Books: 'Kidney glomerulus Diseases'

1

Rotter, Wolfgang. Color atlas of kidney biopsy: Pathology of glomerular diseases. New York: Liss, 1985.

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2

Prabhakar, Sharma S. An update on glomerulopathies: Clinical and treatment aspects. Rijeka, Croatia: InTech, 2011.

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3

Prabhakar, Sharma S. An update on glomerulopathies: Etiology and pathogenesis. Rijeka, Croatia: InTech, 2011.

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4

Wardle, E. N. Glomerulopathies: Cell biology and immunology. Australia: Harwood Academic Press, 1996.

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5

Valaitis, Jonas. Renal glomerular diseases: Atlas of electron microscopy with histopathological bases and immunofluorescence findings : presention of 110 cases of patients undergoing kidney biopsies. Chicago: ACSP Press, 2002.

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6

Churg, Jacob. Renal disease: Classification and atlas of glomerular diseases. 2nd ed. New York: Igaku-Shoin, 1995.

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7

Dickersin, G. Richard. Diagnostic electron microscopy: A text/atlas. New York: Igaku-Shoin, 1988.

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8

Membranes, International Symposium on Renal Basement. Progress in basement membrane research: Renal and related aspects in health and disease : proceedings. London: J. Libbey, 1988.

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9

Elger, M. The vascular pole of the renal glomerulus of rat. Berlin: Springer, 1998.

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10

International Symposium on Renal Basement Membranes (4th 1987 Paris, France). Progress in basement membrane research: Renal and related aspects in health and disease : proceedings of the IVth International Symposium on Renal Basement Membranes and Related Research held in Paris, 21-25 July 1987. London: Libbey, 1988.

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11

1926-, Kincaid-Smith Priscilla, and Dowling J. P, eds. Atlas of glomerular disease: Morphological and clinical correlation. Balgowlah, Australia: AIDS Health Science Press, 1985.

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12

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

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

13

1915-, Senoo Sachimaru, Satellite Symposium on Biopathology of Vascular Wall and Glomerular Dysfunction (1984 : Kurashiki-shi, Japan), and International Congress on Cell Biology (3rd : 1984 : Tokyo, Japan), eds. Glomerular dysfunction and biopathology of vascular wall. Tokyo: Academic Press, 1985.

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14

Valaitis, Jonas M. D. Renal Glomerular Diseases: Atlas of Electron Microscopy with Histopathological Bases and Immunofluorescence Findings. American Society Clinical Pathology, 2002.

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15

M, Dodd S., ed. Tubulointerstitial and cystic disease of the kidney. [Berlin: Springer-Verlag, 1995.

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16

Dodd, Susan M. Tubulointerstitial Cystics Kidney (Chemistry of Plant Protection). Springer-Verlag Telos, 1995.

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17

Qiuhai, Qian, and Ni Qing, eds. Man xing shen xiao qiu shen yan. 8th ed. Beijing Shi: Zhongguo yi yao ke ji chu ban she, 2003.

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18

Winyard, Paul. Human kidney development. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0343.

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The kidneys perform diverse functions including excretion of nitrogenous waste products, homeostasis of water, electrolytes and acid–base balance, and hormone secretion. The simplest functional unit within the kidneys is the nephron, which consists of specialized segments from glomerulus, through proximal tubule, loop of Henle, and distal tubule. Human nephrogenesis starts with two stages of transient kidneys, termed the pronephros and mesonephros, and ends with development of a permanent organ from the metanephros on each side. The latter consists of just a few hundred cells when it is formed in the fifth week of pregnancy but progresses to a nephron endowment of between 0.6 to 1.3 million by the time nephrogenesis is completed at 32–36 weeks of gestation. Key events during this process include outgrowth of the epithelial ureteric bud from the mesonephric duct, interactions between the bud and the metanephric blastema (a specific region of mesenchyme) that cause the bud to branch and mesenchyme to condense, epithelialization of the mesenchyme to form proximal parts of the nephron, and differentiation of segment specific cells. Molecular control of these events is being unpicked with data from human genetic syndromes and animal models, and this chapter highlights several of the most important factors/systems involved. Increased understanding of development is not just relevant to congenital kidney malformations, but may also be important in designing rational therapies for diseases of the mature kidney where recapitulation of developmental pathways is common.

