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1
Liu, Bi-Cheng, Hui-Yao Lan et Lin-Li Lv, dir. Renal Fibrosis : Mechanisms and Therapies. Singapore : Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2.
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Journées Gabriel Richet (1994 Le Coudray Montceaux, France). Molecular and experimental aspects of renal fibrogenesis : Journées Gabriel Richet. Sous la direction de Sraer Jean-Daniel, Ronco Pierre et Rondeau Eric. [Cambridge, MA] : Blackwell Science, 1995.
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Hanssen, Lydia. Die pathophysiologische Bedeutung des Y-box-bindenden Proteins-1 (YB-1) in der renalen Fibrose. [S.l : s.n.], 2012.
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Razzaque, M. S., et T. Taguchi, dir. Renal Fibrosis. S. Karger AG, 2003. http://dx.doi.org/10.1159/isbn.978-3-318-00964-4.
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(Editor), Mohammed S. Razzaque, et Takashi Taguchi (Editor), dir. Renal Fibrosis (Contributions to Nephrology). S. Karger Publishers (USA), 2003.
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Liu, Bi-Cheng, Hui-Yao Lan et Lin-Li Lv. Renal Fibrosis : Mechanisms and Therapies. Springer, 2020.
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Liu, Bi-Cheng, Hui-Yao Lan et Lin-Li Lv. Renal Fibrosis : Mechanisms and Therapies. Springer, 2019.
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Liu, Bi-Cheng, Hui-Yao Lan et Lin-Li Lv. Renal Fibrosis : Mechanisms and Therapies. Springer, 2019.
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Lan, Hui Y., et David J. Nikolic-Paterson, dir. Advances in Mechanisms of Renal Fibrosis. Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-499-0.
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Herrington, William G., Aron Chakera et Christopher A. O’Callaghan. Interstitial renal disease. Sous la direction de Patrick Davey et David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0160.
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Tubulointerstitial renal diseases affect the renal tubules and/or the supporting interstitial tissue around them. The glomeruli are typically spared in early disease. Acute interstitial nephritis is characterized by an inflammatory infiltrate (often containing eosinophils). Chronic tubulointerstitial nephritis (TIN) is characterized by extensive tubular atrophy and interstitial fibrosis. The processes are clinically distinct but a prolonged acute interstitial nephritis will develop into chronic disease. This chapter looks at the etiology of interstitial renal disease, as well as its symptoms and clinical features, demographics, complications, diagnosis, and treatment.
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Bardin, Thomas, et Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.
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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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Galperin, Timur A., Kieron S. Leslie et Antonia J. Cronin. Cutaneous manifestations of end-stage renal disease. Sous la direction de David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0131.
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A broad range of skin diseases occur in patients with end-stage renal disease. Some of these conditions are benign, and make little impact on patients’ lives. Others, however, have a greater impact on quality of life, may be physically disabling, and even life-threatening. Mostly, they result from a combination of factors, such as electrolyte imbalance and co-morbid disease. Uraemic pruritus is the most commonly troublesome and an approach to it is presented. Other non-specific skin manifestations of CKD include skin-colour changes, xerosis, half-and-half nails Specific manifestations include acquired perforating dermatosis, bullous dermatoses, metastatic calcification, and nephrogenic systemic fibrosis. Pathophysiology, clinical presentation, diagnosis, and treatment options are discussed.
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Chen, Dan-Qian, et Zhiyong Guo, dir. New Insights Into Renal Fibrosis and Therapeutic Effects of Natural Products. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-272-9.
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Schiller, Adalbert, Adrian Covic et Liviu Segall. Chronic tubulointerstitial nephritis. Sous la direction de 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 reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.
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Hughes, Jeremy. Proteinuria as a direct cause of progression. Sous la direction de David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.
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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.
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Plebani, Mario, Monica Maria Mion et Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.
