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Sr. Director: La acidosis tubular renal (ATR) se define como la incapacidad del tubulo renal de acidificar la orina independientemente de cualquier reducción en el índice de filtración glomerular. Un subtipo es la ATR tipo I o distal que se caracteriza por la alteración en la secreción de hidrogeniones (H+) en el tubulo contorneado distal. Este defecto puede ser hereditario o adquirido y resulta en la retención de H+, con la consiguiente disminución del bicarbonato plasmático y una orina alcalina1, 2. Las causas más comunes de ATR I son la diabetes mellitus, el sindrome de Sjögren, el mieloma múltiple, la amiloidosis primaria, la sarcoidosis, el transplante renal, la uropatía obstructiva, la enfermedad de células falciformes, los trastornos del metabolismo del calcio, y ciertas drogas 1, 2.
To the editor: Renal tubular acidosis (RTA) is defined as the inability of renal tubule to acidify urine regardless of any reduction in glomerular filtration rate. Type I or distal RTA is a subtype characterized by an impaired hydrogen ion (H+) secretion in the distal convoluted tubule. This defect may be inherited or acquired, and causes H+ retention, with the resultant decrease in plasma bicarbonate and alkaline urine.1,2 Most common cause of RTA I include diabetes mellitus, Sjögren¿s syndrome, multiple myeloma, primary amyloidosis, sarcoidosis, kidney transplant, obstructive uropathy, sickle cell disease, calcium metabolism disorders, and certain drugs.1,2
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To the editor: Renal tubular acidosis (RTA) is defined as the inability of renal tubule to acidify urine regardless of any reduction in glomerular filtration rate. Type I or distal RTA is a subtype characterized by an impaired hydrogen
ion (H+) secretion in the distal convoluted tubule. This defect may be inherited or acquired, and causes H+ retention, with the resultant decrease in plasma bicarbonate and alkaline urine.1,2 Most common cause of RTA I include diabetes mellitus, Sjögren¿s syndrome, multiple myeloma, primary amyloidosis, sarcoidosis, kidney transplant, obstructive uropathy, sickle cell disease, calcium metabolism disorders, and certain drugs.1,2
Thyroid hormone increases membrane cell Na+, K+-ATPase pumps.3 In hypothyroidism, content and function of these pumps are reduced, which causes a decreased elimination of H+, exacerbating the acidotic state caused by RTA. Hypocalcemia in hypothyroid patients is caused by type I RTA.3-6
Two patients with hypocalcemia due to renal tubular acidosis secondary to Hashimoto¿s thyroiditis are reported below. We suggest that this association is mediated by autoimmune mechanisms.
PATIENT 1
A 29-year-old female patient with progressive muscle weakness and quadriplegia, hyperchloremic metabolic acidosis with normal anion gap, and severe hypokalemia, which was corrected with intravenous potassium with clinical improvement. RTA type I, with high titers of anti-peroxidase antibodies (100 U/mL) and > 100 mU/mL of thyroid-stimulating hormone (TSH), was diagnosed. Despite adequate alkali administration, acid-base status was corrected when thyroid function was normalized. After treatment with levothyroxin and potassium citrate, the patient has been asymptomatic for the past 8 years.
PATIENT 2
A 30-year-old female patient with growth retardation due to type I RTA diagnosed in adolescence was admitted to hospital for a spontaneous hip fracture. Patient reported marked fatigue, weakness (quadriparesis), and muscle
cramps for the past two years. Laboratory tests results: TSH > 100 mU/mL, high titers of anti-peroxidase antibodies
(300 U/mL), and low free thyroxin levels (table). Treatment was started with levothyroxin 150 mg/day and calcium
citrate. Densitometry showed severe osteoporosis. Patient has not relapsed after 7 years of hormone replacement
therapy.
Hashimoto¿s thyroiditis is an autoimmune disease, and type I RTA has also been related to autoimmunity.6-8 Antibodies directed against collecting tubule cells could play an outstanding role in this setting, affecting acid-base status and potassium balance. These are the first cases reported in the literature of hypokalemic paralysis caused by type I RTA as a presentation form of Hashimoto¿s thyroiditis.
Taking into account that Hashimoto¿s thyroiditis is the most common cause of hypothyroidism, with a 1% prevalence, type I RTA could be an underdiagnosed associated condition with variable grades of clinical expressivity.
ion (H+) secretion in the distal convoluted tubule. This defect may be inherited or acquired, and causes H+ retention, with the resultant decrease in plasma bicarbonate and alkaline urine.1,2 Most common cause of RTA I include diabetes mellitus, Sjögren¿s syndrome, multiple myeloma, primary amyloidosis, sarcoidosis, kidney transplant, obstructive uropathy, sickle cell disease, calcium metabolism disorders, and certain drugs.1,2
Thyroid hormone increases membrane cell Na+, K+-ATPase pumps.3 In hypothyroidism, content and function of these pumps are reduced, which causes a decreased elimination of H+, exacerbating the acidotic state caused by RTA. Hypocalcemia in hypothyroid patients is caused by type I RTA.3-6
Two patients with hypocalcemia due to renal tubular acidosis secondary to Hashimoto¿s thyroiditis are reported below. We suggest that this association is mediated by autoimmune mechanisms.
PATIENT 1
A 29-year-old female patient with progressive muscle weakness and quadriplegia, hyperchloremic metabolic acidosis with normal anion gap, and severe hypokalemia, which was corrected with intravenous potassium with clinical improvement. RTA type I, with high titers of anti-peroxidase antibodies (100 U/mL) and > 100 mU/mL of thyroid-stimulating hormone (TSH), was diagnosed. Despite adequate alkali administration, acid-base status was corrected when thyroid function was normalized. After treatment with levothyroxin and potassium citrate, the patient has been asymptomatic for the past 8 years.
PATIENT 2
A 30-year-old female patient with growth retardation due to type I RTA diagnosed in adolescence was admitted to hospital for a spontaneous hip fracture. Patient reported marked fatigue, weakness (quadriparesis), and muscle
cramps for the past two years. Laboratory tests results: TSH > 100 mU/mL, high titers of anti-peroxidase antibodies
(300 U/mL), and low free thyroxin levels (table). Treatment was started with levothyroxin 150 mg/day and calcium
citrate. Densitometry showed severe osteoporosis. Patient has not relapsed after 7 years of hormone replacement
therapy.
Hashimoto¿s thyroiditis is an autoimmune disease, and type I RTA has also been related to autoimmunity.6-8 Antibodies directed against collecting tubule cells could play an outstanding role in this setting, affecting acid-base status and potassium balance. These are the first cases reported in the literature of hypokalemic paralysis caused by type I RTA as a presentation form of Hashimoto¿s thyroiditis.
Taking into account that Hashimoto¿s thyroiditis is the most common cause of hypothyroidism, with a 1% prevalence, type I RTA could be an underdiagnosed associated condition with variable grades of clinical expressivity.
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