Acute paralysis due to distal renal tubular acidosis: a case report

Abstract

A 38-year-old woman presented to the emergency department with rapidly progressive quadriparesis. The patient reported sudden onset of diffuse myalgias associated with generalized muscular weakness and numbness during the last week. On the day prior to admission, paresis of limb and neck muscles developed. She denied any sensory, sphincter, visual, respiratory, or language disturbance. There was no history of recent gastrointestinal or respiratory upset. She denied diuretic, laxative or excessive licorice intake. There were no recent vaccinations, she had never experienced a similar event in the past, and there was no significant family history. She did not smoke or drink alcohol.She gave a history of joint pain associated with morning stiffness and Raynaud-like symptoms at her hands for several years. Hypothyroidism developed subacutely as a consequence of post-partum autoimmune thyroiditis after her first pregnancy, when the patient was 30 years old, and levothyroxine treatment had been started. Mild-grade proteinuria (\500 mg/die) had been detected during a biochemical assessment in the beginning of her second pregnancy last year. Also laboratory testing revealed a hypokalemia of 2.8 mEq/L. She had a history of calcium oxalate nephrolithiasis treated with lithotripsy. On admission, physical examination revealed no disturbances of consciousness or cognition; she was hemodynamically stable, the body temperature was 36.6°C, the recumbent blood pressure 120/80 mmHg, the pulse rate 70 beats per minute with regular sinus rhythm, and the respiratory rate 20 breaths per minute. Finger pulse oximetry revealed 98% arterial oxygen saturation and blood glucose concentration measured by a portable meter was 102 mg/dL. Lung fields were clear, and heart sounds were normal. The cranial nerve examination was unremarkable. Head flexion and extension were mildly weak. Motor examination demonstrated 1/5 strength in both the upper and lower extremities; there were neither fasciculation nor muscle tenderness. Deep tendon reflexes were symmetrically hyporeflexic; toes were down going.Blood gas analysis revealed: pH 7.23, PaCO 2 29 mmHg, HCO 3 -12 mmol/L, base excess 14.1 mmol/L. Serum sodium was 137 mEq/L, potassium 0.9 mEq/L, chloride 115 mEq/L, creatinine 0.8 mg/dL, blood urea nitrogen 48 mg/dL, blood glucose 112 mg/dL, creatine kinase 379 U/L. A complete blood count showed 8200 leukocytes, 11.2 g/dL haemoglobin, 362000 platelets. A spot urine sample showed a pH of 7.5 with 50-100 red cells, 5-10 white cells, and a few bacteria per high-power field. ECG revealed diffuse ST and T changes, prolonged PR and QT intervals, decreased P wave amplitude, prolonged QRS complexes and U waves (Fig. 1a).Potassium chloride was given intravenously at a rate of 20 mEq/h. Magnesium sulphate was also infused. At 4 h the serum potassium level was only 1.1 mEq/dL, the pH fell to 7.19, and serum chloride and bicarbonate were 125 and 10.8, respectively. Within 24 h her potassium level normalized, limb power returned to normal, there was recovery of all...

Tenofovir-induced distal renal tubular acidosis: A rare cause of recurrent hypokalaemic paralysis

“…However, in the event of severe hypokalaemia, it is important to avoid rapid alkalisation using sodium bicarbonate alone as it would exaggerate the hypokalaemia by shifting serum potassium intracellularly. 17…”

A distal (type 1) renal tubular acidosis case that mimic coronary ischemia

“…Previous case reports published before about type I RTA was usually consistent of neurological symptoms. 5 Several reports were about quadriparesis related to distal RTA. 6 There is a strong correlation between the severity and development rate of hypokalemia and the neurological symptoms.…”

Distal Renal Tubular Acidosis in HIV/AIDS Patient

“…Specific targets would include the following: that the concentration of plasma bicarbonate is maintained above 20 mmol/L, supplement of potassium is given early to combat the debilitating effect of hypokalaemia, and vitamin D may be necessary later on. However in the event of severe hypokalemia, it is important to avoid rapid alkalization using sodium bicarbonate alone as it would exacerbate the hypokalaemia by shifting serum potassium intracellularly (18).…”