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2
Phipps, Lisa M., Titi Chen, and David C. H. Harris. Radiation nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0091_update_001.
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Radiation nephropathy usually arises after inadvertent exposure of kidneys to radiotherapy. It may manifest as acute nephropathy as early as 6 months after exposure, or later as chronic nephropathy, hypertension, or asymptomatic proteinuria. Glomerular and peritubular endothelium and renal tubular cells are especially radiosensitive. There are no pathognomonic histological features, but renal pathology may be similar to that of haemolytic uraemic syndrome. Radiation nephropathy may be prevented by renal shielding and mitigated by radiation dose fractionation. Control of hypertension is important and angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists appear to have protective effects beyond those of blood pressure control.
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Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. Boston: Nijhoff, 1988.
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Alderson, Helen, Constantina Chrysochou, James Ritchie, and Philip A. Kalra. Ischaemic nephropathy. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0212.
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Ischaemic nephropathy describes loss of renal function or renal parenchyma due to stenosis or occlusion of the renal artery or its branches. In the Western world, this is usually the result of atherosclerotic renovascular disease, but other aetiologies include arteritis, embolic disease, dissection, and fibromuscular disease.Chronic kidney disease is the most common manifestation of ischaemic nephropathy, but hypertension, flash pulmonary oedema, sensitivity to angiotensin blockade, and sensitivity of glomerular filtration rate to blood pressure reduction are all possible manifestations of occlusive diseases of the renal artery or its branches. Proteinuria may also occur.This chapter describes these clinical features and the outcomes of ischaemic nephropathy. It goes on to discuss the haemodynamics and mechanisms and what we understand of the pathophysiology of the condition.
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Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.
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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.
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Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0066_update_001.
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Immunoglobulin A (IgA) nephropathy characteristically causes haematuria and may present as a nephritic illness in older children and young adults. However, it may occur at any age and is commonly asymptomatic, associated first with haematuria alone, later progressing in some patients to hypertension, proteinuria, and progressive loss of glomerular filtration. While this evolution is characteristically slow, over decades, in some it is rapid, leading to early end-stage renal failure. It is common for the disease to present late, as advanced renal disease, or malignant hypertension. It may present with acute kidney injury caused by crescentic disease, but acute kidney injury caused by haematuria may be confused clinically with the same. Henoch–Schönlein purpura is a type of small vessel vasculitis that is most commonly seen in children, but which occurs at all ages, that is associated with IgA deposition. In older children and most adults it merges closely into IgA nephropathy after the acute event. Outcomes in adults are less good. IgA nephropathy is the most common type of glomerulonephritis in most developed countries. The disease is more common in men, and appears to be much less common in black people. The detected incidence is strongly influenced by biopsy policies; the lower your threshold to biopsy patients with haematuria, the more of this condition you discover. There are clear genetic tendencies but the strongest risk seems to come from genes in the human leucocyte antigen complex.
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Porush, J. G., and F. Faubert. Clinician's Manual on Hypertension, Diabetes Mellitus, and Nephropathy. Science Press, 2001.
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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus, Fourth. 4th ed. Springer, 1998.
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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus, Sixth Edition. 6th ed. Informa Healthcare, 2004.
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Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. 3rd ed. Boston: Kluwer, 1997.
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Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. 6th ed. London: Taylor & Francis, 2004.
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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus. 6th ed. Kluwer Academic Publishers, 2006.
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Erikmogensen, Carl. The Kidney and Hypertension in Diabetes Mellitus. Springer, 2012.
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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus. 3rd ed. Springer, 1996.
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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus. 5th ed. Springer, 2000.
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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus. Springer, 2013.
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Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. 2nd ed. Boston: Kluwer Academic, 1994.
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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus. Springer, 2013.
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20
Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus. Springer, 1998.
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21
Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. 4th ed. Boston: Kluwer Academic Publishers, 1998.
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22
Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus. Springer, 2013.
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23
Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. 6th ed. Boston: Kluwer Academic Publishers, 2003.
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24
Carton, James. Renal pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0010.
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This chapter discusses renal pathology, including acute kidney injury (AKI), chronic kidney disease (CKD), nephrotic syndrome, hereditary renal diseases, Alport’s syndrome and thin basement membrane lesion, hypertensive nephropathy, diabetic nephropathy, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy, glomerulonephritis, IgA nephropathy, post-infectious glomerulonephritis, C3 glomerulopathy, anti-glomerular basement membrane disease, monoclonal gammopathy-associated kidney disease, acute tubular injury, acute tubulointerstitial nephritis, reflux nephropathy, and obstructive nephropathy.
