Metabolic acidosis results from either the gain of an acid or the loss of a base. The former is due to exogenous or endogenous acid loads, resulting in normal anion gap metabolic acidosis. The latter is due to the loss of a base from either the gastrointestinal or genitourinary tract, producing a non-anionic gap or hyperchloremic metabolic acidosis. Renal tubular acidosis (RTA) arises from the kidney’s inability to excrete enough acid or retain enough bicarbonate (HCO3), resulting in a clinical syndrome characterized by non-gap metabolic acidosis, hyperchloremia, and impaired urinary acidification.
Here we report a case of a 39-year-old male who presented to the emergency department with ascending weakness and was later diagnosed with distal renal tubular acidosis (distal RTA).
A 39-year-old male presented to the emergency department with a history of bilateral calf muscle tightness for 2 weeks and difficulty walking, which was relived with rest. Later, he developed bilateral leg cramps, for which he was treated with IV fluids and paracetamol in an outside hospital. During his hospital stay, he developed difficulty walking, which worsened over a period of time. The weakness progressed from the calf muscles to his pelvic girdle and shoulder. He also had chest tightness and bulbar weakness symptoms, like difficulty swallowing. patient was diagnosed with Guillain-Barre syndrome and referred to our hospital for IVIG, or plasmapheresis.
On arrival, the patient was conscious and oriented, and his blood pressure was 160/80 mmHg, his pulse rate was 78/min, and his saturation was 98% in room air. The examination of the respiratory and cardiovascular systems was unremarkable. A neurologic exam revealed he had a power of 2/5 in all his limbs; cranial nerves were intact; tongue fasciculations were noted; deep tendon reflexes were mute bilaterally; and the plantar reflex was also mute. Suspecting ascending flaccid paralysis, a provisional diagnosis of GBS was made and advice was given to do a nerve conduction study. In view of the worsening weakness associated with respiratory distress, he was intubated in an emergency and shifted to the ICU for further management. In the ICU, ABG was done, which showed severe hypokalaemia (0.9 meq) with metabolic acidosis. Other Laboratory analysis shows the following: Na+141 mmol/L, Cl– 112 mmol/L, and HCO3– 12 mmol/L, and an arterial blood gas test shows pH 7.22 and pCO2 26 mmHg. Serum creatinine is 1.0mg/dL and urine pH is 6.8. ECG showed diffuse ST segment depression in lead with T wave inversion.
Other causes that used to cause acidosis, which leads to ICU admission, like diabetic ketoacidosis, were ruled out due to the normal range of blood sugar, and acidosis was non-anion gap metabolic acidosis. The toxicology screening was negative, and renal function was normal. In view of non-anion gap metabolic acidosis with hypokalaemia and urine alkaline PH, metabolic acidosis in blood distal RTA was diagnosed. Other findings supporting the diagnosis of distal RTA were Ultrasound imaging shows normal sized kidneys with evidence of numerous calcifications distributed throughout both kidneys with a positive urine anion gap. The patient was treated with IV bicarbonate and potassium. patient has regained power completely from 2/5 to 5/5 within 6 hours of ICU admission, and patient was extubated the next morning and shifted to the ward. We also looked for causes of RTA, like autoimmune workups, which were negative. During the hospital stay, the patient had another episode of weakness, which resolved with potassium correction. Dietary potassium-rich foods were advised, and the patient was discharged with potassium and soda-bicarbonate tablets.
In clinical practice, patients with RTA can present with a wide range of signs and symptoms. An accurate diagnosis of RTA is important when selecting the appropriate treatment strategy. Appropriate attention to clinical and biochemical findings will lead, in most cases, to the correct classification of the patient.
In all cases of metabolic acidosis, the plasma or serum anion gap should be the first laboratory assessment. Analysis of urine biochemistry may also be useful in the evaluation of RTA; in patients with hyperchloremic metabolic acidosis and alkaline urine (i.e., pH 5.5), RTA of some type should be strongly suspected.
The aims of treatment for RTA are not only to correct as much as possible the biochemical abnormalities but also to fundamentally improve growth in children and to prevent the progression of nephrocalcinosis and the development of chronic renal failure at all ages. The basis of therapy is the continuous administration of appropriate amounts of alkali in the form of either bicarbonate or citrate. The amount of alkali administered should compensate for the urinary loss of HCO3 plus the amount of acid generated by the catabolism of proteins and skeletal growth.
Weakness is a common, non-specific symptom. Initial differentials would need to rule out acute emergencies like neurological stroke, the Guillain bare syndrome, and the myasthenia crisis. But we should not ignore common electrolyte disorders like hypokalaemia, which may mimic other disorders. Delays in the identification of electrolyte disorders may lead to unnecessary investigation and treatment.
Dr. Vetriselvan Associate Consultant Critical Care Medicine Kauvery Hospital, Chennai
Dr.R.Arun, Mbbs,MD,MBA, Critical Care Resident Kauvery Hospital, Chennai