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In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘cardiorenal syndrome’, in particular, the measurement of serum creatinine and its use for calculating the glomerular filtration rate which, with the new and more efficient equation, namely Chronic Kidney Disease Epidemiology Collaboration, still remains the most widely used biomarker. The role of newer biomarkers will be explored. The measurement of cystatin C, representing additional information, particularly in paediatric age groups and in the early phase of kidney disease, plays an increasing role. Neutrophil gelatinase-associated lipocalin is a recently developed and very promising new biomarker for the diagnosis of acute kidney injury, while the well-known albumin/creatinine ratio has been re-evaluated as a simple and useful tool for an early identification of kidney disease. Regarding liver diseases, a growing body of evidence demonstrates the usefulness of non-invasive makers of hepatic fibrosis that may avoid the need for a liver biopsy in most patients. A promising field of research is represented by the role of non-alcoholic fatty liver disease in the pathogenesis of cardiovascular disease.
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London, Gerard M. Cardiovascular complications in end-stage renal disease patients. Sous la direction de Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0268.
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Cardiovascular complications are the predominant cause of death in patients with end-stage renal disease (ESRD). The high incidence of cardiovascular complications results from pathology present before ESRD (generalized atherosclerosis, diabetes, hypertension) and an additive effect of multiple factors including haemodynamic overload and metabolic and endocrine abnormalities more or less specific to uraemia or its treatment modalities. These disorders are usually associated and can exacerbate each other. While ischaemic heart disease is a frequent cause of cardiac death, heart failure and sudden death are the most frequent causes of death in ESRD. Cardiomyopathy of overload with development of left ventricular hypertrophy and fibrosis are the most characteristic alterations and major determinants of prognosis. Left ventricular hypertrophy may result in systolic and/or diastolic dysfunction and is a risk factor for arrhythmias, sudden death, heart failure, and myocardial ischaemia. Arterial disease, whether due to atherosclerosis or arteriosclerosis (or both), represents a major contributory factor to the cardiovascular complications. Arterial disease may result in ischaemic complications (ischaemic heart disease, peripheral artery diseases) or arterial stiffening with direct consequences on left ventricular afterload, decreased coronary perfusion, and microvascular abnormalities (inward remodelling and microvessel rarefaction).
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Glockner, James F., Kazuhiro Kitajima et Akira Kawashima. Magnetic resonance imaging. Sous la direction de Christopher G. Winearls. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0015_update_001.
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Magnetic resonance imaging (MRI) provides excellent anatomic detail and soft tissue contrast for the evaluation of patients with renal disease. MRI needs longer scan time than computed tomography (CT); however, no radiation is involved. Gadolinium-based contrast agents (GBCAs) are used to help provide additional image contrast during MRI. MRI is indicated for characterization of renal mass, staging of malignant renal neoplasms, and determination of vena cava involvement by the renal tumour. Magnetic resonance (MR) angiography is widely accepted as a non-invasive imaging work-up of renal artery stenosis. MR urography is an alternative to CT urography to assess the upper urinary tract but does not identify urinary calculi. Diffusion-weighted imaging is a functional MR technique being used to characterize parenchymal renal disease and renal tumours. Nephrogenic systemic fibrosis is a rare but debilitating and potentially life-threatening condition which has been linked to exposure of GBCAs in patients with severe renal insufficiency. The risk versus benefit must be assessed before proceeding.
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Nahas, A. M. El. Renal Scarring - A Multi-Organ Approach to Fibrosis (Experimental Nephsology, 1995 , Vol 3, No 2-3). S. Karger AG (Switzerland), 1995.
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Henderson, Lorna K., Brian J. Nankivell et Jeremy R. Chapman. Chronic allograft dysfunction. Sous la direction de Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0286.
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Despite improvements in short-term renal allograft survival, long-term survival has not appreciably changed. Excepting death with a functioning graft, most late graft loss results from chronic allograft dysfunction. Immune and non-immune-mediated injuries contribute to graft dysfunction over time, ultimately leading to a non-specific and irreversible histological end-point of fibrosis, tubular atrophy, and glomerulosclerosis. Screening and early identification of pathology is crucial to allow timely intervention in order to prevent permanent nephron damage and graft loss. This chapter outlines assessment of renal dysfunction following transplantation, defines the causes of chronic allograft failure, and their pathophysiology, and evaluates current therapeutic strategies used to improve or stabilize chronic allograft dysfunction.