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Lambert, Heather. Primary vesicoureteric reflux and reflux nephropathy. Edited by Adrian Woolf. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0355_update_001.
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Vesicoureteric reflux (VUR) describes the flow of urine from the bladder into the upper urinary tract when the ureterovesical junction fails to perform as a one-way valve. Most commonly, VUR is primary, though it can be secondary to bladder outflow obstruction and can occur in several multiorgan congenital disorders. There is good evidence of a genetic basis with a greatly increased risk of VUR in children with a family history of VUR. VUR is a congenital disorder, which largely shows improvement or complete resolution with age. Fetal VUR may be associated with parenchymal developmental defects (dysplasia). Postnatally non-infected, non-obstructed VUR does not appear to have a detrimental effect on the kidneys. However there is an association of VUR with urinary tract infection and acquired renal parenchymal defects (scarring). The parenchymal abnormalities detected on imaging, often termed reflux nephropathy, may be as a result of reflux-associated dysplasia or acquired renal scarring or both. It is difficult to distinguish between the two on routine imaging. Higher grades of VUR are associated with more severe reflux nephropathy. The precise role of VUR in pyelonephritis and scarring is not clear and it may be that VUR simply increases the risk of acute pyelonephritis. Whilst most VUR resolves during childhood, it is associated with an increased risk of urinary tract infection and burden of acute disease. Investigation strategies vary considerably, related to uncertainties about the natural history of the condition and the effectiveness of various interventions. The long-term prognosis is chiefly related to the morbidity of reflux nephropathy leading in some cases to impairment of glomerular filtration rate, hypertension, proteinuria, and pregnancy-related conditions including hypertension, pre-eclampsia, and recurrent urinary tract infection. Management is controversial and ranges from simple observation with or without provision of rapid access to diagnosis and treatment of urinary tract infections; to long-term prophylactic antibiotics or various antireflux surgical procedures.
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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Diabetic renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0164.
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Diabetic nephropathy is kidney damage occurring as a result of diabetes mellitus. Overt diabetic nephropathy is defined as proteinuria greater than 0.5 g/day. Diabetic nephropathy has a complicated pathogenesis including glomerular hypertension with hyperfiltration and advanced glycation end products. Poor glycaemic control is associated with progression to microalbuminuria and overt diabetic nephropathy. The lifetime risk is fairly equivalent for type 1 and type 2 diabetes mellitus. Early disease is usually asymptomatic. Hyperglycaemia causes an osmotic diuresis and, thus, diabetes can present with polyuria. Hypertension develops with microalbuminuria; oedema indicates abnormal sodium and water retention and, occasionally, the development of nephrotic syndrome. Patients with diabetes, perhaps due to accompanying cardiac disease, are particularly susceptible to fluid overload and uraemic symptoms. End-stage renal disease can occur as early as when the estimated glomerular filtration rate is 15 ml/min 1.73 m−2.
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Winston, Jonathan, Etti Zeldis, John A. Grimaldi, and Esteban Martínez. HIV-Associated Nephropathy, End-Stage Renal Disease, Dialysis, and Kidney Transplant. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0044.
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Antiretroviral therapy has changed the phenotype of HIV-related kidney disease to a more chronic disease model. In addition to HIV-associated nephropathy (HIVAN), patients with HIV may experience kidney dysfunction related to other chronic illnesses, such as diabetes, hypertension, and hepatitis C. Patients with HIV should be monitored for the development of chronic kidney disease and the potential nephrotoxicity of antiretroviral therapy. For patients with HIV who progress to end-stage renal disease, the outcomes on dialysis and management of the dialysis procedure are similar to the outcomes of patients without HIV. Renal transplantation is a promising treatment option for HIV patients with end-stage renal disease, despite certain barriers inherent in the transplant evaluation process. Concomitant HIV and end-stage renal disease, with the stress of dialysis, can exacerbate psychiatric illness.
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Raine, Tim, James Dawson, Stephan Sanders, and Simon Eccles. Pharmacopoeia. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199683819.003.0005.
