found, normal kidneys, when administered even 16-20 mmol/kgBW NaHCO 3 (i.e. even over 1,400 mmol/24h), lead to only a slight increase in serum bicarbonate concentration (33-36 mmol/L). 10 However, it is common for patients with renal failure to be unable to handle a bicarbonate load and are at risk of developing alkalosis. In experimental models with dogs with renal failure, a significant increase in their reabsorption was found compared International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 20 to normal controls, which was independent of: a) the state of extracellular fluid volume, b) the need for increased H + excretion, and c) the concentration of PTH levels. 9 Diaconu et al. reported a 69-year-old man hospitalized with metabolic alkalosis (pH 7.61, bicarbonate 53.2 mmol/L, K + 2.6 mmol/L), acute kidney injury (serum creatinine 355.45 mmol/L), and liver toxicity in the context of excessive use of baking soda as an alternative treatment for gout. 6 Finally, few cases of patients with renal failure and metabolic alkalosis due to excessive soda intake have been published to date. 1,3,4,8,11 (Table 2), among which our case is the most severe. Study pH HCO 3 - PaCO 2 PaO 2 BE K + CI - Ca 2+ Dose soda Renal function Our patient >7.8 >70 47 69 39.2 2.6 - 0.66 5-8 teaspoon soda 24h + 1 teaspoon before every meal CRF (serum creatinine 336 mmol/L) Fitzgibbons & Snoey 1997 7.56 58 64.9 73 31.2 55 - - Several tablespoons soda/24th CRF (serum creatinine 256.4 mmol/L) Forslund 2008 7.57 85 13.3 17.8 49.6 2.3 46 0.75 >50 gr/24h Hemodialyzed Ajbani et al 2011 7.59 56 60 59 35 1.7 53 0.87 Unspecified amount of soda CRF (serum Cr 291.8 mmol/L) Yi et al 2012 7.60 53 54 76 - 2.7 65 - 3-5 teaspoon/24h CRF (serum Cr 336 mmol/L) Diaconu et al 2022 7.61 53.2 53 - - 2.6 78 - 20 gr of baking soda dissolved in 2 L of water per 24h ARF (serum Cr 355.5 mmol/L) Razavi 2000 7.52 38 49 63 - 3.6 95 0.92 He reported taking a couple of tablespoons every day CRF (serum creatinine 168 mmol/Ll) Table 2: Studies with patients with renal failure who developed severe metabolic alkalosis due to ingestion of large amounts of baking soda (CRF=chronic renal failure, ARF = acute renal failure, HCO 3- = bicarbonates in mmol/L, PaCO 2 = arterial partial carbon dioxide pressure in mmHg, PaO 2 = arterial partial oxygen pressure in mmHg, BE = base excess in mmol/L, K + = serum potassium in mmol/L, CI - = serum chloride in mmol/L and Ca 2+ = blood ionized calcium in mmol/L) Although metabolic alkalosis occurs less frequently than metabolic acidosis in patients with renal failure, the former, because it significantly increases morbidity and mortality, should be considered as a possible diagnosis when treating a patient with sleep apnea, resistant hypertension, hyperhydration, muscle weakness and cramps, heart arrhythmias and spasms, as well as spontaneous gastric rupture. 8 Our patient had two causes of metabolic alkalosis, excessive amount soda intake and vomiting. Vomiting leads to volume contraction (hypovolemia), hypokalemia (due to losses from the stomach contents, but mainly due to the stimulation of aldosterone secretion due International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 21 to hypovolemia and the subsequent increased Na + -K + exchange in the distal tubule, aiming to increase intravascular volume), and hypochloremia. 12 Furthermore, in chronic metabolic alkalosis, K + deficiency is often associated with increased intracellular K + concentration. The resulting hypokalemia can cause arrhythmias, decreased cardiac output, syncope, or seizures (mainly in severe cases), as in our case. There is certainly a relationship between hypokalemia and metabolic alkalosis. In particular, K + deficiency: a) reduces glomerular filtration rate (GFR) through vasoconstriction, which reduces the filtered bicarbonate load and this secondarily contributes to the maintenance of metabolic alkalosis, b) stimulates the rate of proximal and distal H + secretion and c) leads to an adaptive increase in ammonium (NH 4+ ) enzymatic synthesis (increased proximal ammonogenesis), while isolated K + deficiency does not cause significant alkalosis, unless accompanied by hypovolemia. Hypovolemia (through secretion of angiotensin-II and norepinephrine), hypokalemia (through exchange in the distal tubules of filtered Na + with K + , instead of H + ), and hypochloremia (due to inhibition of the action of CI - -HCO 3- -ATPase, which facilitates distal bicarbonate excretion) perpetuate and exacerbate metabolic alkalosis. 