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Sayer, John A., et Roslyn J. Simms. Nephronophthisis. Sous la direction de Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0317_update_001.
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Nephronophthisis (NPHP) is a clinically heterogeneous autosomal recessive cystic kidney disease and the leading genetic cause of end-stage renal failure in children and young adults. Whilst enlarged dysplastic cystic kidneys are associated with infantile NPHP, more typically renal ultrasound reveals normal kidney size and corticomedullary cysts in a child with polyuria and secondary enuresis. Extrarenal manifestations occur in 10–15% including retinal degeneration, cerebellar vermis hypoplasia and liver fibrosis, requiring referral to other specialists. Mutations in 18 genes have been identified to cause NPHP, but a genetic diagnosis still cannot be found in many patients. NPHP is classified as a ciliopathy because of the localization of the protein products of the associated genes. Currently there is no specific therapy for NPHP.
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Kang, Duk-Hee, et Mehmet Kanbay. Urate nephropathy. Sous la direction de 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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Denton, Christopher P., et Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.
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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.
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Tsai, Ching-Wei, Sanjeev Noel et Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.
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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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Izzedine, Hassan, et Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Sous la direction de Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.
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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.
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Izzedine, Hassan, et Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Sous la direction de 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 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.
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Segall, Liviu, et Adrian Covic. Immune-mediated tubulointerstitial nephritis. Sous la direction de Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.
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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.
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Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Sous la direction de David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0139.
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Experimental studies show that podocyte death first causes focal scars, but beyond approximately 40% loss is lethal to a glomerulus. Podocytes have limited ability to regenerate, although some degree of replacement may occur from stem cells located near the urinary pole of Bowman’s capsule. It is not yet known whether this plays a significant part in ameliorating damage in disease processes. In one interpretation, foot process effacement may be seen as an adaptation by the podocyte to remain attached to the glomerular basement membrane after injury, at the expense of proteinuria. Podocyte dysfunction is closely associated with proteinuria, which in turn is strongly associated with progressive loss of glomerular filtration rate. Continuing podocyte damage and loss could therefore account for progressive renal disease. In this hypothesis, drugs that protect against progression of renal disease may have their primary protective effects on podocytes themselves, rather than or as well as on haemodynamic factors or on fibrotic processes.
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Alchi, Bassam, et David Jayne. The patient with antiphospholipid syndrome with or without lupus. Sous la direction de 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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Lee, Olivia T., Jennifer N. Wu, Frederick J. Meyers et Christopher P. Evans. Genitourinary aspects of palliative care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0084.
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Genitourinary tract diseases in the palliative care setting most commonly involve urinary tract obstruction, intractable bleeding, fistulae, and bladder-associated pain. Sources of obstruction in the lower urinary tract include benign prostatic hyperplasia, invasive prostate or bladder cancer, urethral stricture, or bladder neck contracture. Upper tract obstruction includes intraluminal or extraluminal blockage of the renal collecting system and ureters, such as transitional cell carcinoma, fibroepithelial polyps, stricture, stones, pelvic or retroperitoneal malignancy, fibrosis, or prior radiation. Untreated, obstructive uropathy leads to elevated bladder, ureter, and kidney pressures, bladder dysfunction, urolithiasis, renal failure, pyelonephritis, or urosepsis. Intractable haematuria can cause problematic anaemia, frequent transfusions, clot retention, haemorrhagic shock, and death. In addition, urinary tract fistulae such as vesicovaginal and vesicoenteric fistulae are common in patients who have had prior pelvic surgery or radiation especially in the setting of immunocompromise, poor nutrition, and infection. Untreated, these symptoms lead to rash, skin breakdown, ulcers, chronic infection, and sepsis. Lastly, pelvic and bladder pain, depending on aetiology can be treated with oral medications, intravesical therapies, or surgical therapies such as palliative resection or urinary diversion. Selection of tests and treatment modalities in the palliative care setting should be based on using the least invasive means to achieve the most relief in suffering. Some genitourinary conditions are potentially fatal, and in the acute or subacute setting, require re-evaluation of the end-of-life goals and wishes of the patient and family.
