sodium-bicarbonate and Bone-Diseases--Metabolic

sodium-bicarbonate has been researched along with Bone-Diseases--Metabolic* in 2 studies

Other Studies

2 other study(ies) available for sodium-bicarbonate and Bone-Diseases--Metabolic

ArticleYear
Primary Sjögren's syndrome manifesting as sclerotic metabolic bone disease.
    BMJ case reports, 2021, Jan-11, Volume: 14, Issue:1

    Primary Sjögren's syndrome (pSS) is a chronic slowly progressive autoimmune disease characterised by lymphocytic infiltration of salivary and lacrimal glands with varying degree of systemic involvement. Renal involvement, a recognised extraglandular manifestation of pSS, is commonly related to tubular dysfunction and generally manifests as distal renal tubular acidosis (RTA), proximal RTA, tubular proteinuria and nephrogenic diabetes insipidus. Untreated long-standing RTA is known to cause metabolic bone disease. Here, we present the report of a patient with sclerotic metabolic bone disease related to pSS with combined distal and proximal RTA and negative workup for other causes of sclerotic bone disease. A significant clinical and biochemical improvement, including recovery of proximal tubular dysfunction, was noted with alkali therapy. This case suggests the need to consider pSS in the diagnostic algorithm of a patient presenting with sclerotic bone disease.

    Topics: Absorptiometry, Photon; Acidosis, Renal Tubular; Adult; Alkaline Phosphatase; Back Pain; Bone Density; Bone Diseases, Metabolic; Female; Humans; Potassium Citrate; Radionuclide Imaging; Sjogren's Syndrome; Skeleton; Sodium Bicarbonate

2021
[Osteopenia and renal calcification in a 4.5 year old child with primary distal renal tubular acidosis treated for idiopathic renal hypercalciuria].
    Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego, 2001, Volume: 10, Issue:58

    We present a case of a 4.5 years old boy suffering from hypercalciuria caused by a not diagnosed distal renal tubular acidosis. In the age of 2.5 years, after a banal infection the routine analysis showed a presence of numerous calcium phosphates in urine. Other diagnostic procedures showed: hypercalciuria, hyperphosphaturia, rather high calcemia and high values of UCa/cr and UPO4/cr ratios. HCO3 in serum 21.2 mmol/l, pH of urine 7.0. Kidneys and urinary tract-usg normal. These results induced the family doctor to make the diagnosis: idiopathic renal hypercalciuria. He advised the therapy with hydrochlorothiazide and limitations of calcium and vitamins D3 oral supply. This decision caused an illusory positive effect: decreased the UCa/cr ratio (to 0.96 mmol/mmol) without any reduction of calcemia. After a period of 12 months the UCa/cr ratio increased up to 1.31 and calcification of renal pyramids appeared. We diagnosed the distal renal tubular acidosis (some medical informations suggested the essential distal renal tubular acidosis) and osteopenia (DXA BMD L1-L4 below -1 s.d.). The therapy with NaHCO3 (about 2.6 mmol/kg) normalized the levels of HCO3a and calcium in serum, decreased the UCa/cr ratio to values 0.09-0.16 mmol/mmol.

    Topics: Acidosis, Renal Tubular; Bone Diseases, Metabolic; Calcinosis; Calcium; Child, Preschool; Humans; Kidney Diseases; Male; Sodium Bicarbonate

2001