19

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by 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.

20

Fervenza, Fernando C. Evaluation of Kidney Function, Glomerular Disease, and Tubulointerstitial Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0472.

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Several measures are used to evaluate kidney function: serum creatinine, urinalysis, renal clearance, and renal imaging. Creatinine is an end product of muscle catabolism and is commonly used as a filtration marker. Dysmorphic erythrocytes in the urinary sediment indicate bleeding in the upper urinary tract. A urine pH less than 5.5 excludes type 1 renal tubular acidosis. A pH greater than 7 suggests infection. Acidic urine is indicative of a high-protein diet, acidosis, and potassium depletion. Alkaline urine is associated with a vegetarian diet, alkalosis and urease-producing bacteria. Clearance of p-aminohippurate is a measure of renal blood flow. Kidney function is evaluated to determine disease states such as glomeruluar disease or tubulointerstitial disease. Clinical manifestations of glomerular injury can vary from the finding of isolated hematuria or proteinuria, or both. In addition, some patients who present with advanced renal insufficiency, hypertension, and shrunken, smooth kidneys are presumed to have chronic glomerulonephritis. Acute and chronic interstitial disease preferentially involves renal tubules.

21

Sharpstone, P., and J. A. Trafford. Renal Glomerular Diseases. Springer, 2012.

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22

Sharpstone, P., and J. A. Trafford. Renal Glomerular Diseases. Springer Netherlands, 2012.

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23

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. The kidney in systemic disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0170.

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Many systemic diseases can affect the kidney, including autoimmune conditions, malignancies, infections, and vascular diseases. Autoimmune conditions can cause inflammation of the glomeruli or tubules, or deposition of inflammatory proteins (AA amyloidosis). Malignancy can cause infiltration of normal renal tissue, immunoglobulin deposition in the renal vessels, glomeruli or tubules, or paraneoplastic renal dysfunction as occurs in secondary focal segmental glomerulosclerosis. Infections can cause inflammation in glomeruli, in association with immune complex deposition. Vascular disease and vasculitis reduce kidney blood supply and cause renal ischaemia. This chapter provides an overview of these diseases.

24

Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Edited by 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.

25

Dickersin, Richard G. Diagnostic Electron Microscopy: A Text/Atlas. Springer, 2013.

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26

Dickersin, Richard G. Diagnostic Electron Microscopy: A Text/Atlas. 2nd ed. Springer, 2000.

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27

Dickersin, Richard G. Diagnostic Electron Microscopy: A Text/Atlas. Springer London, Limited, 2006.

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28

Wiles, Kate, Kate Bramham, and Catherine Nelson-Piercy. Kidney disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0044.

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This chapter describes the physiological adaptations to pregnancy in women with and without renal disease, reports pregnancy outcomes in women with both acute kidney injury and chronic kidney disease, and discusses a management strategy for antenatal and peripartum care. Acute kidney injury (AKI) is difficult to define in pregnancy because of the physiological increase in glomerular filtration. A normal creatinine can mask renal injury in pregnancy. This chapter considers important causes of AKI in pregnancy including pre-eclampsia, HELLP syndrome, thrombotic microangiopathy, acute fatty liver of pregnancy, systemic lupus erythematosus, urinary tract infection, and obstruction. The trend in the developed world for delaying pregnancy and the increasing prevalence of obesity mean that greater numbers of pregnancies will be complicated by chronic kidney disease. Maternal and fetal complications increase with worsening prepregnancy renal function including the development of pre-eclampsia, fetal growth restriction, premature delivery, and fetal loss. Prepregnancy counselling and the intrapartum management for women with lupus nephritis, immunoglobulin A nephropathy, polycystic kidney disease, and diabetic nephropathy are discussed. Renal replacement therapies in pregnancy including both dialysis and renal transplantation are considered, and practical guidance on renal biopsy, anaesthesia, and the pharmacology of renal disease in pregnancy is offered.

29

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Chronic kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0163.

