Gotowe bibliografie tematyczne / Renal Fanconi syndrome

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Gotowa bibliografia na temat „Renal Fanconi syndrome”

Autor: Grafiati

Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Renal Fanconi syndrome"

Papadopoulos, N. M., R. Costello, L. Charnas, M. D. Adamson, and W. A. Gahl. "Electrophoretic examination of proteinuria in Lowe's syndrome and other causes of renal tubular Fanconi syndrome." Clinical Chemistry 35, no. 11 (1989): 2231–33. http://dx.doi.org/10.1093/clinchem/35.11.2231.

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Abstract Urine samples from 26 patients with five different causes of renal tubular Fanconi syndrome were examined by zone electrophoresis on agarose gel and immunofixation. The tubular disorders associated with Lowe's syndrome, cystinosis, and idiopathic Fanconi syndrome exhibited urine protein electrophoretic characteristics that differentiated them from normal and from each other. In particular, Lowe's syndrome urine exhibited four discrete bands in the gamma globulin zone. Electrophoresis of urinary proteins may be useful in distinguishing among the different metabolic disorders causing re

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Garcia, Agustin A. "Ifosfamtoe-Induced Fanconi Syndrome." Annals of Pharmacotherapy 29, no. 6 (1995): 590–91. http://dx.doi.org/10.1177/106002809502900607.

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Objective: To report a case of possible ifosfamide-induced Fanconi syndrome in an adult with cancer. Case Summary: A 20-year-old man was treated for an osteosarcoma with a chemotherapy regimen that included ifosfamide, methotrexate, and doxorubicin. Three months after completing therapy he developed polyuria, polydypsia, and bilateral ankle pain. Laboratory findings showed decreased serum concentrations of phosphorus, uric acid, calcium, potassium, and bicarbonate; elevated blood urea nitrogen and creatinine; and increased urinary excretion of phosphorus, potassium, calcium, citrate, and prote

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Hall, A. M., P. Bass, and R. J. Unwin. "Drug-induced renal Fanconi syndrome." QJM 107, no. 4 (2013): 261–69. http://dx.doi.org/10.1093/qjmed/hct258.

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Vilasi, Annalisa, Pedro R. Cutillas, Anthony D. Maher, et al. "Combined proteomic and metabonomic studies in three genetic forms of the renal Fanconi syndrome." American Journal of Physiology-Renal Physiology 293, no. 2 (2007): F456—F467. http://dx.doi.org/10.1152/ajprenal.00095.2007.

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The renal Fanconi syndrome is a defect of proximal tubular function causing aminoaciduria and low-molecular-weight proteinuria. Dent's disease and Lowe syndrome are defined X-linked forms of Fanconi syndrome; there is also an autosomal dominant idiopathic form (ADIF), phenotypically similar to Dent's disease though its gene defect is still unknown. To assess whether their respective gene products are ultimately involved in a common reabsorptive pathway for proteins and low-molecular-mass endogenous metabolites, we compared renal Fanconi urinary proteomes and metabonomes with normal (control) u

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Ahn, Jin-Ok, Sang-Min Kim, Woo-Jin Song, et al. "Transient Fanconi Syndrome After Treatment with Firocoxib, Cefadroxil, Tramadol, and Famotidine in a Maltese." Journal of the American Animal Hospital Association 55, no. 6 (2019): 323–27. http://dx.doi.org/10.5326/jaaha-ms-6786.

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ABSTRACT Fanconi syndrome is a renal proximal tubulopathy characterized by excessive urinary loss of glucose, amino acids, several electrolytes, and bicarbonate. Here, we report the case of transient Fanconi syndrome in a dog following administration of firocoxib, cefadroxil, tramadol, and famotidine. A 10 mo old Maltese was presented with lethargy, anorexia, vomiting, and weight loss. Transient Fanconi syndrome without azotemia was associated with firocoxib, cefadroxil, tramadol, and famotidine treatment. The dog received supportive care including IV fluids, gastroprotectants, and oral nutrit

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Bommer, Nick X., Serena E. Brownlie, Linda R. Morrison, Marge L. Chandler, and James W. Simpson. "Fanconi Syndrome in Irish Wolfhound Siblings." Journal of the American Animal Hospital Association 54, no. 3 (2018): 173–78. http://dx.doi.org/10.5326/jaaha-ms-6439.

