scholarly journals Hypokalemia: A potentially life-threatening complication of tenofovir therapy

2017 ◽  
Vol 5 ◽  
pp. 2050313X1774101 ◽  
Author(s):  
Abhilash Koratala ◽  
Rupam Ruchi
Keyword(s):  
Cardiac Arrest ◽  
Fanconi Syndrome ◽  
Transcriptase Inhibitor ◽  
Tubular Dysfunction ◽  
Nucleotide Analog ◽  
Life Threatening ◽  
Proximal Tubular ◽  
Life Threatening Complication ◽  
Renal Proximal Tubular ◽  
Reverse Transcriptase Inhibitor

Tenofovir is a nucleotide analog reverse transcriptase inhibitor approved for the treatment of HIV and hepatitis B infections. It is widely prescribed and an integral part of the recommended regimens for the treatment of HIV infection in antiretroviral-naive patients. Tenofovir is implicated in renal proximal tubular dysfunction, which can be associated with Fanconi syndrome and hypokalemia. When the hypokalemia is severe, it can lead to life-threatening complications. We describe the case of a 59-year-old woman who suffered a cardiac arrest secondary to severe hypokalemia from tenofovir use.

scholarly journals Tenofovir Nephrotoxicity: 2011 Update

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Beatriz Fernandez-Fernandez ◽  
Ana Montoya-Ferrer ◽  
Ana B. Sanz ◽  
Maria D. Sanchez-Niño ◽  
Maria C. Izquierdo ◽  
...  
Keyword(s):  
Significant Risk ◽  
Kidney Injury ◽  
Transcriptase Inhibitor ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Tubular Dysfunction ◽  
Cell Secretion ◽  
Risk Patients ◽  
Proximal Tubular ◽  
Reverse Transcriptase Inhibitor

Tenofovir is an acyclic nucleotide analogue reverse-transcriptase inhibitor structurally similar to the nephrotoxic drugs adefovir and cidofovir. Tenofovir is widely used to treat HIV infection and approved for treatment of hepatitis B virus. Despite initial cell culture and clinical trials results supporting the renal safety of tenofovir, its clinical use is associated with a low, albeit significant, risk of kidney injury. Proximal tubular cell secretion of tenofovir explains the accumulation of the drug in these mitochondria-rich cells. Tenofovir nephrotoxicity is characterized by proximal tubular cell dysfunction that may be associated with acute kidney injury or chronic kidney disease. Withdrawal of the drug leads to improvement of analytical parameters that may be partial. Understanding the risk factors for nephrotoxicity and regular monitoring of proximal tubular dysfunction and serum creatinine in high-risk patients is required to minimize nephrotoxicity. Newer, structurally similar molecular derivatives that do not accumulate in proximal tubules are under study.

Outcome of renal proximal tubular dysfunction with Fanconi syndrome caused by sodium valproate

2016 ◽  
Vol 58 (10) ◽  
pp. 1023-1026 ◽  
Author(s):  
Sawako Yamazaki ◽  
Toru Watanabe ◽  
Seiichi Sato ◽  
Hideto Yoshikawa
Keyword(s):  
Sodium Valproate ◽  
Fanconi Syndrome ◽  
Tubular Dysfunction ◽  
Proximal Tubular Dysfunction ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

Approach to the patient with renal Fanconi syndrome, glycosuria, or aminoaciduria

2018 ◽  
Author(s):  
Detlef Bockenhauer ◽  
Robert Kleta
Keyword(s):  
Fanconi Syndrome ◽  
Tubular Dysfunction ◽  
Renal Fanconi Syndrome ◽  
Renal Glycosuria ◽  
Proximal Tubular Dysfunction ◽  
Wide Range ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Low Molecular Weight Proteins ◽  
Filtration Capacity

Up to 80% of filtered salt and water is returned back into the circulation in the proximal tubule. Several solutes, such as phosphate, glucose, low-molecular weight proteins, and amino acids are exclusively reabsorbed in this segment, so their appearance in urine is a sign of proximal tubular dysfunction. An entire orchestra of specialized apical and basolateral transporters, as well as paracellular molecules, mediate this reabsorption. Defects in proximal tubular function can be isolated (e.g. isolated renal glycosuria, aminoacidurias, or hypophosphataemic rickets) or generalized. In the latter case it is called the Fanconi–Debre–de Toni syndrome, based on the initial clinical descriptions. However, in clinical practice it is usually referred to as just the ‘renal Fanconi syndrome’. Severity of proximal tubular dysfunction can vary, and may coexist with some degree of loss of glomerular filtration capacity. Causes include a wide range of insults to proximal tubular cells, including a number of genetic conditions, drugs and poisons.

scholarly journals Glycine Amidinotransferase (GATM), Renal Fanconi Syndrome, and Kidney Failure

