Renal Tubular Acidosis Due to Amphotericin B Nephrotoxicity

Patterson, Rodney M.

doi:10.1001/archinte.1971.00310140069007

Cited by 41 publications

(3 citation statements)

References 13 publications

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“…[2][3][4][7][8][9] The majority of cases were either secondary to ingestion of medications such as dyazide, toluene abuse, or associated with a maternal systemic disorder, such as diabetes, chronic hepatitis, alcoholism, and SLE. 2,[6][7][8][9][10][11] All these cases were chronic and persisted after delivery. The majority of patients (86%) presented with preterm labor and the use of Betamimetics and intravenous fluids for control of uterine activity worsened the electrolyte abnormality.…”

Section: Discussionmentioning

confidence: 99%

Transient Renal Tubular Acidosis in Pregnancy

Muhieddine

Adra²,

Khalil³

et al. 2000

Am J Perinatol

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Renal tubular acidosis in pregnancy is a very rare disorder. Most cases are either inherited or secondary to maternal disease or ingestion of toxic chemicals. We report a 22-year-old woman, previously healthy, who presented at 27 weeks of gestation with preterm labor. Investigation revealed renal tubular acidosis with no obvious etiology. Labor was stopped with various tocolytic drugs and her electrolyte imbalance was corrected. She was delivered at 36 weeks, by cesarean for a nonreassuring fetal heart tracing, of an appropriate-for-gestational-age infant weighing 2905 g. Evaluation 3 and 6 months postpartum revealed gradual, but complete resolution of the acidosis and electrolyte abnormality. The infant is now 7 months old, is growing normally with normal electrolytes, and with no evidence of acidosis.

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Section: Discussionmentioning

confidence: 99%

Transient Renal Tubular Acidosis in Pregnancy

Muhieddine

Adra²,

Khalil³

et al. 2000

Am J Perinatol

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“…Secondary, or acquired dRTA, has been reported in conditions including autoimmune diseases (Sjögren syndrome, 118 systemic lupus erythematosus, 119 rheumatoid arthritis 120 ), dysproteinemic syndromes (hypergammaglobulinemia, 121 amyloidosis 122 ), vitamin D toxicosis, 123 kidney transplantation (most frequently dRTA), 124,125 sickle cell disease, 126,127 exposure to drugs and toxins (amphotericin B, 128,129 lithium carbonate, 130 amiloride, 131 vanadium, 132,133 zonisamide 134 ), obstructive uropathy, 82 and other conditions. 3,5 Mechanisms suspected in acquired dRTA secondary to disease processes include absent or defective function of H + -ATPase in the A-intercalated cells of the collecting duct (Sjögren syndrome) 135,136 ; immune complex deposition in the kidneys (systemic lupus erythematosus) 137 ; suspected deposition of autoantibodies affecting tubular pumps (rheumatoid arthritis) 138 ;…”

Section: Secondary Distal (Type 1) Rtamentioning

confidence: 99%

A review of renal tubular acidosis

Kunchur,

Mauch,

Parkanzky

et al. 2024

J Vet Emergen Crit Care

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ObjectiveTo review the current scientific literature on renal tubular acidosis (RTA) in people and small animals, focusing on diseases in veterinary medicine that result in secondary RTA.Data SourcesScientific reviews and original research publications on people and small animals focusing on RTA.SummaryRTA is characterized by defective renal acid–base regulation that results in normal anion gap hyperchloremic metabolic acidosis. Renal acid–base regulation includes the reabsorption and regeneration of bicarbonate in the renal proximal tubule and collecting ducts and the process of ammoniagenesis. RTA occurs as a primary genetic disorder or secondary to disease conditions. Based on pathophysiology, RTA is classified as distal or type 1 RTA, proximal or type 2 RTA, type 3 RTA or carbonic anhydrase II mutation, and type 4 or hyperkalemic RTA. Fanconi syndrome comprises proximal RTA with additional defects in proximal tubular function. Extensive research elucidating the genetic basis of RTA in people exists. RTA is a genetic disorder in the Basenji breed of dogs, where the mutation is known. Secondary RTA in human and veterinary medicine is the sequela of diseases that include immune‐mediated, toxic, and infectious causes. Diagnosis and characterization of RTA include the measurement of urine pH and the evaluation of renal handling of substances that should affect acid or bicarbonate excretion.ConclusionsCommonality exists between human and veterinary medicine among the types of RTA. Many genetic defects causing primary RTA are identified in people, but those in companion animals other than in the Basenji are unknown. Critically ill veterinary patients are often admitted to the ICU for diseases associated with secondary RTA, or they may develop RTA while hospitalized. Recognition and treatment of RTA may reverse tubular dysfunction and promote recovery by correcting metabolic acidosis.

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“…The dose is increased each day by 5 mg/ day, up to a maximum of 1 mg/kg per day. The appearance of renal failure usually limits the dose to 0.7 mg/kg per day [92].…”

Section: Systemic Therapy Of Candida Infectionmentioning

confidence: 99%

Candida infection in surgical patients

Solomkin

Simmons

1980

World j. surg.

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Candida infections have become a common and serious problem in non‐neutropenic general surgical patients. This paper reviews the etiologic factors, pathogenesis of systemic candidiasis, and the more common syndromes of infection in surgical patients. Prophylactic and systemic therapy is detailed. The most significant factor inCandida infections is depression of host immune function. Significant abnormalities of T‐cells, monocytes, and neutrophils have been described in patients with systemicCandida infection and in patients shown to be at high risk of such infection (burned, malnourished, or septic patients). Systemic infection is a consequence of high density colonization at 1 or more sites. Topical therapy with nystatin, amphotericin B, or the imidazole derivatives is usually effective in terminating local colonization of skin lesions, the gastrointestinal tract, or the bladder. If local colonization is not controlled, the patient may progress to systemic infection. The primary diagnostic difficulty is determining when conversions to systemic infection has occurred. Serologic testing and blood culture techniques appear to be of value only late in the course of infection. For this reason, the assessment of culture results from multiple sites appears to be of value. Treatment is begun with systemic amphotericin if the patient is immunodepressed or has ≥ 3 sites positive forCandida. In nonneutropenic patients, relatively short therapy appears effective. Treatment of endocarditis requires several (4–6) weeks of therapy, and current evidence suggests that early surgery with valve replacement may improve survival.

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Renal Tubular Acidosis Due to Amphotericin B Nephrotoxicity

Cited by 41 publications

References 13 publications

Transient Renal Tubular Acidosis in Pregnancy

Transient Renal Tubular Acidosis in Pregnancy

A review of renal tubular acidosis

Candida infection in surgical patients

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