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ABSTRACT Three juvenile male Irish wolfhound littermates presented with marked polyuria and polydipsia. The four female siblings were apparently unaffected. Diagnostic testing revealed glucosuria with normoglycemia, generalized aminoaciduria, hypokalemia and metabolic acidosis consistent with Fanconi syndrome. Renal ultrasonographic and histologic findings are presented. Cases were managed with a supplementation regimen based on a treatment protocol for Fanconi syndrome in basenjis. These dogs did not have angular limb deformities as documented previously in juvenile canine siblings with Fanco

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Sabrina, Lissa, and Sidharta Salim. "Fanconi Syndrome and Osteomalacia Induced by Tenofovir." Cermin Dunia Kedokteran 51, no. 4 (2024): 207–9. http://dx.doi.org/10.55175/cdk.v51i4.875.

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Introduction: Tenofovir disoproxil fumarate (TDF), an antiviral nucleoside analog reverse transcriptase inhibitor, has been used for the treatment of HIV and HBV in the past decades. TDF nephrotoxicity has been reported and could lead to renal failure and Fanconi Syndrome (FS). Case: A 58-year-old female HBsAg carrier with TDF treatment since 2013 presented with osteomalacia. She had glucosuria, albuminuria, vitamin D insufficiency, hypophosphatemia, and occasional hypokalemia episodes. Laboratory results showed amino aciduria, which indicates renal tubulopathy. The diagnosis of Fanconi syndro

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Gou, Manting, and Zhongshu Ma. "Osteomalacia, renal Fanconi syndrome, and bone tumor." Journal of International Medical Research 46, no. 8 (2018): 3487–90. http://dx.doi.org/10.1177/0300060518763708.

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We herein report two cases of Fanconi syndrome with refractory hypophosphatemic osteomalacia that was difficult to correct by phosphorus replacement therapy. The pathological result was a bony giant cell tumor and osteosarcoma, respectively. Interestingly, after resection of the tumors, the patient with osteosarcoma recovered completely but the patient with the bony giant cell tumor had a relapse. Although she underwent nine operations, her symptoms and laboratory tests did not improve. These findings indicate that Fanconi syndrome can result from a bone tumor.

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Watanabe, Toru. "Renal Fanconi syndrome in distal renal tubular acidosis." Pediatric Nephrology 32, no. 6 (2017): 1093. http://dx.doi.org/10.1007/s00467-017-3638-z.

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Tolaymat, A., A. Sakarcan, and R. Neiberger. "Idiopathic Fanconi syndrome in a family. Part I. Clinical aspects." Journal of the American Society of Nephrology 2, no. 8 (1992): 1310–17. http://dx.doi.org/10.1681/asn.v281310.

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Fanconi syndrome is a rare cause of rickets in children. Only six families with Fanconi syndrome following an autosomal dominant pattern of inheritance have been reported. In this report, the results of clinical studies performed in three generations of a family of 39 members with autosomal dominant Fanconi syndrome are presented. Twenty-one members of this family provided blood and urine for biochemical evaluation. Many family members have one or more tubular reabsorptive abnormalities; however, the complete Fanconi syndrome was not present in most members. Three children with the complete sy

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Rozprawy doktorskie na temat "Renal Fanconi syndrome"

Hall, A. "The role of mitochondria in the renal Fanconi syndrome." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19323/.

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Clinically, the renal proximal tubule (PT) seems to be vulnerable to mitochondrial dysfunction (MD), which can affect normal transport processes (including reabsorption of low molecular weight proteins [LMWPs]), resulting in the renal Fanconi syndrome. I wanted to explore why the PT is vulnerable to MD, and how this leads to impaired LMWP transport: (1) Using the OK cell line, to model uptake of LMWPs in the PT, I found respiratory chain (RC) inhibitors had minimal effect on the uptake of fluorescent-labelled albumin, and also had a relatively small impact on [ATP], which was maintained largel

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Albardeiro, Ana Isabel Espadinha. "Clínica de animais de companhia: síndrome de Fanconi no cão." Master's thesis, Universidade de Évora, 2014. http://hdl.handle.net/10174/13544.