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Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, where the abnormalities have been present for >3 months and have implications for health. It is characterized by a reduced estimated glomerular filtration rate (eGFR) or other renal abnormalities. CKD is staged according to the eGFR or the degree of albuminuria. The KDIGO (Kidney Disease: Improving Global Outcomes) criteria for CKD is either an eGFR that is <60 ml/min 1.73 m−2 and has been present for >3 months, or one or more markers of kidney damage, when these have been present for >3 months.

30

Progress in basement membrane research: Renal and related aspects in health and disease : Proceedings of the IVth International Symposium on Renal Basement ... Research held in Paris, 21-25 July 1987. Libbey, 1988.

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31

ROTTER, W. Rotter Color Atlas of Kidney Biopsy - Pathology of Glomerular Diseases. John Wiley & Sons Inc, 1985.

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32

Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Screening for kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0353.

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Renal disease is common and, with routine reporting of estimated glomerular filtration rates, impairment of renal function is increasingly being recognized. As renal impairment is usually asymptomatic until very advanced, chronic kidney disease (CKD) guidelines have been developed to improve the identification and screening of at-risk populations. Target groups include patients with vascular risk factors (e.g. diabetes mellitus and hypertension); patients with certain multisystem diseases which can cause renal impairment; patients with urological conditions; patients on nephrotoxic medication; and immediate relatives of patients with established renal disease. Kidney function should also be checked during intercurrent illness and perioperatively in all patients with CKD or suspected CKD. The frequency of screening is dictated by the CKD stage.

33

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Inherited renal diseases. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0169.

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The causes of inherited renal diseases can be divided into cystic, glomerular, tubular, and systemic diseases. By far, the most common of these in clinical practice is adult polycystic kidney disease (APKD). This chapter reviews APKD, other inherited cystic renal diseases, inherited glomerular and tubular diseases, and inherited systemic diseases with renal involvement.

34

Yaqoob, Muhammad M. Acidosis in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0148.

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Metabolic acidosis becomes increasingly common as chronic kidney disease progresses. It is associated with a number of complications, including bone disease, altered protein synthesis and degradation, skeletal muscle wasting, and lately progressive glomerular filtration rate loss. Experimental and clinical studies suggest a role for alkali therapy to lessen these complications. Recent controlled studies support this notion, and suggest that correction of metabolic acidosis in patients with chronic kidney disease slows the rate of decline of renal function and the development of end-stage renal disease, although more definitive evidence is needed on the long-term benefits of alkali therapy, type of alkali supplements, and the optimal level of serum bicarbonate.

35

Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.

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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.

36

Ho, Kwok M. Kidney and acid–base physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0005.

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Anatomically the kidney consists of the cortex, medulla, and renal pelvis. The kidneys have approximately 2 million nephrons and receive 20% of the resting cardiac output making the kidneys the richest blood flow per gram of tissue in the body. A high blood and plasma flow to the kidneys is essential for the generation of a large amount of glomerular filtrate, up to 125 ml min−1, to regulate the fluid and electrolyte balance of the body. The kidneys also have many other important physiological functions, including excretion of metabolic wastes or toxins, regulation of blood volume and pressure, and also production and metabolism of many hormones. Although plasma creatinine concentration has been frequently used to estimate glomerular filtration rate by the Modification of Diet in Renal Disease (MDRD) equation in stable chronic kidney diseases, the MDRD equation has limitations and does not reflect glomerular filtration rate accurately in healthy individuals or patients with acute kidney injury. An optimal acid–base environment is essential for many body functions, including haemoglobin–oxygen dissociation, transcellular shift of electrolytes, membrane excitability, function of many enzymes, and energy production. Based on the concepts of electrochemical neutrality, law of conservation of mass, and law of mass action, according to Stewart’s approach, hydrogen ion concentration is determined by three independent variables: (1) carbon dioxide tension, (2) total concentrations of weak acids such as albumin and phosphate, and (3) strong ion difference, also known as SID. It is important to understand that the main advantage of Stewart over the bicarbonate-centred approach is in the interpretation of metabolic acidosis.

37

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.

38

Little, Mark, and Alan Salama. The kidney. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0025.

