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At least 703 records · Page 39Linked to original sources
PubMed1986

Hyperkalemic distal renal tubular acidosis in salt-losing congenital adrenal hyperplasia.

Functional indices of distal urinary acidification were assessed in two male infants, aged 1 and 3 months, with salt-losing congenital adrenal hyperplasia. In both cases the diagnosis was sustained by the presence of elevated plasma levels of 17-hydroxyprogesterone, hyponatremia, hyperkalemia, metabolic acidosis and increased plasma renin activity. Both patients were unable to lower urinary pH below 5.9 either during acute ammonium chloride-induced acidosis or after i.v. administration of furosemide. One patient also failed to decrease urine pH below 5.5 and to increase urinary potassium excretion during sodium sulfate infusion. Oral sodium bicarbonate loading was given to both patients but failed to induce a significant increase in the urine minus blood PCO2 gradient. This gradient remained low also after neutral phosphate administration. Repeated studies after acute administration of fludrocortisone in one case or after prolonged administration of hydrocortisone in the other resulted in complete normalization of all functional studies. We conclude that salt-losing congenital adrenal hyperplasia can lead to hyperkalemic distal renal tubular acidosis in early infancy. The defective renal secretion of hydrogen ion and potassium is probably related to the abolishment of the negative potential difference in the cortical collecting tubule induced by the impaired reabsorption of sodium.

Acidosis, Renal Tubular↗
PubMed1995

Proximal renal tubular acidosis secondary to FK506 in pediatric liver transplant patients.

We hereby report our experience with an index case of a pediatric liver transplant patient in whom FK506 administration was associated with the development of proximal renal tubular acidosis (RTA), as well the prevalence of acidosis and renal dysfunction in all pediatric liver transplant patients in our institution followed long term during a 6-year period. Data were grouped according to immunosuppressant regime: cyclosporine (CsA) only, FK506 only, or CsA with conversion to FK506. A 23-month-old female treated with FK506 after orthotopic liver transplantation (OLT) performed 15 months earlier presented with a 1-wk history of fever, watery diarrhea and metabolic acidosis. Although the acidosis did not improve following correction of her hydration status, administration of oral bicarbonate was effective. Discontinuation of this therapy resulted in acidosis. Since other indirect measurements of renal tubular function were normal, the patient was judged to have an isolated proximal RTA. In our group of pediatric liver transplant patients converted from CsA to FK506, FK506 administration was associated with a decline in serum bicarbonate (19 +/- 1 vs. 16 +/- 1 mEq/l, p < 0.02); neither blood urea nitrogen nor serum creatinine differed between the two groups. The number of rejection episodes/patient/month was comparable, allowing clinically relevant comparison of relative drug nephrotoxicities. We conclude that proximal RTA may be a relatively common treatable complication of FK506 administration in children.

Acidosis, Renal Tubular↗
PubMed2001

Proximal renal tubular acidosis associated with osteomalacia.

Vitamin D deficiency is relatively common among older persons and those with spinal cord injuries. We report a case of proximal renal tubular acidosis in a 44-year-old quadriplegic nursing home resident who had limited sunlight exposure. Laboratory studies showed a low level of serum bicarbonate, a normal serum anion gap, and a positive urine anion gap. There was no history of diarrhea. Serum calcium and phosphorus levels were 6.9 mg/dL and 3.7 mg/dL, respectively. Proximal renal tubular acidosis due to osteomalacia was suspected, which was confirmed by a low serum 25-hydroxycholecalciferol level (< 5 ng/mL) with an elevated serum parathyroid hormone level. Treatment with vitamin D and a calcium supplement led to normalization of laboratory values.

Acidosis, Renal Tubular↗
PubMed1990

Trimethoprim/sulfamethoxazole-induced renal tubular acidosis.

A child was evaluated for growth failure at the University of California, San Diego. On two occasions the patient had renal bicarbonate wasting, acidosis, and growth failure associated with trimethoprim/sulfamethoxazole (TMP/SMZ) administration. On both occasions, the acidosis resolved and the growth rate normalized following a period without receiving TMP/SMZ. Renal tubular acidosis and growth failure may occur as a result of TMP/SMZ therapy in children.

Acidosis, Renal Tubular↗
PubMed2002

[Severe hypokalemia with paralysis in a patient with distal renal tubular acidosis as an initial expression of Sjögren's syndrome].

In a 33-year-old woman with a recent flaccid paralysis of the arms and legs, laboratory tests demonstrated a severe hypokalemia with hyperchloremic metabolic acidosis and abnormally acidified urine. The urinary anion gap was positive in the presence of acidosis, thus establishing the diagnosis of distal renal tubular acidosis. The patient made a full recovery after potassium and alkali replacement. Further investigation revealed Sjögren's syndrome as the underlying cause.

Acid-Base Equilibrium↗