12 Of course, alkalosis also moves K + intracellularly to exchange it with H + , with the aim of improving alkalemia, thus creating conditions for exchange of K + with Na + and exacerbation of hypokalemia, which is what our patient had. The clinical picture of metabolic alkalosis results from the accompanying conditions, such as hypovolemia, hypokalemia, hypocalcemia, hypoxemia, and reduced tissue perfusion. Thus, our patient had hypotension and manifestations of it (he fell and hit his face twice on the day of his admission to the hospital). Also, in severe prolonged metabolic alkalosis, myocardial contractility and its response to endogenous inotropes are reduced. 12 Both explain the hypotension of metabolic alkalosis, 13 which our patient also had. Accordingly, the patient presented had manifestations of hypocalcemia (tremor of the arms, spasms, paresthesias, numbness) and disturbances of the level of consciousness due to hypoxemia, alkalosis and the resulting reduced blood and O 2 supply to the brain. He could have had a coma, which is known to complicate severe metabolic alkalosis. Finally, our patient, despite not having particular manifestations from the cardiovascular system, showed prolongation of the QT interval on the electrocardiogram, which was restored with the treatment applied. International Journal of Pharmaceutical Science and Health Care Volume 15, Number 6, 2025 Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 DOI: 10.5281/zenodo.17360940 1 Case Report ©2025 RS Publicaon, rspublica[email protected] 22 The decrease in ionized calcium in metabolic alkalosis in patients with CRF is due to its reduced release from the bones (during the process of neutralizing H + ), although the manifestations of hypocalcemia are due to the increased binding of proteins to calcium (alkalosis intensifies this binding), events that contribute to the manifestation of tetany 14 and spasms, which our patient also had in the upper arms and face, numbness and paresthesias around the mouth. Treatment of chloride-sensitive metabolic alkalosis includes administration of 0.9% NaCl (hydration to restore hypovolemia) and correction of electrolyte disturbances (hypochloremia, hypokalemia, and hypocalcemia). In more severe cases, acetazolamide (as was done in our patient) or NH 4 CI may be used. 15 In our case, 2 L of 0.9% NaCl were initially given (first 2 hours) and immediately afterwards, 0.9% NaCl and KCl were added to the next 6 L of serum (3-4 amps of 10% KCl in each L of 0.9 NaCI) and calcium (4 amps of 10 ml of 10% calcium gluconate were added to 100 ml of 0.9% NaCl, which were administered one of them each day during the first few days), so as to restore the deficit that existed, as well as acetazolamide from the day of his admission (tabl 250 mgx3/24h). Both the serum K + , as well as the CI - , the bicarbonates and the blood pH were fully restored on the 4 th day of his admission to the hospital. There are several reports of acetazolamide administration for the correction of metabolic alkalosis in critically ill patients. 16,17 It inhibits carbonic anhydrase, an enzyme that catalyzes the reaction of H + with HCO 3to produce CO 2 with H 2 O. This helps in the reabsorption of HCO 3from the urine filtrate. Inhibition of the action of this enzyme contributes to an increase in the excretion of bicarbonate in the urine (along with Na + ), which in the distal tubule also contributes to an increased excretion of K + (the increased supply of Na + to the distal tubule enhances the excretion of K + ). All of this results in the desired removal of bicarbonate and the undesirable removal of K + (the latter is treated with exogenous administration). The administration of 0.9% NaCl, in addition to improving the serum levels of CI - of patients with chloride-sensitive metabolic alkalosis, also contributes to the restoration of bicarbonate levels, as when the concentration of CI - in the lumen of the distal tubules increases, the CI - -HCO 3- -ATPase is activated and increases the excretion of bicarbonate in the urine. Regarding K + , the restoration of its levels in the serum of patients with metabolic alkalosis increases its concentration in the distal tubular cells, so that now the exchange of Na + in the tubular lumen is with K + and not