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Kidney dysfunction is common in patients with rheumatological disease, be it secondary to renal (usually glomerular) involvement by a multisystem rheumatological disorder, renal impairment due to nephrotoxic medication use, or incidentally noted during a rheumatological work-up. It is therefore important for the rheumatologist to know how to assess kidney function biochemically and radiologically, to appreciate when an organ-threatening process is present, and to understand the basic steps to take in the event of acute kidney injury. This chapter reviews assessment of kidney function with respect to estimating excretory function, and the degree of proteinuria and haematuria. It provides an in-depth review of the causes, assessment, and management of acute kidney injury as encountered in rheumatological practice, and a summary of the causes and approach to chronic kidney disease.

39

Little, Mark, and Alan Salama. The kidney. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0025_update_002.

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Kidney dysfunction is common in patients with rheumatological disease, be it secondary to renal (usually glomerular) involvement by a multisystem rheumatological disorder, renal impairment due to nephrotoxic medication use, or incidentally noted during a rheumatological work-up. It is therefore important for the rheumatologist to know how to assess kidney function biochemically and radiologically, to appreciate when an organ-threatening process is present, and to understand the basic steps to take in the event of acute kidney injury. This chapter reviews assessment of kidney function with respect to estimating excretory function, and the degree of proteinuria and haematuria. It provides an in-depth review of the causes, assessment, and management of acute kidney injury as encountered in rheumatological practice, and a summary of the causes and approach to chronic kidney disease.

40

Bramham, Kate, and Catherine Nelson-Piercy. Specific renal conditions in pregnancy. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0298.

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Pre-pregnancy glomerular filtration rate, proteinuria, and blood pressure are usually more important in determining the risk of pregnancy in patients with chronic kidney disease, but some diseases may be exacerbated in pregnancy, or appear more liable to complications. This chapter considers immunoglobulin A nephropathy, systemic lupus erythematosus (which may also be associated with some manifestations in the infant), diabetic nephropathy, polycystic kidney disease, reflux nephropathy, single kidney, urological disorders, and angiomyolipomata. Distinguishing underlying renal disease exacerbation from pre-eclampsia and other complications of pregnancy can be challenging. Renal biopsy is sometimes indicated.

41

Turner, Neil. Mechanisms of progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0136.

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Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.

42

Hwang, Young-Hwan, and York Pei. Autosomal dominant polycystic kidney disease management. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0309_update_001.

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Management of patients with autosomal dominant polycystic kidney disease (ADPKD) currently comprises non-specific measures including promotion of healthy lifestyle, optimization of blood pressure control, and modification of cardiovascular risk factors. A high water intake of 3–4 L per day in patients with glomerular filtration rate greater than 30 mL/min/1.73 m2 may decrease the risk of kidney stones, but its potential benefit in reducing renal cyst growth is presently unproven. Maintenance of a target blood pressure of 130/80 mmHg is recommended by expert clinical guidelines though this is unlikely to slow cyst growth. It is unclear whether pharmacological blockade of the renin–angiotensin axis confers an extrarenal protective effect. Recognition of the variable clinical presentations of cyst infection, cyst haemorrhage, or nephrolithiasis is important for early diagnosis and optimal management of these complications. Most patients with ADPKD do well on dialysis and after transplantation. Nephrectomy may be needed to make space for a donor kidney, or if kidney size or infection is an issue after end-stage renal failure is reached. Recent advances in ADPKD have led to the identification of multiple potential therapeutic targets with more than 10 clinical trials completed or currently in progress. Given the promising results of the TEMPO trial, tolvaptan may well be the first disease-modifying drug to be approved for clinical use. Several other classes of drugs (e.g. somatostatin analogues, triptolide, metformin, and glucosylceramide synthase inhibitors) with good long-term safety profiles are promising candidates which may be repurposed for this disease. In the future, identifying patients with different risks of renal disease progression by their genotype and/or kidney volume will likely assume an important role for the clinical management of ADPKD.

43

Barakat, Amin Y., and Russell W. Chesney, eds. Pediatric Nephrology for Primary Care. American Academy of Pediatrics, 2008. http://dx.doi.org/10.1542/9781581104356.