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O estágio curricular para conclusão do Mestrado Integrado em Medicina Veterinária decorreu no Hospital Veterinário da Universidade de Évora, durante seis meses, com início no dia 1 de outubro de 2013 e término no dia 30 de março de 2014, sob coorientação da Dra. Leonor Pinho. É elaborado, inicialmente, um relatório de estágio que inclui uma relação de toda a casuística acompanhada no hospital durante este período, bem como uma descrição relativamente extensa e esquematizada da área da medicina preventiva e uma descrição sumariada relativa aos casos mais ou menos prevalecentes dentro de cada ár

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Passos, Marta Cristina de Caldas. "Síndrome de Fanconi em cães." Bachelor's thesis, Universidade Técnica de Lisboa. Faculdade de Medicina Veterinária, 2009. http://hdl.handle.net/10400.5/1134.

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Dissertação de Mestrado Integrado em Medicina Veterinária<br>A síndrome de Fanconi é uma doença renal caracterizada por uma disfunção generalizada dos túbulos renais proximais da qual resultam perdas urinárias excessivas de solutos. Estas perdas vão ser responsáveis pelo desenvolvimento de alterações metabólicas e manifestações clínicas que, no seu conjunto, constituem a síndrome. A gravidade das perdas urinárias dos vários solutos é variável entre os animais afectados, bem como a sua expressão sintomatológica. Trata-se de uma doença rara que foi descrita inicialmente em humanos por Guido

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Książki na temat "Renal Fanconi syndrome"

Bockenhauer, Detlef, and Robert Kleta. Approach to the patient with renal Fanconi syndrome, glycosuria, or aminoaciduria. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0041_update_001.

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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 latt

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Walsh, Stephen B. Approach to the patient with renal tubular acidosis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0036.

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The renal tubular acidoses are a collection of syndromes characterized by defective urinary acidification. These syndromes have classically caused some confusion, and many opine that the widely used numerical system (type 1, 2) should be abandoned. We consider distal renal tubular acidosis and proximal renal tubular acidosis separately, and briefly cover hypoaldosteronism. Distal (Type 1) renal tubular acidosis is a syndrome of hypokalaemia, metabolic acidosis, kidney stones, nephrocalcinosis, and osteomalacia or rickets. It is caused by failure of the acid secreting α‎‎‎-intercalated cells in

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Fervenza, Fernando C., An S. De Vincent Rajkumar, An S. De Vriese, and Sanjeev Sethi. Other consequences from monoclonal immunoglobulins/fragments. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0155_update_001.

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Renal damage secondary to deposition of monoclonal immunoglobulin can occur due to accumulation of either light chains, heavy chains, or both. These include myeloma kidney (cast nephropathy), light-chain and heavy-chain amyloidosis, and light- and heavy-chain deposition disease. Renal damage secondary to deposition of both chains is far less common. In the great majority of these cases the M-component is immunoglobulin G, but the spectrum of renal lesions associated with monoclonal gammopathy is extensive and depends on the physiochemical properties of the immunoglobulin produced.This chapter

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Speeckaert, Marijn, and Joris Delanghe. Tubular function. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0008.

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Assessment of tubular function is more complicated than the measurement of glomerular filtration rate. Different functions may be affecting according to the different segments of tubule involved. Key tests include concentrating and diluting capacity, and fractional excretion of sodium. Tubular proteinuria occurs when glomerular function is normal, but when the proximal tubules have a diminished capacity to reabsorb and to catabolize proteins, causing an increased urinary excretion of the low-molecular-mass proteins that normally pass through the glomerulus. Proximal tubular dysfunction is char

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Freda, Benjamin J., and Gregory L. Braden. Other toxic acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0085.