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PharmacopoeiaUsers are advised to always check local prescribing guidelines and formularies and to consult the BNF when prescribing drugs.Dose see Table 5.1, and see Table 5.2 on how to commence a patient on an ACEi Indications heart failure, hypertension, diabetic nephropathy, prophylaxis of cardiovascular events ...
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Gnudi, Luigi, Giorgio Gentile, and Piero Ruggenenti. The patient with diabetes mellitus. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0149_update_001.
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About one third of patients with type 1 diabetes develop diabetic nephropathy long-term (usually not before at least 10 years of diabetes), though this proportion is falling as standards of care have risen. Nephropathy is strongly associated with other microvascular complications of diabetes, so that some degree of retinopathy is to be expected, and evidence of neuropathy is common. Patients with type 2 diabetes are equally susceptible, but this is an older group in which vascular disease and other pathologies are also more likely. The rise in type 2 diabetes accounts for diabetes being the most common recorded cause of end stage renal disease (ESRD) in the developed world.Diabetic nephropathy is characterized by a progression through hyperfiltration, microalbuminuria, hypertension, overt proteinuria, nephrotic syndrome, loss of GFR, to ESRD. Risk factors for developing it include genetic factors (though no major single gene effects have been identified), and quality of glycaemic control.The risk of progression can at early stages be reduced by improved glycaemic control, and control of hypertension also slows progression. However angiotensin converting enzyme inhibitors or receptor blockers (ACEi, ARB) are the standard of care for patients with microalbuminuria or overt proteinuria, as they have been shown to reduce the risk of renal endpoints. Combination therapy with both ACEi and ARB together has been associated with a high risk of AKI, hyperkalaemia and other adverse effects so is not generally recommended. Other promising agents in combination are under investigation but none adequately proven at this stage.Patients who reach ESRD have reduced survival on all modalities compared to age-matched patients with other diagnoses. Best rehabilitation and survival for those who are suitable is through renal transplantation, though combined pancreas-renal transplantation may offer still better outcomes for selected patients.
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Haymann, Jean-Philippe, and Francois Lionnet. The patient with sickle cell anaemia. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0167.
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In sickle cell anaemia (SCA) a single mutation in the haemoglobin beta-globin gene is responsible for a pleomorphic phenotype leading to acute and chronic life-threatening complications. Healthcare management programmes, patient and family education, infection prophylaxis (especially in childhood), and long-term treatment for some patients (such as hydroxyurea) have significantly improved survival, giving rise to some new long-term issues.Sickle cell-associated nephropathy (SCAN) leads in some cases to chronic renal failure with a significant impact on survival. SCAN is characterized by an increased effective plasma renal flow and glomerular filtration rate, glomerular hypertrophy, and damaged vasa recta system leading to albuminuria and impaired urinary concentration.Early onset of hyperfiltration occurs in 60% of SCA patients often associated with microalbuminuria. SCAN risk factors are still under investigation, but may be related to chronic haemolysis at an early time point. Other lesions in patients with sickle cell anaemia include papillary necrosis, and recurrent acute kidney injury in association with crises or infections.ACEI are recommended if there is proteinuria. There is no current agreement on whether angiotensin-converting enzyme inhibitors (ACEI) should be introduced earlier, but systematic screening for microalbuminuria and hypertension, and avoidance of nephrotoxic agents are strongly advised.Patients with sickle cell trait (carriers for sickle cell anaemia) are prone to microscopic haematuria and abnormalities of the vasa recta have been described. A very rare tumour, renal medullary carcinoma, is largely restricted to this group (in whom it is still extremely rare). Increased risk of other renal problems is still largely hypothetical rather than proven.The prevalence of nephropathies in other sickle cell diseases (in particular haemoglobin SC disease) is much lower.
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Orth, Stephan R. Smoking in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0103.
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Smoking has been acknowledged as the number one preventable cause of death in most countries. The adverse effects of smoking on the kidney are less known. Prospective, population-based, observational studies, and evidence from experimental work indicate that smoking (a) is a relevant risk factor for chronic kidney disease (CKD) in the general population and (b) is associated with an increased risk of deterioration in renal function in CKD patients. The latter is especially true for patients with diabetic nephropathy or hypertensive renal damage. The conclusion is that smoking is an important renal risk factor and nephrologists should make greater efforts to motivate patients to stop smoking, not least because smoking cessation improves the prognosis of CKD.
