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Fanconi syndrome - Etiology, Clinical Features, Pathology, Diagnosis and Treatment

📌 𝐅𝐨𝐥𝐥𝐨𝐰 𝐨𝐧 𝐈𝐧𝐬𝐭𝐚𝐠𝐫𝐚𝐦:-   / drgbhanuprakash   📌𝗝𝗼𝗶𝗻 𝗢𝘂𝗿 𝗧𝗲𝗹𝗲𝗴𝗿𝗮𝗺 𝗖𝗵𝗮𝗻𝗻𝗲𝗹 𝗛𝗲𝗿𝗲:- https://t.me/bhanuprakashdr 📌𝗦𝘂𝗯𝘀𝗰𝗿𝗶𝗯𝗲 𝗧𝗼 𝗠𝘆 𝗠𝗮𝗶𝗹𝗶𝗻𝗴 𝗟𝗶𝘀𝘁:- https://linktr.ee/DrGBhanuprakash Fanconi syndrome - Etiology, Clinical Features, Pathology, Pathophysiology, Diagnosis and Treatment Introduction ------------------- Fanconi syndrome is categorized under Type 2 renal tubular acidosis in which the Inability of the proximal convoluted tubule cells to reabsorb HCO3- Fanconi syndrome "not to be confused with Fanconi anemia" which is a defect in the proximal convoluted tubule in which amino acids, glucose, HCO3-, and PO43- are excreted rather than reabsorbed. Fanconi anemia • Hereditary autosomal recessive disorder due to a DNA crosslink repair defect resulting in bone marrow failure Unlike other renal tubular defects e.g. Barrter, Gitleman, and Liddle syndromes, Fanconi syndrome is not a defect of a specific transporter, rather, it is a global defect in the PCT. Causes of Fanconi syndrome include ------------------------------------------------------------ • Hereditary e.g. cystinosis, Wilson disease, tyrosinemia, glycogen storage disease type 1, Galactosemia • Ischemia • Heavy metals e.g. lead poisoning • Multiple myeloma due to PCT light chain reabsorption • Drugs e.g. expired tetracyclines, tenofovir, ifosfamide, cisplatin • Light chain nephropathy e.g., multiple myeloma • Amyloidosis • Vitamin D deficiency • Paroxysmal nocturnal hemoglobinuria • Drugs: ifosfamide, tenofovir, expired tetracyclines, aminoglycosides • Heavy metal poisoning e.g., lead, cadmium, mercury Clinical Presentation --------------------------------- The presentation of patients with Fanconi syndrome may be associated with a deficiency of any of the excreted solutes: • Polyuria → polydipsia, hypovolemia Polyuria The production of an abnormally large amount of urine. Quantitatively defined as the passage of greater than 3 liters of urine in 24 hours. Polydipsia A condition of excessive thirst. It can be caused by organic e.g., dehydration, hypovolemia, hyperglycemia, diabetes insipidus, or non-organic conditions e.g., psychogenic polydipsia. • Hypophosphatemic rickets in children; osteomalacia in adults due to loss of potassium Due to phosphaturia and hypophosphatemia; vitamin D resistant rickets and osteomalacia are more severe among patients with Fanconi syndrome. • Growth failure, due to acidosis and hypophosphatemia • Nephrocalcinosis - Calcium stones are formed because calcium tends to precipitate in an alkaline solution. Calcium stones may be seen bilaterally. • Calcium stones are formed because calcium tends to precipitate in an alkaline solution. Calcium stones may be seen bilaterally. Failure of the PCT to reabsorb HCO3- can result in a proximal renal tubular acidosis "Type II RTA" in patients with Fanconi syndrome. Diagnostics ------------------- Serum • Hyperchloremic metabolic acidosis,i.e., normal anion gap • Hypokalemia that worsens with alkaline therapy The degree of hypokalemia is usually mild when compared to type 1 RTA. However, hypokalemia worsens with the initiation of alkaline therapy. Severe hypokalemia may also be present in the case of Fanconi syndrome. • Hypouricemia • Hypophosphatemia Urine • Urine pH less than 5.5 Urine pH may be greater than 5.5 before acidosis sets in • Bicarbonate infusion test: Urine pH rises above 7.5, and the fractional excretion of bicarbonate is less than 15% following IV sodium chloride administration. Supplemental potassium should be given during the infusion because sodium chloride may induce hypokalemia. • Negative urine anion gap Fanconi syndrome • Aminoaciduria • Glucosuria despite normal or low serum glucose • Phosphaturia Treatment ----------------- Alkali therapy with orally administered potassium citrate • Potassium citrate is required in order to correct the hypokalemia that occurs with the initiation of alkali therapy. Thiazide diuretics if alkali are not tolerated or effective • Thiazide diuretics result in volume depletion and enhanced bicarbonate reabsorption.

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