To see the other types of publications on this topic, follow the link: Immunosuppression. eng.
Books on the topic 'Immunosuppression. eng'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 23 books for your research on the topic 'Immunosuppression. eng.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Kuypers, Dirk R. J., and Maarten Naesens. Immunosuppression. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0281_update_001.
Full textAbstract:
Combination immunosuppressive therapy produces excellent short-term results after kidney transplantation. Long-term graft survival has improved, but less dramatically. Death with a functioning graft remains the primary cause of graft loss. Dosing of current immunosuppressive therapy balances between careful clinical interpretation of time-driven immunological risk assessments and drug-related toxicity on the one hand, and the use of simple surrogate drug exposure indicators like blood/plasma concentrations on the other. The combined use of calcineurin-inhibitors (CNIs) with mycophenolic acids and corticosteroids has been fine-tuned over the last decade, based on empirically derived observations as well as on the results of large multicentre randomized clinical studies. Corticosteroid withdrawal and avoidance are feasible, at least in patients with a low immunological risk, but CNI-free protocols have had few long-term successes. Some minimization strategies have increased risk of developing acute rejection or (donor-specific) anti-HLA antibodies, with deleterious effects on the graft. Mammalian target of rapamycin inhibitors (mTORi) have shown limited benefit in early CNI replacement regimens and their long-term use as primary drug is hampered by intolerance. In the setting of particular malignant disease occurring after transplantation, such as squamous cell carcinoma of the skin and Kaposi’s sarcoma, mTORi seem promising. Induction agents (anti-interleukin 2 receptor monoclonal antibodies, antithymocyte globulins) effectively diminish the risk of early immunological graft loss in recipients with moderate to high immunological risk but at the price of more infectious or malignant complications. While personalized transplantation medicine is only in its early stages of development, attempts are made to quantitatively measure the clinical degree of immunosuppression, to tailor immunosuppressive therapy more specifically to the patient’s individual profile, and to monitor graft status by use of invasive (e.g. surveillance renal biopsies) and non-invasive biomarkers. These scientific endeavours are a necessity to further optimize the current immunosuppressive therapy which will remain for some time to come.
2
(Editor), M. H. Sayegh, and Giuseppe Remuzzi (Editor), eds. Current and Future Immunosuppressive Therapies Following Transplantation. Springer, 2001.
Find full text
3
Schmidt, Jens. Extramuscular complications occurring in myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0004.
Full textAbstract:
Extra-muscular complications affecting patients suffering from the idiopathic inflammatory myopathies (IIM) are common, and appear in recognizable patterns affecting the skin, lungs, joints, oesophagus or heart, although these complications rarely all occur simultaneously. During the initial presentation of symptoms, involvement of organs other than muscle can aid the confirmation of the correct IIM subtype. Extra-muscular manifestations can be severe and life-threatening, e.g. with respiratory or cardiac involvement. Escalations of immunosuppression and other treatment modalities will likely be required in such cases since standard immunosuppression usually is not sufficient for an effective treatment of e.g. interstitial lung disease. IIM patients should therefore be regularly checked for extra-muscular manifestations, and management altered as appropriate.
4
Lopes, Eurides, and Jennifer Husson. Solid Organ Transplantation in HIV-Infected Individuals. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0025.
Full textAbstract:
End-organ disease has become a major cause of morbidity and mortality in HIV-infected patients due to increased life expectancy, increasing the demand for organ transplantation in these patients. The care of HIV-infected transplant recipients warrants a multidisciplinary team approach, including the transplant team, pharmacists, infectious disease specialists, nurses, and patients and their families. The immunosuppression of HIV-infected recipients post-transplant does not appear to further advance HIV disease. The post-transplant risk for HIV-infected recipients of opportunistic infections does not appear to be increased by immunosuppression. However, the overall rate of infections is high, and it is even higher in hepatitis C virus (HCV) co-infected transplant recipients. HIV/HCV co-infected recipients have worse outcomes compared to both liver and kidney HIV-infected recipients.
5
Wilson, John W., and Lynn L. Estes. Clinical Approach to Patients With Infection. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199797783.003.0066.