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Rodriguez-Iturbe, Bernardo, and Mark Haas. Immunoglobulin A-dominant post-infectious glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0078_update_001.
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Immunoglobulin A (IgA)-dominant post-infectious glomerulonephritis is usually associated with infections with Staphylococcus aureus. It is most commonly seen in patients over 60, and particularly in men. The renal lesion is acute and severe, and commonly includes crescent formation, although the described histological features vary widely. IgA is the dominant immunoglobulin and in later phases when capillary deposits are resolving it may be impossible to distinguish the condition from IgA nephropathy without the use of electron microscopy. Diabetes appears to be a risk factor. Complement levels are frequently low but may be normal. Clinically there is often severe nephrotic syndrome and hypertension may be less prominent.
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Turner, Neil, Teena Tandon, and Rajiv Agarwal. APOL1 and renal disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0341_update_001.
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Although apolipoprotein L1 (APOL1) is not known to be a direct cause of renal disease, it has emerged as a powerful cofactor in several important conditions. APOL1 gene polymorphisms account for the restriction of HIV-associated collapsing focal segmental glomerulosclerosis (FSGS) to those with African ancestry. In Africa, the disease-predisposing alleles seem to have been selected for because they convey resistance to some strains of trypanosomiasis. The same alleles are associated with increased susceptibility to primary FSGS, and are probably able to fully account for the excess of FSGS in black races. Two high-risk alleles have been labelled G1 and G2. To have increased susceptibility, individuals must usually have two copies, that is, it is recessive, but the gene frequency is high in West and Southern Africa and in those descended from those regions. The same alleles convey susceptibility to other more common renal diseases. Numerically the most significant association is with nephropathy previously attributed to hypertension. Recent evidence suggests that the gene may increase rate of progression in renal disease of various types, including diabetes. The mechanism is not known.
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Woywodt, Alexander, and Diana Chiu. The glomerulus and the concept of glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0042.
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The key features of glomerular diseases—haematuria, proteinuria, loss of glomerular filtration rate, and hypertension—were recognized in the nineteenth century, and some earlier, but Richard Bright is usually given credit for synthesizing the concepts of renal disease, and glomerulonephritis came under the heading of Bright’s disease for almost a century. Separation into different types was based on first clinical syndromes, but in the early twentieth century, pathological description was improving and with the introduction of percutaneous renal biopsies in the 1950s, in the 1960s histopathological definitions assumed the ascendancy. A unifying classification of glomerular disease remains work in progress. Current classifications are pathologically based but increasingly include the results of other investigations (including genotype and a variety of immunological and other tests). This chapter follows this pragmatic, hybrid approach, categorizing glomerular disease by pattern on renal biopsy except where aetiological factors are clearly identified (e.g. HIV nephropathy), or associated multisystem disease is defined (e.g. lupus nephritis), or the immunopathogenesis is well characterized (e.g. antiglomerular basement membrane disease).
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Bissell, Lesley-Anne, Dwomoa Adu, and Paul Emery. The patient with rheumatoid arthritis, mixed connective tissue disease, Sjögren syndrome, or polymyositis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0166.
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Renal disease is a well-recognized cause of ill health and death in rheumatoid arthritis. Three broad categories of renal disease occur. The first—and by far the most common—arises from the nephrotoxicity of the drugs used in the treatment of arthritis, particularly with non-steroidal anti-inflammatory drugs. Disease-modifying antirheumatic drugs such as gold and D-penicillamine may lead to proteinuria and a glomerulonephritis in 10–30% of patients. Ciclosporin is associated with significant nephrotoxicity and hypertension. A second major but diminishing cause of renal disease in rheumatoid arthritis is amyloidosis. Thirdly, rheumatoid arthritis may be associated with the development of glomerulonephritis. The main types described are a mesangial proliferative glomerulonephritis with or without immunoglobulin A deposits, a membranous nephropathy, and a focal segmental necrotizing glomerulonephritis of the vasculitic type.Renal disease in mixed connective tissue disease and polymyositis is infrequent, but the former can be associated with a membranous and mesangial proliferative glomerulonephritis.Sjögren syndrome is rarely associated with clinically significant renal disease, but patients can present with proteinuria, acidosis, or hyperchloraemia. Interstitial nephritis and immune complex glomerulonephritis reflect the exocrinopathy and circulating immune complex disease pathognomonic of Sjögren syndrome. Evidence for effective treatment of the renal complications is lacking. Corticosteroids and cyclophosphamide are most commonly used, with newer biological drugs, such as rituximab, showing promise.
