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Abstract

Introduction: Renal tubular acidosis type 1 (RTA type 1), also known as distal renal tubular acidosis, is a disorder characterized by the inability of the distal nephron to secrete hydrogen ions and reabsorb bicarbonate (HCO3-) in the presence of metabolic acidosis, leading to a chronic state of metabolic acidosis with a normal anion gap. This disorder has an estimated prevalence of 0.46- 1.60 per 10,000 people. RTA type 1 can often go undiagnosed in hospital settings due to its nonspecific presentation, such as weakness, fatigue or cramps, causing physicians to focus on empirically correcting low electrolyte levels rather than investigating the underlying cause. Early and accurate diagnosis is crucial to ensure appropriate management and prevent long-term complications associated with chronic acidosis.

Case Presentation: A 61-year-old lady with a known history of diabetes, essential hypertension, and asthma, presented to the emergency department with complaints of a progressively worsening body weakness, dry cough unresponsive to albuterol therapy over the past five days. Notably, she denied experiencing fever, shortness of breath, chest pain, palpitations, vomiting, or any changes in bowel movements. Apart from a tachycardia of 103 bpm and a respiratory rate of 20 bpm, no other abnormalities were noted on vital signs. Her examination showed mild wheezing and pharyngeal erythema. The patient was noted to have a hemoglobin of 6.8 g/dl on complete blood count with all other values within normal parameters. Her serum analysis highlighted significant electrolyte imbalances, with potassium at 2.4 mmol/L, sodium 149mmol/L chloride at 121 mmol/L, and bicarbonate at 14.2 mmol/ and a glucose of 73mg/dL. Her arterial blood gas analysis was indicative of hyperchloremic non-anion gap metabolic acidosis.

Further evaluation revealed her to be positive for both COVID-19 and Streptococcus. Chest X- ray was normal. She was admitted for Covid, severe anemia, and hypokalemia. Further evaluation of the hypokalemia revealed a urine electrolyte analysis to be notable for sodium at 197 mmol/L, potassium at 40.6 mmol/L, chloride at 219 mmol/L and anion gap of 18.6. Her findings were indicative of type 1 renal tubular acidosis (RTA). She was managed with the administration of sodium bicarbonate 650 mg orally twice daily and IV potassium. Additionally, the patient received one unit of packed red blood cells to address her low hemoglobin levels after which her symptoms resolved completely. She was advised to follow-up with her primary care physician for further management for her Type 1 RTA.

Conclusion: Although she tested positive for COVID-19 and Streptococcus, her primary symptoms were driven by anemia and renal tubular acidosis. Upon receiving targeted treatment for these conditions, her symptoms significantly improved. Hypokalemia management should not be empirically corrected alone and further evaluation to determine the underlying cause is essential, as different management strategies may be required. This case highlights the importance of comprehensive diagnostic workups in patients with complex presentations to ensure appropriate and effective treatment. Ultimately, personalized treatment plans based on thorough evaluations can lead to better patient outcomes.

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Comprehensive Diagnosis and Management of Renal Tubular Acidosis Type 1: A Case Report

Introduction: Renal tubular acidosis type 1 (RTA type 1), also known as distal renal tubular acidosis, is a disorder characterized by the inability of the distal nephron to secrete hydrogen ions and reabsorb bicarbonate (HCO3-) in the presence of metabolic acidosis, leading to a chronic state of metabolic acidosis with a normal anion gap. This disorder has an estimated prevalence of 0.46- 1.60 per 10,000 people. RTA type 1 can often go undiagnosed in hospital settings due to its nonspecific presentation, such as weakness, fatigue or cramps, causing physicians to focus on empirically correcting low electrolyte levels rather than investigating the underlying cause. Early and accurate diagnosis is crucial to ensure appropriate management and prevent long-term complications associated with chronic acidosis.

Case Presentation: A 61-year-old lady with a known history of diabetes, essential hypertension, and asthma, presented to the emergency department with complaints of a progressively worsening body weakness, dry cough unresponsive to albuterol therapy over the past five days. Notably, she denied experiencing fever, shortness of breath, chest pain, palpitations, vomiting, or any changes in bowel movements. Apart from a tachycardia of 103 bpm and a respiratory rate of 20 bpm, no other abnormalities were noted on vital signs. Her examination showed mild wheezing and pharyngeal erythema. The patient was noted to have a hemoglobin of 6.8 g/dl on complete blood count with all other values within normal parameters. Her serum analysis highlighted significant electrolyte imbalances, with potassium at 2.4 mmol/L, sodium 149mmol/L chloride at 121 mmol/L, and bicarbonate at 14.2 mmol/ and a glucose of 73mg/dL. Her arterial blood gas analysis was indicative of hyperchloremic non-anion gap metabolic acidosis.

Further evaluation revealed her to be positive for both COVID-19 and Streptococcus. Chest X- ray was normal. She was admitted for Covid, severe anemia, and hypokalemia. Further evaluation of the hypokalemia revealed a urine electrolyte analysis to be notable for sodium at 197 mmol/L, potassium at 40.6 mmol/L, chloride at 219 mmol/L and anion gap of 18.6. Her findings were indicative of type 1 renal tubular acidosis (RTA). She was managed with the administration of sodium bicarbonate 650 mg orally twice daily and IV potassium. Additionally, the patient received one unit of packed red blood cells to address her low hemoglobin levels after which her symptoms resolved completely. She was advised to follow-up with her primary care physician for further management for her Type 1 RTA.

Conclusion: Although she tested positive for COVID-19 and Streptococcus, her primary symptoms were driven by anemia and renal tubular acidosis. Upon receiving targeted treatment for these conditions, her symptoms significantly improved. Hypokalemia management should not be empirically corrected alone and further evaluation to determine the underlying cause is essential, as different management strategies may be required. This case highlights the importance of comprehensive diagnostic workups in patients with complex presentations to ensure appropriate and effective treatment. Ultimately, personalized treatment plans based on thorough evaluations can lead to better patient outcomes.

 

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