Full textAbstract:
•Define the host: Identify factors that influence the type of infection, disease progression, and prognosis, which include:• Host factors such as patient age, immune status (eg, immunosuppression or the absence of a spleen), the presence of foreign bodies (eg, central venous catheter, permanent pacemaker, intracardiac defibrillator, prosthetic heart valves, prosthetic joints), or other comorbid conditions, ...
6
Tyndall, Alan, and Jacob M. van Laar. Stem cell therapies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0085.
Full textAbstract:
Since the start of the international project in 1997, over 1500 patients have received a haematopoietic stem cell transplant (HSCT), mostly autologous, as treatment for a severe autoimmune disease, with overall 85% 5-year survival and 43% progression-free survival. Around 30% of patients in all disease subgroups had a complete response, often durable despite full immune reconstitution. In many cases, e.g. systemic sclerosis, morphological improvement such as reduction of skin collagen and normalization of microvasculature was documented, beyond any predicted known effects of intense immunosuppression alone. It is hoped that the results of the three running large prospective randomized controlled trials will allow modification of the protocols to reduce the high transplant-related mortality which relates to regimen intensity, age of patient, and comorbidity. Multipotent mesenchymal stromal cells (MSC) have been recently tested in various autoimmune diseases, exploiting their immune modulating properties and apparent low acute toxicity. MSC display immune privilege in that the patient requires no immunosuppression prior to allogeneic MSC infusion. Despite encouraging small phase I/II studies, no positive data from randomized prospective studies are as yet available in the peer-reviewed literature.
7
Tyndall, Alan, and Jacob M. van Laar. Stem cell therapies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0085_update_003.
Full textAbstract:
Since the start of the international project in 1997, over 2000 patients have received a haematopoietic stem cell transplant (HSCT), mostly autologous, as treatment for a severe autoimmune disease, with overall 85% 5-year survival and 43% progression-free survival. Around 30% of patients in all disease subgroups had a complete response, often durable despite full immune reconstitution. In many cases, e.g. systemic sclerosis, morphological improvement such as reduction of skin collagen and normalization of microvasculature was documented, beyond any predicted known effects of intense immunosuppression alone. It is hoped that the results of the three running large prospective randomized controlled trials will allow modification of the protocols to reduce the high transplant-related mortality which relates to regimen intensity, age of patient, and comorbidity. Multipotent mesenchymal stromal cells (MSC) have been recently tested in various autoimmune diseases, exploiting their immune modulating properties and apparent low acute toxicity. MSC display immune privilege in that the patient requires no immunosuppression prior to allogeneic MSC infusion. Despite encouraging many small phase I/II studies, only 2 prospective controlled trials which achieved their primary endpoints have been published.
8
Norman, Douglas J., Laurence Turka, Thomas E. Young, and O. Barry Mangum. Primer on Transplantation. 2nd ed. Blackwell Publishing Limited, 2001.
Find full text
9
Hodgkiss, Andrew. Further clinical issues. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0012.
Full textAbstract:
The clinical challenges arising when a person with a severe mental illness, such as schizophrenia or bipolar disorder, develops a cancer are surveyed. Delayed diagnosis and access to oncological treatment, factors contributing to reduced adherence, and the interruption of specialist community psychiatric care are discussed. Long-term psychotropic medication may complicate end-of-life care, and access to palliative care is usually limited for those in secure mental health inpatient units. The striking inverse relationship between neurodegenerative disorders (Alzheimer-type dementia) and proliferative disorders (cancers) is considered.Psychiatric aspects of haematopoietic stem cell transplantation (HSCT) are reviewed, including psychopathology arising from drugs used to prevent graft-versus-host disease and from infections complicating chronic immunosuppression. Cognitive impairment and suicide after HSCT are considered.
10
Smith, Ian. Kidney Transplant. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0029.
Full textAbstract:
Renal transplantation is the preferred treatment for pediatric patients who have end-stage renal disease. A successful transplant improves intellectual and behavioral development, quality of life, and survival, with the survival at 10 years being as high as 83% (Kim et al., 1991). We can optimize the chance of success by understanding the pathophysiology involved and applying this knowledge to guide our management of perioperative fluid balance, electrolyte anomalies, anemia, blood pressure control, and comorbidities. Also critical is an appreciation of the effects and consequences of the various immunosuppressive agents that are used. Close communication is required between the pediatrician, surgeon, and anesthesiologist.
