ANTHONY SEBASTIAN, M.D.; ELISABETH MCSHERRY, M.D.; IRIS UEKI, B.A.; R. CURTIS MORRIS JR., M.D.
A 29-year-old man with renal amyloidosis, nephrotic syndrome, and chronic renal failure had the classic physiologic features of the Fanconi syndrome and hyperchloremic acidosis associated with inappropriately alkaline urine and striking bicarbonaturia. Sodium bicarbonate loading studies demonstrated that the maximal renal tubular reabsorption of bicarbonate (Tm HCO3-) was reduced by some 20 to 30%; tubular reabsorption of bicarbonate (T HCO3-) at normal plasma bicarbonate concentrations was reduced by more than 15%. Such reductions of Tm HCO3- and T HCO3- at normal plasma bicarbonate concentration characterize a renal acidification defect physiologically distinct from that of adult patients with classic renal tubular acidosis or that described in patients with uremic acidosis. The magnitude of reduction of Tm HCO3- and T HCO3- at normal plasma bicarbonate concentrations suggests that the impairment in renal bicarbonate reabsorption involves the acidification process of the proximal nephron.
ANTHONY SEBASTIAN, ELISABETH MCSHERRY, IRIS UEKI, R. CURTIS MORRIS. Renal Amyloidosis, Nephrotic Syndrome, and Impaired Renal Tubular Reabsorption of Bicarbonate. Ann Intern Med. 1968;69:541–548. doi: 10.7326/0003-4819-69-3-541
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Published: Ann Intern Med. 1968;69(3):541-548.
Nephrology, Nephrotic Syndrome.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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