[Nephrotoxicity caused by amphotericin B].

F Mota Hernández; R Gastelbondo; P N Saracho

PubMed · 7317148

[Nephrotoxicity caused by amphotericin B].

F Mota Hernández·R Gastelbondo·P N Saracho

Abstract

A six-year-old child with coccidioidomycosis is reported. The patient was given amphotericin B, that brought about disturbances in renal function with renal failure, which turned reversible on discontinuance of treatment. The earliest manifestations of nephrotoxicity were observed following administration of a total dose of 1,000 mgs. The findings were: glycosuria, cylindruria, high urinary pH followed by metabolic acidosis, hypokalemia, decreased capacity of renal concentration and clearance of endogenous creatinine. Oral administration of postassium bicarbonate and interruption of amphotericin B were followed by reversal of kidney lesion manifestations.

Explore related subjects

Acidosis, Renal Tubular Acute Kidney Injury Amphotericin B Bicarbonates Child Coccidioidomycosis Creatinine Humans Hypokalemia Male Potassium Compounds Case Reports English Abstract Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

F Mota Hernández, R Gastelbondo, P N Saracho. [Nephrotoxicity caused by amphotericin B].. https://pubmed.ncbi.nlm.nih.gov/7317148/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Sibling cases of Vici syndrome: sleep abnormalities and complications of renal tubular acidosis.

Vici syndrome is a rare congenital disorder characterized by albinism, agenesis of the corpus callosum, and developmental delays. Cardiac complications usually cause poor prognosis. We report sibling cases of Vici syndrome, and address complications of renal tubular acidosis. We also demonstrate the significance of serial examinations of brain natriuretic peptides, and discuss the possible early use of a beta-blocker to control cardiomyopathy. A sleep study including polysomnography indicated functional brainstem involvement, in which muscle atonia during non-rapid sleeping eye movements, and bursts of rapid eye movements increased. These findings provide new clues for medical care of patients with Vici syndrome.

Acidosis, Renal Tubular↗

PubMed2007

Inadequate dietary intake but not renal tubular acidosis is associated with bone demineralization in primary biliary cirrhosis.

BACKGROUND: Metabolic bone disease associated with primary biliary cirrhosis (PBC) is inadequately characterized. Renal tubular acidosis (RTA) may lead to bone loss through chronic mobilization of skeletal calcium salts to buffer increased acid load. AIM: To evaluate the prevalence of RTA in PBC and establish the relationships among bone mineral density (BMD), renal function and nutritional status. METHODS: We enrolled 69 female patients with compensated PBC and 35 control patients with chronic hepatitis C. RTA was searched in all patients, and 24-h dietary recalls were collected at enrolment. BMD was measured by dual-energy X-ray absorptiometry at the femur neck, lumbar spine and radius ultradistalis sites. RESULTS: No patients received a diagnosis of RTA. BMD values (Z-scores) showed only little deviation from normal population with no difference between PBC and controls. Osteopoenic PBC patients (T-score < 1) showed significantly lower daily phosphorus intake [median: 672 (288-1374) vs. 921 (253-1923) mg/day; P = 0.037], with a trend towards lower caloric intake than their nonosteopoenic counterparts. CONCLUSIONS: Renal tubular acidosis is uncommon in compensated PBC. Cholestasis is not associated with an increased risk of bone demineralization. Inadequate dietary intake may be a preventable factor contributing to bone loss in PBC.

Acidosis, Renal Tubular↗

PubMed2007

Distal RTA with nerve deafness: clinical spectrum and mutational analysis in five children.

Distal renal tubular acidosis (RTA) with nerve deafness is caused by mutations in the ATP6V1B1 gene causing defective function of the H+ -ATPase proton pump. We report five acidotic children (four males) from four unrelated families: blood pH 7.21-7.33, serum bicarbonate 10.8-14.7 mEq/l, minimum urinary pH 6.5-7.1 and fractional excretion of bicarbonate in the presence of normal bicarbonatemia 1.1-5.7%. Growth retardation and nephrocalcinosis, but not hypercalciuria, were common presenting manifestations. Hearing was normally preserved in one of the patients whose sister was severely deaf. One child was homozygous for a known mutation in exon 1: C>T (R31X). Three children were homozygous for a splicing mutation, intron 6 + 1G>A. The other patient was a compound heterozygote, having this mutation and a previously unreported mutation in exon 10: G>A (E330K). Our report shows that hearing loss is not always present in the syndrome of distal renal tubular acidosis with nerve deafness and the absence of hypercalciuria at diagnosis and describes a new mutation responsible for the disease in the ATP6V1B1 gene.

Acidosis, Renal Tubular↗