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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.
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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.
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Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0182_update_001.
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AbstractSchistosomiasis is a parasitic disease that affects millions of people in 78 countries, where it is held responsible for considerable morbidity and mortality. It is caused by a blood fluke, which provokes an immunological response to hundreds of its antigens. This induces multi-organ pathology through the formation of tissue granulomata or circulating immune complexes. In addition, it is amyloidogenic and carcinogenic, through the interaction of immunological perturbation with confounding metabolic and genetic factors. The primary targets of schistosomiasis are urinary and hepatointestinal.The lower urinary tract is mainly affected in S. haematobium infection, and may lead to chronic pyelonephritis and/or obstructive nephropathy. The colon and liver are the targets of S. mansoni and S. japonicum infection, leading to hepatic fibrosis, portal hypertension, and liver failure. S. mansoni may also lead to immune complex glomerulonephritis, which is discussed elsewhere. Both S. haematobium and S. mansoni ova may be carried with the venous circulation to the lungs, where they provoke granulomatous and immune-mediated endothelial injury leading to cor-pulmonale. Ova may be subsequently carried with the arterial circulation to form ‘metastatic’ granulomas in other tissues, notably the brain (S. japonicum), spinal cord (S. haematobium), skin, conjunctiva, and genital organs.Schistosomiasis is preventable. World Health Organization programmes have successfully eradicated or reduced the incidence of infection in many countries, particularly Egypt and China. Prevention strategies include health education, raising hygiene standards, and interruption of the parasite’s life cycle by snail control and mass treatment. The search for a vaccine continues. Effective antiparasitic treatment is now possible with high elimination rates. Available agents include praziquantel and artemether for all species, metrifonate for S. haematobium, and oxamniquine for S. mansoni. Successful outcome correlates with early intervention, before fibrosis has occurred.
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Ferro, Charles J., and Khai Ping Ng. Recommendations for management of high renal risk chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0099.
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Poorer renal function is associated with increasing morbidity and mortality. In the wider population this is mainly as a consequence of cardiovascular disease. Renal patients are more likely to progress to end-stage renal disease, but also have high cardiovascular risk. Aiming to reduce both progression of renal impairment and cardiovascular disease are not contradictory. Focusing on the management of high-risk patients with proteinuria and reduced glomerular filtration rates, it is recommended that blood pressure should be kept below 140/90, or 130/80 if proteinuria is > 1 g/24 h (protein:creatinine ratio (PCR) >100 mg/mmol or 0.9 g/g). These targets may be modified according to age and other factors. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor antagonists should form part of the therapy for patients with proteinuria > 0.5 g/24 h (PCR > 50 mg/mmol or 0.45 g/g). Use of ACEIs or angiotensin receptor blockers in patients with lower levels of proteinuria may be indicated in some patient groups even in the absence of hypertension, notably in diabetic nephropathy. Evidence that other agents that reduce proteinuria bring additional benefits is weak at present. The best studies of ‘dual-blockade’ with various combinations of ACEIs, ARBs, and renin inhibitors have shown additional hazard with little evidence of additional benefit. Hyperlipidaemia—regardless of lipid levels, statin therapy is indicated in secondary cardiovascular prevention, and in primary prevention where cardiovascular risk is high, noting that current risk estimation tools do not adequately account for the increased risk of patients with CKD. There is not substantial evidence that lipid lowering therapy impacts on average rates of loss of GFR in progressive CKD. Non-drug lifestyle interventions to reduce cardiovascular risk, including stopping smoking, are important for all. Acidosis—in more advanced CKD it is justified to treat acidosis with oral sodium bicarbonate. Diet—sodium restriction to < 100 mmol/day (6 g/day) and avoidance of excessive dietary protein are justified in early to moderate CKD. Recommendations to limit levels of protein to 0.8 g/kg body weight are suggested by some, but additional protective effects of this are likely to be slight in patients who are otherwise well managed. Low-protein diets may carry some risk. Lower-protein diets may however be used to prevent symptoms in advanced CKD not treated by dialysis.