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Astroza, Gastón M., Michael E. Lipkin et Glenn M. Preminger. Intracorporeal techniques of stone fragmentation. Sous la direction de John Reynard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0018.
Texte intégralRésumé :
The use of intracorporeal lithotripsy for the management of larger ureteral and intrarenal calculi has dramatically improved. Although the choice of intracorporeal fragmentation is frequently based on the location and composition of the stone to be treated, the experience of the clinician and availability of equipment often dictates this decision. Several different modalities of intracorporeal lithotripsy are currently available. Ultrasonic lithotripsy is mainly used for the fragmentation of large renal calculi during percutaneous nephrolithotripsy procedures. Ultrasound is used rarely via an ureteroscopic approach. Significant advances in laser fibres and power generation systems have propelled laser lithotripsy to the treatment of choice for fragmentation of most ureteral stones. Pneumatic lithotripsy consists of a pneumatically driven piston which will fragment stones by direct contact.
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Lopez, Berenice, et Patrick J. Twomey. Biochemical investigation of rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0062.
Texte intégralRésumé :
It is important for rheumatologists to have an understanding of biochemical tests including an awareness of their limitations. The biological variability of an analyte both within and between individuals, the limitations of the measurement technology, the sensitivity of laboratory internal quality control and external quality assurance procedures, as well as interlaboratory variations in practices including sample collection procedures, may all impact on the interpretation of a result. Biochemical tests are often requested to monitor organ-specific dysfunction arising as an adverse consequence of pharmacotherapy or as a component of a systemic rheumatic disease, although dysfunction may also reflect infection or coincidental pathology. Patients with rheumatic diseases are at high risk of renal and hepatic disease. Serum creatinine and its derivative estimated glomerular filtration rate (eGFR) are the most readily available surrogate markers of GFR and are used to assess renal impairment and monitor its course. However, the use of creatinine alone lacks sensitivity and a substantial loss of function must occur before creatinine levels are increased. Additional biochemical screening for kidney damage can be performed by assessment of glomerular integrity, including proteinuria or albuminuria and haematuria. A wide spectrum of rheumatic diseases can affect the liver with various degrees of involvement and hepatic pathology. These often present with cholestatic or hepatitic biochemical profiles. The medical management of rheumatic diseases also involves medications that are hepatotoxic, and routine monitoring of liver function is recommended. This approach is not problem-free and may be improved by quantitative determinations of non-invasive markers of liver fibrosis in the future. Together with imaging techniques, biochemical tests play an important role in the assessment and differential diagnosis of metabolic bone disease.
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Zoccali, Carmine, Davide Bolignano et Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Sous la direction de David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.
Texte intégralRésumé :
Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.
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Radović, Milan, et Adalbert Schiller. Balkan endemic nephropathy. Sous la direction de Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.
Texte intégralRésumé :
Balkan endemic nephropathy (BEN) is a chronic, slowly progressive tubulointerstitial nephritis, with familial clustering, occurring in several endemic rural regions in countries of the Balkan Peninsula. BEN is characterized by anaemia, tubular proteinuria, renal shrinkage, and slowly declining glomerular filtration rate (GFR). Up to one-third of patients may also develop upper urothelial tumours. The aetiology of BEN is unclear; chronic exposure to aristolochic acid and a polygenic predisposition are the most likely contributing factors. The major pathological characteristics of BEN are symmetrically shrunken, smooth-shaped kidneys, with interstitial fibrosis, mild interstitial inflammation, and tubular atrophy. Diagnosis is usually based upon positive family history of BEN, past or current residence in endemic regions, tubular proteinuria, tubular dysfunctions (such as urine acidification defects, salt wasting, and impaired excretion of ammonia, uric acid, and phosphate), scant urinary sediment, bilateral and symmetrically reduced kidney size, accompanied by severe anaemia, disproportionate to the degree of GFR reduction. There is no specific therapy for BEN; patients should therefore be treated as all patients with chronic kidney disease, in general. The use of distant water supplies or moving to another residence area should be advised to affected families. Careful evaluation for urothelial cancers is mandatory in patients with haematuria.