11
Sarwal, Minnie M., and Ron Shapiro. Paediatric renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0290.
Full textAbstract:
Approximately 1 in 65,000 children develops end-stage renal disease (ESRD) each year with almost 1200 children (aged 0–19 years) in the United States developing ESRD annually. Kidney transplantation is the primary method of treating ESRD in the paediatric population. The special issues in children and adolescents with ESRD include achieving normal growth and cognitive development. This chapter discusses the advances in surgical techniques, patient selection, transplant evaluation/preparing for transplantation, postoperative management (including fluid management in infants and small children), and the evolution of immunosuppressive drugs that have resulted in improved quality of life and a reduction in the mortality rate of children with chronic renal failure.
12
Houssiau, Frédéric A. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0163_update_001.
Full textAbstract:
Major progress has been achieved in the field of lupus nephritis (LN) treatment over the last decade. Glucocorticoids and other immunosuppressants (including cyclophosphamide) are now used in a more patient-friendly way, minimizing their untoward effects. Mycophenolate mofetil is now an option, both for induction and maintenance immunosuppression. Ever increased standards for optimal global care have further contributed to lower end-stage renal disease rates.Better understanding of the mechanisms underlying lupus raises hopes for more targeted therapies with biologics. Thus, the anti-B-lymphocyte stimulator belimumab has been officially labelled for non-renal lupus by the medical agencies, which has not happened for more than 50 years, when cortisone and hydroxychloroquine were approved.These exciting developments should, however, not disguise the fact that LN still impacts survival of lupus patients and that no cure can be offered so far.
13
Todd, Stacy, and Nick Beeching. Fungal infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0315.
Full textAbstract:
Fungi, comprising yeasts, moulds, and higher fungi, have a worldwide distribution and are uncommon causes of disease in healthy individuals. However, over the last 20 years, invasive fungal disease (IFD) has become an increasing cause of morbidity and mortality. This is probably due to the increasing numbers of patients with underlying host conditions, which predispose to opportunistic IFD (e.g. transplant and anti-tumour necrosis factor immunosuppression, HIV, or chronic lung disease), and to increased recognition of endemic IFD (e.g. histoplasmosis), which cause disease in both immunocompetent and immunocompromised hosts in selected geographic locations. Diagnosis of IFD remains a challenge. Symptoms are often non-specific, and a definite diagnosis requires invasive sampling with appropriate laboratory testing of these samples. Non-invasive tests are being developed, but their positive and negative predictive values still need validation. Diagnostic criteria (‘proven, probable, and possible’) established primarily for use in research and clinical trials can also prove useful in clinical environments. However, the most important step in identifying patients with IFD is to consider the diagnosis in those at risk. This chapter will focus on the commonest causes of IFD (Candida spp., Aspergillus spp., Cryptococcus spp., and histoplasmosis).
14
Keogh, Karina A. Vasculitis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0277.
Full textAbstract:
The vasculitic syndromes are a heterogeneous group of rare disorders characterized by degrees of inflammation and necrosis of blood vessels with a wide variety of clinical manifestations. Intensive care treatment is most commonly required for vasculitis involving small blood vessels, including capillaries. Involvement of these vessels in the lung causes alveolar haemorrhage, which may lead to respiratory failure. In the kidneys it may cause glomerulonephritis leading to renal failure. Severe cardiac, neurological, and gastrointestinal manifestions can also be seen. Non-vasculitic manifestations may also be present, such as pulmonary nodules secondary to granulomatous inflammation in granulomatosis with polyangiitis. Diagnosis is based primarily on history and physical exam in conjunction with radiographic and serological testing. Intensive care unit admission is typically secondary to end organ damage due to inflammation, or because of side effects from the cytotoxic therapies, particularly infection. Treatment of vasculitis includes supportive management in conjunction with immunosuppression. Standard treatment of severe disease consists of corticosteroids and cytotoxic drugs.
15
Fox, Simon, Brian Angus, Angela Minassian, and Thomas Rawlinson. Infection in the Immunocompromised Host (Oxford Specialist Handbook). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789987.001.0001.
