Diagnosis Of Distal Renal Tubular Acidosis Research Articles

O12 Pulseless electrical activity arrest in a young woman: could renal tubular acidosis due to Sjögren’s syndrome be the underlying cause?

O12 Pulseless electrical activity arrest in a young woman: could renal tubular acidosis due to Sjögren’s syndrome be the underlying cause?

Cause of respiratory paralysis: kidney, not the lung

Hypokalemia is a common electrolyte abnormality and if neglected, it may be fatal. This type of electrolyte abnormality is seen in distal renal tubular acidosis (RTA). Respiratory paralysis in distal RTA due to hyokalemia is a rare clinical entity described in the literature. Here we discuss one such case: a 25-year-old female presented with complaints of acute onset symmetrical weakness of bilateral lower limbs that rapidly progressed to involve trunk, upper limb and neck. Later on, she developed respiratory paralysis and was put on mechanical ventilation. Diagnosis of distal RTA with hypokalemia was made and managed successfully.

Hypokalemic respiratory paralysis due to distal renal tubular acidosis as the presenting manifestation of Sjögren's syndrome

Hypokalemic respiratory paralysis in Sjögren's syndrome (SS) with distal renal tubular acidosis (RTA) is very rare. In the literature, only five such cases have been reported. We report a 48-year-old lady, who presented with respiratory paralysis, bulbar weakness, and flaccid quadriplegia. She had severe hypokalemia (1.11 mEq/L), metabolic acidosis (pH = 7.09), hyperchloremia (120.8 mEq/L), and normal anion gap (11.2). An ammonium chloride test was consistent with the diagnosis of distal RTA. She recovered completely with potassium and alkali supplementations. Clinical features, positive Schirmer's test, and autoantibody screening were suggestive of diagnosis of SS. Hypokalemic periodic paralysis and respiratory involvement may occur as a first and rare complication of SS with distal RTA. Immunosuppressive therapy is not indicated except in the presence of systemic vasculitis. Potassium and alkali supplementations are the mainstay of the therapy. Patients with secondary hypokalemic periodic paralysis should be investigated for this possibility.

Renal involvement in primary Sjogren syndrome of childhood: case report and literature review

Renal tubular acidosis (RTA) is common in adults with primary Sjogren syndrome (pSS) but to date this condition has only been identified in 12 pediatric cases of pSS. Here we present the case of a 13-year-old, otherwise asymptomatic girl in whom the search for the etiology of incidentally found nephrocalcinosis led to diagnosis of distal RTA and nephrogenic diabetes insipidus secondary to SS-associated tubulointerstitial nephritis. Immunosupressive treatment and alkali/electrolyte supplementation resulted in stable renal function over the 6-year follow-up. A review of the literature focuses on two aspects of pSS: (1) the difficulties in diagnosing pSS in childhood and (2) clinical-pathological features, treatment and outcome of renal tubulointerstitial disease in childhood pSS. SS should be considered in older children, particularly females with otherwise unexplained RTA. A careful search for other renal dysfunctions is necessary, and renal biopsy may be of value in assessing the extent of renal damage and the need for immunomodulatory therapy.

Neem Extract Poisoning as a Cause of Renal Tubular Acidosis

Context: We report on systemic toxicity caused by ingestion of large quantities of ‘neem extract’, a traditional medicine widely used throughout the Indian subcontinent and increasingly imported to the developed world. There are case reports of neem extract causing renal impairment and liver damage in a microvesicular pattern but no cases of distal renal tubular acidosis (RTA) have been reported thus far. Case details: A 51-year old Solomon Islander was transferred to a Sydney Hospital with encephalopathy and a metabolic acidosis. A diagnosis of distal RTA was made requiring four days of continuous veno-venous hemodialysis. He also showed signs of bone marrow suppression, coagulopathy and liver damage, which were successfully managed with supportive care. Further history following the resolution of his encephalopathy revealed ingestion of large quantities of ‘neem extract’ over the preceding three months. Discussion: Liver damage is the predominant toxicity reported thus far with ‘neem extract’ and almost exclusively in children. This is the first report of neem extract causing distal RTA with evidence of mitochondrial toxicity. Physicians should be aware of the increasing use of ‘neem extract’ as a complimentary medicine and the potential toxicities this may lead to.

Distal Renal Tubular Acidosis in HIV/AIDS Patient

We report a case of renal tubular acidosis (RTA) in a patient with HIV infection and AIDS. A 33-year-old HIV-positive man with Hepatitis C and tuberculous lymphadenitis was admitted due to deep venous thrombosis and generalized muscle weakness. He had never received anti-retroviral medication. The blood gases and serum electrolytes showed hyperchloremic normal anion gap metabolic acidosis with severe hypokalemia and alkaline urine. Diagnosis of distal RTA was made. His renal function and serum globulin level remained within normal range throughout his illness. Clinicians should be alert to renal tubular disorders in HIV/AIDS patients even in the absence of anti-retroviral therapy or hypergammaglobulinemic state.

Bone disease in primary biliary cirrhosis: Lack of association with distal renal tubular acidosis

Primary biliary cirrhosis (PBC) might be complicated by osteoporosis, whose etiology remains unknown but seems to be multifactorial. Prevalence rates of 30% to 60% for distal renal tubular acidosis (DRTA) have been reported in PBC patients, generally as incomplete DRTA. Although it is undisputed that a reduced bone mineral density (BMD) is the expected outcome among patients who have been suffering from longstanding chronic metabolic acidosis, it is unclear if incomplete DRTA is also associated with metabolic bone disease in PBC patients. The present study was undertaken to compare the BMD of PBC patients with and without DRTA. The BMD of 23 PBC patients (11 with DRTA and 12 without), all with normal clearance of creatinine, was assessed by dual energy radiograph absorptiometry. The diagnosis of DRTA was made if the urine pH was above 5.4 in all samples after the oral acid overload, showing tubular inability to acidify urine in the presence of test-induced systemic metabolic acidosis. Densitometric signs of osteoporosis were found in 82% of DRTA cases and in 83% of patients without DRTA (difference not significant). There were no significant differences in BMD measurement, T and Z scores of patients with and without DRTA. The present study could not support a correlation between the presence of DRTA and the bone loss observed in PBC patients.