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Turner, Neil. Crescentic (rapidly progressive) glomerulonephritis. Sous la direction de Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0070.
Texte intégralRésumé :
Crescent formation refers to the appearance of proliferating cells in Bowman’s space in response to severe glomerular inflammation. Any aggressive ‘nephritic’ diseases that cause basement membrane breaks may provoke this. Specific serum proteins appear to be responsible for provoking crescent formation as it is largely abolished by defibrination in animal models. The cells in the crescent are initially mostly hypertrophying and proliferating parietal epithelial cells that normally line Bowman’s capsule. Foci of proliferation of these cells (extracapillary proliferation) are the first steps of crescent formation. Monocytes are frequently seen in established crescents. At this stage recovery of glomerular structure and function is possible in many circumstances. However, if Bowman’s capsule is ruptured, fibroblast ingress followed by fibrosis and glomerulosclerosis are likely. Crescentic nephritis is a histological description, but it fits closely with the clinical picture of rapidly progressive glomerulonephritis (RPGN), in which renal function is lost over days to weeks. The diseases most likely to cause this clinical picture are small vessel vasculitis, anti-GBM disease, lupus nephritis, and post-infectious glomerulonephritis. Any ‘nephritic’ disease may provoke crescent formation, but it is frequently encountered in immunoglobulin A nephropathy/Henoch–Schönlein purpura, and in post-infective glomerulonephritis. Recognizing the clinical picture is important as aggressive immunosuppression can be effective in saving glomerular function in some of the conditions causing it.
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Hajhosseiny, Reza, Kaivan Khavandi et David J. Goldsmith. Sudden cardiac death in chronic kidney disease. Sous la direction de David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0108.
Texte intégralRésumé :
Epidemiological data demonstrate the unique vulnerability of chronic kidney disease (CKD) subjects to cardiovascular disease, the most catastrophic being sudden cardiac death (SCD). In patients with declining kidney function there is a continuum of cardiovascular risk. In those individuals who survive to reach end-stage renal disease (ESRD), the risk of suffering a cardiac event is extremely high. Some of this risk is explained by the common risk factors and traditional cardiovascular events, namely atherosclerotic plaque fissure and rupture, but there is now evidence of a distinct ‘later CKD’ mechanism, notably arrhythmias. This appears particularly true in later stages of CKD and corresponds with the multifaceted range of myocardial and vascular insults operating. The physiological milieu of disordered vessel autoregulation, sequestered vasoprotective agents, loss of conduit and small artery elasticity/compliance, a stiffened and fibrotic myocardium, with calcified and diseased coronary arteries, all within an inflammatory environment, all contribute to arrhythmia generation. The final insult is changes in volume and electrolyte status. Risk stratification tools would be helpful in guiding clinicians to recognize those subjects likely to benefit from specific interventional strategies. These might include the novel, or emerging serum, haemodynamic, or electrocardiographic biomarkers in CKD. Current tools—such as those used for stratifying risk for SCD and determining the need for ICD implantation—are not valid in ESRD patients. Beta blockers appear likely to be generally advisable, blood pressure permitting, for patients with significant cardiomyopathy. Evidence for implantable cardiac defibrillators (ICD) is lacking. There is good reason to think that young dialysis patients at high risk of sudden death may benefit, but the risk/benefit ratio for older patients is less likely to be advantageous. These hypotheses need further investigation.