ReviewPediatric nephrology (Berlin, Germany)2015
Drug-induced acid-base disorders.
Review in Pediatric nephrology (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 56 citations in OpenAlex.
- Acetazolamide for the Management of Diuretic-Induced Chloride Depletion Alkalosis: A Systematic Review.Journal of clinical medicine · 2025Review
- Renal calcification in children with renal tubular acidosis: What a paediatrician should know.World journal of clinical pediatrics · 2023Review
- Propofol-Related Infusion Syndrome: A Bibliometric Analysis of the 100 Most-Cited Articles.Cureus · 2023Review
- Genetic Diagnosis and Treatment of Inherited Renal Tubular Acidosis.Kidney diseases (Basel, Switzerland) · 2023Review
- Tuberous Sclerosis Complex with Renal Stones and Distal Renal Tubular Acidosis: Case Report and Literature Review.Oman medical journal · 2023Article
- Molecular Aspects of Distal Kidney Tubular Acidosis in Children, Its Long-Term Outcome, and Relationship with Hyperammonemia.Turkish archives of pediatrics · 2022Article
- Long-Term Tubular Dysfunction in Childhood Cancer Survivors; DCCSS-LATER 2 Renal Study.Cancers · 2022Article
- Article
- Role of Drug-Gene Interactions and Pharmacogenetics in Simvastatin-Associated Pulmonary Toxicity.Drug safety · 2021Observational
- Application of Dendrimers for Treating Parasitic Diseases.Pharmaceutics · 2021Review
- Article
- Bicarbonate Therapy in Renally Compromised Critically Ill Patients with Metabolic Acidosis: Study of Clinical Outcomes and Mortality Rate.International journal of general medicine · 2021Article
- Screening and function discussion of a hereditary renal tubular acidosis family pathogenic gene.Cell death & disease · 2020Article
- Distal renal tubular acidosis: genetic causes and management.World journal of pediatrics : WJP · 2019Review
- Development of an in silico prediction model for chemical-induced urinary tract toxicity by using naïve Bayes classifier.Molecular diversity · 2019Article
- Serum markers and development of delayed neuropsychological sequelae after acute carbon monoxide poisoning: anion gap, lactate, osmolarity, S100B protein, and interleukin-6.Clinical and experimental emergency medicine · 2018Article
- Metabolic acidosis and anaemia associated with dorzolamide in a patient with impaired renal function.British journal of clinical pharmacology · 2018Article
- Improving outcomes for patients with distal renal tubular acidosis: recent advances and challenges ahead.Pediatric health, medicine and therapeutics · 2018Review
- Na(+), K(+), Cl(-), acid-base or H2O homeostasis in children with urinary tract infections: a narrative review.Pediatric nephrology (Berlin, Germany) · 2016Review
- The Anion Gap is a Predictive Clinical Marker for Death in Patients with Acute Pesticide Intoxication.Journal of Korean medical science · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal anti-inflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g., anesthetics, sedatives) or hyperventilation (e.g., salicylates, epinephrine, nicotine).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.