Full textAbstract:
There is an increasing number of patients who are immunocompromised either by malignancy, new therapies, or infection. This handbook aims to provide a clinically relevant guide for use by specialist trainee and consultant medical staff caring for immunocompromised patients in a hospital setting, including but not limited to the areas of infectious diseases, haematolo-gy, oncology, transplant medicine, HIV and genitourinary medicine, rheumatology, and general medicine. Divided into three sections, the handbook takes both a patient-centred approach, and a pathogen-centred approach. This includes the assessment, investigation, and management of different clinical syndromes presenting in patients with primary immunodeficiency, HIV infection, immunodeficiency as a result of therapeutic immunosuppression, haematological and solid organ malignancy, and immunodeficiency related to organ transplant. Medical conditions resulting in defective immunity (e.g. diabetes mellitus and chronic renal failure) are also covered in addition to travel in the immunocompromised. Furthermore, it includes guidance on the investigation and management of viral, bacterial, parasitic, and fungal infections of particular relevance to the immunocompromised host.
16
Segall, Liviu, and Adrian Covic. Immune-mediated tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.
Full textAbstract:
Immune-mediated tubulointerstitial nephritides (TINs) are generally encountered in the context of systemic or extrarenal autoimmune diseases, such as sarcoidosis, Sjögren syndrome, systemic lupus erythematosus, inflammatory bowel disease, TIN and uveitis (TINU) syndrome, and immunoglobulin G4-related disease. The pathogenesis of these TINs is complex and more or less unclear; it usually involves leucocyte activation, autoantibodies, immune complex deposition, complement activation, and release of inflammatory cytokines and growth factors. Tubulointerstitial inflammation most commonly has a chronic pattern, although acute forms of TIN may also occur. Furthermore, inflammation may be granulomatous (as in sarcoidosis or Crohn’s disease) or non-granulomatous. Immunofluorescence staining can sometimes reveal immune complex deposits and even antitubular basement membrane autoantibodies. Systemic immunosuppressive therapies are almost always required to prevent progression to irreversible interstitial fibrosis, tubular atrophy, and end-stage renal disease.
17
Steiner, Lisa A. Infections of the Hand. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0047.
Full textAbstract:
Hand infections can be delineated by type and location of infection, by a polymicrobial vs single microbial colonization, and by the type of organism. They are most often caused by superficial injury or trauma. Early identification and timely treatment can significantly improve the morbidity associated with hand infections. In addition to determining the source and mechanism of infection, it is important to identify tetanus immunization status, prior injury to the affected area, immune status, occupation, and hand dominance. Some hand infections (eg, paronychia, felon, herpetic whitlow, and cellulitis) can be treated in the emergency department and discharged with close follow-up. Deep space abscesses and infections caused by bite wounds involving tendons will require either observation, admission, or surgery depending on their severity. Take into account a patient’s comorbidities—diabetes, immunosuppression, injection drug use, inability to follow up for re-evaluation, and ability to fill antibiotic prescriptions—upon disposition.
18
Kulkarni, Kunal, James Harrison, Mohamed Baguneid, and Bernard Prendergast, eds. Transplantation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198729426.003.0030.
Full textAbstract:
Organ transplantation is now a well-established therapy for patients with end-stage organ failure. Over the last 20 years, the results of transplantation have improved incrementally for many reasons, including better recipient selection, improved anaesthetic and surgical techniques, the introduction of more effective antiviral agents, and better post-transplant immunosuppressive management. The problem of early graft loss from acute rejection is now uncommon, and the main challenges today are chronic allograft rejection and the side effects of non-specific suppression of the immune response. Randomized clinical trials continue to inform and further improve clinical practice. Because transplantation today is largely successful, the traditional endpoints of 1-year patient and graft survival are no longer sufficient, and more sophisticated endpoints are needed that reflect graft function and quality of life after transplantation. This chapter brings together studies which recognize this need for clinical trials which improve practice and focus on more broadly defined endpoints.
19
Wiles, Kate, and Catherine Nelson-Piercy. Contraception in patients with kidney disease. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0293_update_001.