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Chronic kidney disease (CKD) is often the result of incomplete recovery of renal function from a variety of causes of acute tubulointerstitial injury. Exposure to ethylene glycol, chlorinated hydrocarbons, paraquat, or toxic mushrooms often causes severe acute kidney injury (AKI), leading to chronic tubulointerstitial nephritis (TIN) and CKD, including end-stage renal disease. Ethylene glycol intoxication often leads to chronic TIN and CKD from direct renal tubular toxicity and from interstitial calcium oxalate deposition. Chlorinated hydrocarbon exposure can cause dialysis-dependent AKI, but

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Schiller, Adalbert, Adrian Covic, and Liviu Segall. Chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.

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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably red

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Ronco, Pierre M. Kidney involvement in plasma cell dyscrasias. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0150.

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Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-ch

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Levtchenko, Elena N., and Mirian C. Janssen. Cystinosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0339_update_001.

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Cystinosis is a rare autosomal recessive disease caused by mutations in the lysosomal cystine transporter cystinosin encoded by the CTNS gene (17p.13.2). Cystinosis is characterized by lysosomal cystine accumulation throughout the body with renal Fanconi syndrome being the most common presenting symptom of a multisystem disorder. It must be distinguished from cystinuria in which formation of cystine stones is the core problem. When left untreated, kidney dysfunction gradually progresses towards end-stage renal failure during the first 10 years of life. The advent of renal replacement therapy a

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Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal pheno

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Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.

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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of

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Części książek na temat "Renal Fanconi syndrome"

Bien, Christian G., Christian E. Elger, Ali R. Afzal, et al. "Renal Fanconi Syndrome." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8518.

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Cutillas, P. R., A. G. W. Norden, R. Cramer, A. L. Burlingame, and R. J. Unwin. "Urinary Proteomics of Renal Fanconi Syndrome." In Proteomics in Nephrology. KARGER, 2003. http://dx.doi.org/10.1159/000074596.

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Morris, R. Curtis. "Cellular Mechanisms of Type 2 Renal Tubular Acidosis/Fanconi Syndrome." In Nephrology. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_118.

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Roth, Karl S. "Studies on a Physiological Model for the Hunman Renal Fanconi Syndrome." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_98.

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Sirac, Christophe, Frank Bridoux, Marie Essig, Olivier Devuyst, Guy Touchard, and Michel Cogné. "Toward Understanding Renal Fanconi Syndrome: Step by Step Advances through Experimental Models." In Contributions to Nephrology. KARGER, 2011. http://dx.doi.org/10.1159/000313962.

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Besouw, M., E. Cornelissen, D. Cassiman, L. Kluijtmans, L. van den Heuvel, and E. Levtchenko. "Carnitine Profile and Effect of Suppletion in Children with Renal Fanconi Syndrome due to Cystinosis." In JIMD Reports. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/8904_2014_312.

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Bockenhauer, Detlef, and Robert Kleta. "Renal Fanconi Syndromes and Other Proximal Tubular Disorders." In Pediatric Kidney Disease. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-52972-0_32.

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Bockenhauer, Detlef, and Robert Kleta. "Renal Fanconi Syndromes and Other Proximal Tubular Disorders." In Pediatric Kidney Disease. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-11665-0_35.

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Orita, Yoshimasa, Yoshifumi Fukuhara, Takeshi Nakanishi, Masaru Horio, and Hiroshi Abe. "Disorder of Coupled Transport in Renal Brush Border Membrane Vesicles from Rabbits with Experimental Fanconi Syndrome Induced by Anhydro-4-Epitetracycline as a Model of Membrane Disease." In Membranes and Membrane Processes. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4899-2019-5_4.

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Pezeshk, Parham, and John Carrino. "Fanconi Syndrome and Renal Tubular Acidosis." In Imaging of Arthritis and Metabolic Bone Disease. Elsevier, 2009. http://dx.doi.org/10.1016/b978-0-323-04177-5.00038-0.

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Streszczenia konferencji na temat "Renal Fanconi syndrome"

Yildirim, Gözde Atasever, Fatma Derya Bulut, Bahriye Atmiş, et al. "GP287 Fanconi bickel syndrome and renal tubular dysfunction." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.346.

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