Severe hypokalaemia and respiratory arrest due to renal tubular acidosis in a patient with Sjögren syndrome

Oda, Hiroshi; Imai, Hirokazu; Kodama, Takahito; Hamai, Keiko; Komatsuda, Atsushi; Wakui, Hideki; Miura, Akira B.

doi:10.1093/ndt/14.9.2201

Cited by 26 publications

(16 citation statements)

References 9 publications

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“…In addition to proteinuria and urinary concentration defects, renal tubular acidosis and Bartter's and Gitelman's syndromes have also been reported in Sjögren's syndrome (Table 2) [3,4,7,8]. Interstitial nephritis predominates in kidney biopsies of patients with Sjögren's syndrome, but glomerular alterations have been reported [8].…”

Section: Discussionmentioning

confidence: 98%

“…The pattern of dysfunction ranges from Fanconi syndrome, nephrogenic diabetes insipidus and renal tubular acidosis to Bartter's or Gitelman's syndrome and other forms of tubular dysfunction [9,10].The key electrolyte in all of these disorders is potassium; all types of lesion are associated with severe hypokalemia, which in some cases may even result in muscle paralysis/rhabdomyolysis and respiratory arrest [3,7]. Attention should be paid to the presence of renal tubular disorders in any autoimmune disease associated with hypokalemia.…”

Section: Discussionmentioning

confidence: 99%

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A woman with red eyes and hypokalemia: A case of acquired Gitelman syndrome

Schwarz

Barisani

Bauer

et al. 2006

Wien Klin Wochenschr

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Gitelman syndrome is a rare hereditary disorder of the thiazide-sensitive NaCl transporter in the distal renal tubular cells, but mimicking of such hereditary tubular disorders has been described in different autoimmune diseases (Sjögren syndrome, SLE, ...). A 62-year-old woman with painful red eyes and sicca syndrome presented at the ophthalmological department. The diagnostic evaluation identified a Sjögren syndrome with early endophthalmitis as the reason for the red eyes. Results of laboratory examination indicated severe hypokalemia, metabolic alkalosis and hypomagnesemia, although this had not been seen years earlier. Together with the urine analysis, a rare case of an acquired Gitelman syndrome was diagnosed. Substitution with potassium and magnesium improved the initial symptoms of weakness, but renal electrolyte wasting persisted even after treatment of Sjögren syndrome. In patients with autoimmune disease, laboratory analysis of serum electrolytes should be performed because different acquired tubular disorders can lead to severe hypokalemia.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

A woman with red eyes and hypokalemia: A case of acquired Gitelman syndrome

Schwarz

Barisani

Bauer

et al. 2006

Wien Klin Wochenschr

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“…Palkar et al [8] also reported a case of Sjögren's syndrome that presented with acute quadriparesis, bulbar weakness, atrial fibrillation, and ventricular ectopics due to hypokalemic dRTA. Severe hypokalemia may rarely cause sudden lifethreatening paralysis [6][7][8][9][10]. Furthermore, if adequate treatment is not received, muscle paralysis may lead to respiratory arrest [9].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, if adequate treatment is not received, muscle paralysis may lead to respiratory arrest [9]. Sjögren's syndrome was reported as the underlying etiology of the hypokalemic dRTA of a patient who suddenly developed respiratory arrest and was transferred to the emergency department [7,8,10]. Although respiratory arrest associated with Sjögren's syndrome is very rare, this complication is very severe and can be fatal.…”

Section: Discussionmentioning

confidence: 99%

An Unusual Initial Presentation of Sjögren’s Syndrome: Severe Hypokalemic Paralysis Secondary to Distal Renal Tubular Acidosis

Şengül

Bunul

Yazıcı³

et al. 2013

EAJM

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Sjögren's syndrome is mainly affects the exocrine glands. Patients usually complain of persistent dryness of the mouth and eyes. However, nonexocrine organs such as the kidneys are often affected in these patients. Distal renal tubular acidosis (dRTA) and interstitiel nephritis are common in Sjögren's syndrome. Nonetheless, severe hypokalemia and paralysis secondary to dRTA are unusual initial manifestation of Sjögren's syndrome. Here, we describe a case of a 48 year old women admitted to the emergency setting with severe hypokalemic paralysis and diagnosed Sjögren's syndrome.

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“…RTA commonly is asymptomatic unless hypokalemia ensues as happened in this case [6][7][8][9]. Furthermore, if adequate treatment is not received, muscle paralysis may progress to respiratory arrest [10][11][12].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2008

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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...

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Severe hypokalaemia and respiratory arrest due to renal tubular acidosis in a patient with Sjögren syndrome

Cited by 26 publications

References 9 publications

A woman with red eyes and hypokalemia: A case of acquired Gitelman syndrome

A woman with red eyes and hypokalemia: A case of acquired Gitelman syndrome

An Unusual Initial Presentation of Sjögren’s Syndrome: Severe Hypokalemic Paralysis Secondary to Distal Renal Tubular Acidosis

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

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