Renal Tubular Acidosis

Bennett, William M.; Hempel, Karl; Berland, John E.; Porter, George A.

doi:10.1001/archinte.1968.03640010083014

Cited by 7 publications

(2 citation statements)

References 24 publications

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“…A reduction in renal H+ secretory capacity explains why acidosis in children and adults with the Fanconi syndrome (31)(32)(33)(34), infants with RTA (28), and some patients with unexplained osteomalacia can be resistant to correction with alkali therapy (35,36). At normal plasma bicarbonate concentrations, patients with marked reductions of Tm HC03-excrete massive amounts of bicarbonate, whereas most patients with classic RTA excrete relatively trivial amounts.…”

Section: Discussionmentioning

confidence: 99%

An experimental renal acidification defect in patients with hereditary fructose intolerance

Rc¹

1968

J. Clin. Invest.

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tively trivial bicarbonaturia, as well as (d) a urinary pH of greater than 6.That the fructose-induced renal acidification defect involves a reduced H+ secretory capacity of the proximal nephron is supported by the magnitude of the reduction in T HCO3-(20-30%o) and the simultaneous occurrence and the persistence throughout administration of fructose of impaired tubular reabsorption of phosphate, alpha amino nitrogen and uric acid.A reduced H+ secretory capacity of the proximal nephron also appears operative in two unrelated children with hyperchloremic acidosis, Fanconi's syndrome, and cystinosis. In both, T HCO3-was reduced 20-30%o at plasma bicarbonate concentrations ranging from 20-30 mEq/liter. The bicarbonaturia disappeared at plasma bicarbonate concentrations ranging from 15-18 mEq/liter, and during moderate degrees of acidosis, urinary pH decreased to less than 6, and the excretion rate of acid was normal.

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Section: Discussionmentioning

confidence: 99%

An experimental renal acidification defect in patients with hereditary fructose intolerance

Rc¹

1968

J. Clin. Invest.

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“…In addition, it should be emphasized that “hyperkalemia does not occur in stable chronic renal failure until renal function is very severely impaired” (1). The acquired form of RTA may be a consequence of various diseases: hypergammaglobulinemic conditions (4–6), metabolic diseases (7, 8), and renal disorders [nephrotic syndrome (9–11), pyelonephritis (12–14), chronic glomerulonephritis (15), medullary sponge kidney (16)]. It has occurred following renal transplantation (2) and the administration of certain drugs such as tetracycline (17), amphotericin B (18), sulfonamides and mercaptopurine (19).…”

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confidence: 99%

Hyperkalemia and Coma Associated with Renal Tubular Acidosis in an Old Patient with Refractory Edema Due to the Nephrotic Syndrome: Furosemide‐Bicarbonate Therapy

Szende¹,

J²,

Takó³

et al. 1972

J American Geriatrics Society

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In a 70‐year‐old man, renal tubular acidosis and hyperkalemia occurred together with the nephrotic syndrome and stable chronic renal failure associated with diuretic‐refractory edema. Apparently an extreme medullary hyaline sclerosis accompanying nephroarteriosclerosis was the anatomical basis of the insufficiency of distal potassium and hydrogen‐ion secretion. The patient was refractory even to excessive doses of exogenous aldosterone. Therefore the edema was attributed exclusively to an increase of proximal tubular sodium reabsorption. The renal tubular acidosis was predominantly of the distal type, but the high daily bicarbonate requirement indicated also the presence of a proximal component. Hyperkalemia presumably was caused by the lack of aldosterone effect, but excessive proximal tubular sodium reabsorption also may have played a part. With or without the influence of diuretics, a definite correlation could be demonstrated between the osmolal clearance and the potassium clearance. The decrease of hyperkalemia caused by furosemide, ethacrynic acid and hydrochlorothiazide was attributed to an enhanced sodium‐for‐potassium exchange in the distal tubules due to the increased sodium load induced by these drugs. The “refractory edema” could be drained off by high doses of furosemide (1600 mg a day) even in the presence of progressive impairment of renal function. By the intravenous infusion of high doses of furosemide and bicarbonate, the acidotic and hyperkalemic coma of this patient with “refractory edema” was successfully combatted several times.

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Proximal tubular dysfunction associated with Burkitt's lymphoma

Goldsweig¹,

Champlain²,

Davidman³

1978

Cancer

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Generalized aminoaciduria, uricosuria, glycosuria and phosphaturia were discovered in a patient with advanced Burkitt's lymphoma with renal infiltration. The literature is reviewed and three pathogenetic mechanisms are discussed. It is presumed that proximal tubular dysfunction in this case was related to the marked peritubular infiltrate causing cell mediated immunological injury or direct tubular destruction by tumor.

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Renal Tubular Acidosis

Cited by 7 publications

References 24 publications

An experimental renal acidification defect in patients with hereditary fructose intolerance

An experimental renal acidification defect in patients with hereditary fructose intolerance

Hyperkalemia and Coma Associated with Renal Tubular Acidosis in an Old Patient with Refractory Edema Due to the Nephrotic Syndrome: Furosemide‐Bicarbonate Therapy

Proximal tubular dysfunction associated with Burkitt's lymphoma

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