Full textAbstract:
Three per cent of women of childbearing age have chronic kidney disease, and although end-stage renal failure impacts on fertility, conception and high-risk pregnancy do occur. Following renal transplantation, the patient should understand the potential impact of a pregnancy on transplant function and vice versa. Surveys show that a large proportion of pregnancies in female renal patients are unplanned. The effectiveness of a particular contraceptive method is dependent upon acceptability to the patient and compliance. Contraceptive decision-making needs to balance acceptability and safety with the risk of an unplanned pregnancy. Oestrogen-containing contraceptive methods are considered unacceptable for many renal patients because of their association with increased blood pressure and thrombotic and vascular events. Progesterone-only methods have an advantageous safety profile. The progesterone-only pill (desogestrel preparations), intrauterine system (Mirena®), and implant (Nexplanon®) are safe and effective in women with CKD. Concerns regarding the intrauterine system (Mirena®) in women taking immunosuppression are unfounded and observational evidence does not demonstrate an increased risk of infection. Sterilization is effective and should be considered to be irreversible. The effectiveness of barrier methods is reduced when ‘typical use’ is compared to ‘perfect use’. Unplanned pregnancy rates are high with fertility awareness methods and reliance on lactational amenorrhoea is not advocated.Interactions between drugs which are commonly prescribed in the renal population and different contraceptive methods are outlined in this chapter.
20
Reddy, Ugan, and Nicholas Hirsch. Diagnosis, assessment, and management of myasthenia gravis and paramyasthenic syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0244.
Full textAbstract:
Diseases that affect the neuromuscular junction (NMJ) interfere with normal nerve transmission and cause weakness of voluntary muscles. The two most commonly encountered are acquired myasthenia gravis (MG) and the Lambert–Eaton myasthenic syndrome (LEMS). Acquired MG is an autoimmune disease in which antibodies are directed towards receptors at the NMJ. In 85% of patients, IgG antibodies against the postsynaptic acetylcholine receptor (AChR) are found (seropositive MG). The thymus gland appears to be involved in the production of these which cause an increase rate of degradation of AChR resulting in a decreased receptor density resulting in a reduced postsynaptic end-plate potential following motor nerve stimulation and leading to muscle weakness. Although all voluntary muscles can be affected, ocular, bulbar, respiratory, and proximal limb weakness predominates. In the majority of seronegative patients, an antibody directed towards a NMJ protein called muscle specific tyrosine kinase (MUSK) is found. Anti-MUSK MG is characterized by severe bulbar and respiratory muscle weakness. Diagnosis of MG requires a high degree of clinical suspicion coupled with pharmacological and electrophysiological testing, and detection of the various causative antibodies. Treatment of MG involves enhancing neuromuscular transmission with long-acting anticholinesterase agents and immunosuppression. Acute exacerbations are treated with either plasma exchange or intravenous immunoglobulin. Myasthenic crisis is associated with severe muscle weakness that necessitates tracheal intubation and mechanical ventilation. LEMS is an autoimmune disease in which IgG antibodies are directed towards the pre-synaptic voltage-gated calcium channels at the NMJ. It is often associated with malignant disease (usually small cell carcinoma of the lung). Autonomic dysfunction is prominent and patients show abnormal responses to neuromuscular blocking drugs.
21
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.
Full textAbstract:
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 phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.
22
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.
Full textAbstract:
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 drug-induced CTIN largely depends on the history of exposure to a nephrotoxic drug. Clinical investigations may show modest elevation in serum creatinine, evidence of tubular dysfunction (e.g. renal tubular acidosis), or Fanconi syndrome (i.e. aminoaciduria, glycosuria, hypophosphataemia, and hypouricaemia). Urinalysis may be normal or show low-grade proteinuria (< 1.5 g/day) and/or pyuria. Diagnosis depends on renal biopsy, which reveals variable cellular infiltration of the interstitium, tubular atrophy, and fibrosis. Analgesic nephropathy is possibly still the most common category of CTIN worldwide. The amount of phenacetin-acetaminophen combination required to cause CTIN has been estimated to be at least 2–3 kg over many years. Lithium-induced CTIN occurs in a small subset of patients receiving long-term lithium therapy, who have had repeated episodes of lithium toxicity, with high serum drug levels. CTIN induced by ciclosporin or tacrolimus is common among patients receiving kidney, heart, liver, and pancreas transplants. The mechanism appears to be dependent largely on the potent vasoconstrictive effects of these drugs. The recognition of a potential association between a patient’s renal disease and exposure to a drug is crucial, because, unlike many other forms of renal disease, drug-induced CTIN can be prevented and even reversed, by avoiding additional drug exposure.
23
Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.
Full textAbstract:
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.