2018 ◽  
Vol 29 (7) ◽  
pp. 1849-1858 ◽  
Author(s):  
Markus Reichold ◽  
Enriko D. Klootwijk ◽  
Joerg Reinders ◽  
Edgar A. Otto ◽  
Mario Milani ◽  
...  
Keyword(s):  
Kidney Failure ◽  
Fanconi Syndrome ◽  
Genetic Disorder ◽  
Subsequent Development ◽  
Mitochondrial Morphology ◽  
Missense Mutations ◽  
Renal Fanconi Syndrome ◽  
Biopsy Specimens ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

Background For many patients with kidney failure, the cause and underlying defect remain unknown. Here, we describe a novel mechanism of a genetic order characterized by renal Fanconi syndrome and kidney failure.Methods We clinically and genetically characterized members of five families with autosomal dominant renal Fanconi syndrome and kidney failure. We performed genome-wide linkage analysis, sequencing, and expression studies in kidney biopsy specimens and renal cells along with knockout mouse studies and evaluations of mitochondrial morphology and function. Structural studies examined the effects of recognized mutations.Results The renal disease in these patients resulted from monoallelic mutations in the gene encoding glycine amidinotransferase (GATM), a renal proximal tubular enzyme in the creatine biosynthetic pathway that is otherwise associated with a recessive disorder of creatine deficiency. In silico analysis showed that the particular GATM mutations, identified in 28 members of the five families, create an additional interaction interface within the GATM protein and likely cause the linear aggregation of GATM observed in patient biopsy specimens and cultured proximal tubule cells. GATM aggregates-containing mitochondria were elongated and associated with increased ROS production, activation of the NLRP3 inflammasome, enhanced expression of the profibrotic cytokine IL-18, and increased cell death.Conclusions In this novel genetic disorder, fully penetrant heterozygous missense mutations in GATM trigger intramitochondrial fibrillary deposition of GATM and lead to elongated and abnormal mitochondria. We speculate that this renal proximal tubular mitochondrial pathology initiates a response from the inflammasome, with subsequent development of kidney fibrosis.

Changes in soluble adhesion molecules correlate with renal proximal tubular dysfunction at cardiac surgery

2002 ◽  
Vol 19 (Supplement 27) ◽  
pp. 18-19
Author(s):  
S. J. Allen ◽  
M. A. Armstrong ◽  
T. J. McMurray ◽  
S. W. Macgowan ◽  
S. P. Penugonda ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Adhesion Molecules ◽  
Tubular Dysfunction ◽  
Soluble Adhesion Molecules ◽  
Proximal Tubular Dysfunction ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

scholarly journals ECMO For Pediatric Cardiac Arrest Caused by Bronchial Rupture and Severe Lung Injury: a Case Report About a Life-threatening Rescue at an Adult ECMO Center

2021 ◽  
Author(s):  
Xiaoqiong Chu ◽  
Weibiao Chen ◽  
Yafei Wang ◽  
Luqi Zhu ◽  
Mengqin Zhang ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Cardiac Arrest ◽  
Chest Trauma ◽  
Total Duration ◽  
Case Presentation ◽  
Bronchial Rupture ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Experienced Adult ◽  
Severe Lung

Abstract BackgroundBronchial rupture in children is a rare but dangerous complication after chest trauma that has been associated with increased mortality. Veno-venous (V-V) extracorporeal membrane oxygenation (ECMO) is reported as one of the treatments for this life-threatening complication.Case presentationA 4-year-old boy who suffered from bronchial rupture and traumatic wet lung complicated by cardiac arrest after chest trauma was admitted to an adult ECMO center. He had two cardiac arrests-one before and one during the operation. The total duration of cardiac arrest was 30 minutes. V-V ECMO was initiated because of severe hypoxia and carbon dioxide retention during the operation. ECMO was performed for 6 days, and mechanical ventilation lasted 11 days. On the 31st day after the operation, he recovered completely and discharged without neurological deficit.ConclusionV-V ECMO can be considered for support in children with severe acute respiratory failure after bronchial rupture. In an emergency, V-V ECMO can be carried out effectively in a qualified and experienced adult ECMO center. But the application of ECMO in children is different from that in adults and requires more refined management.

scholarly journals Cardiac arrest in Wilson's disease after curative liver transplantation: a life-threatening complication of myocardial copper excess?

2019 ◽  
Vol 6 (1) ◽  
pp. 228-231 ◽  
Author(s):  
Emanuele Bobbio ◽  
Niklas Forsgard ◽  
Anders Oldfors ◽  
Piotr Szamlewski ◽  
Entela Bollano ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Cardiac Arrest ◽  
Wilson’S Disease ◽  
Wilson's Disease ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Copper Excess
Sign in / Sign up

Export Citation Format

Share Document