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This clinical resource is purpose-built to help primary caregivers take a lead role in diagnosis, evaluation, and treatment of diverse pediatric kidney diseases. Diagnose and manage renal diseases with confidence. The resource book has clear, concise overviews of the full range of renal conditions you're likely to encounter; evidence-based discussion of each condition's clinical course, pathogenesis, and etiology; expert management recommendations and valuable clinical pearls, tables, algorithms, and clinical calculators to help with differential diagnosis and patient workups; advice on when to treat vs when to refer; practical implications of recent research findings; and how-to diagnostic solutions. Contents include evaluating patient presentation; history and physical examination; examination of the urine; use of the clinical laboratory; imaging of the kidney and urinary tract; prenatal and perinatal diagnosis; guidelines for patient referral; proven approaches to common conditions; congenital abnormalities; urinary tract infection; hematuria and proteinuria; glomerular disease; renal tubular disease; water and electrolyte disorders; acute kidney injury; chronic renal failure; hypertension; genetic diseases; and kidney in systemic disease.

44

Burdmann, Emmanuel A. Syphilis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0192.

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Syphilis is an infectious disease caused by the bacterium Treponema pallidum. The transmission route is usually sexual, but prenatal contamination (congenital syphilis) and transmission by infected blood can also occur. The most frequent presentation of syphilis nephropathy is proteinuria, and the most common form of associated glomerular disease is membranous glomerulopathy. Kidney disease usually reverts with antibiotic therapy. Syphilis must always be considered in proteinuric HIV-infected patients. Renal biopsy is necessary to differentiate between HIV-associated nephropathy and syphilis-induced glomerulopathies, since both kidney diseases have analogous clinical presentations, but syphilis-induced glomerulopathies may recover with syphilis successful treatment.

45

Wenzel, Ulrich, Thorsten Wiech, and Udo Helmchen. The effect of hypertension on renal vasculature and structure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0211.

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The concept of hypertensive nephrosclerosis was introduced by Volhard and Fahr in 1914 and has been extensively used in the literature since then, but its existence is controversial. While it is indisputable that malignant hypertension is a cause of end-stage renal disease (ESRD), there remains controversy as to whether the so-called benign nephrosclerosis can also lead to ESRD.Pressure, if it is great enough, will eventually disrupt any structure. Obviously, this is also true of blood pressure. It is therefore not surprising that an experimentally induced great increase in pressure disrupts the integrity of the blood-vessel wall. Such vascular lesions may be caused or at least influenced by several factors: humoral factors such as angiotensin II, catecholamines, mineralocorticoids, and vasopressin may increase vascular permeability, thereby damaging the vessel walls independently of, or superimposed upon, elevated blood pressure.Nephrosclerosis (literally, hardening of the kidney, Greek derivation: nephros, kidney; sclerosis, hardening) refers to diseases with predominant pathological changes occurring in the pre-glomerular vasculature and secondary changes involving the glomeruli and interstitium. Therefore, it is appropriate to describe first those vascular lesions, which, at least under defined experimental conditions, are believed to be caused solely by the presence of hypertension.

46

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

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Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-chain amyloidosis), or granular precipitates (in monoclonal immunoglobulin deposition disease). They may disrupt organ structure and function, inducing life-threatening complications. All of the pathologic entities related to immunoglobulin deposition principally involve the kidney, which is not only explained by the high levels of renal plasma flow and glomerular filtration rate, but also by the sieving properties of the glomerular capillary wall and by the prominent role of the renal tubule in LC handling and catabolism.The different renal (and other) manifestations are related to the unique physicochemical characteristics of each paraprotein or immunoglobulin fragment, and the rate of their production.

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Carrero, Juan Jesús, Hong Xu, and Bengt Lindholm. Diet and the progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0101.

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The dietary management of non-dialysed CKD patients has focused on limiting the intake of substances which lead to accumulation of urea, potassium, phosphorus, and sodium. Recent advances in nutritional epidemiology have given us the opportunity to examine the relationships between diet and CKD. This chapter focuses on evidence relating to retarding progression of renal impairment in the early to mid stages of CKD. Limits may need to change if GFR falls. The hypothesis that a high dietary protein intake leads to progressive CKD through a mechanism of glomerular hyperfiltration has been taught for decades, and it appears effective in animals. However, the evidence that low-protein diets (LPDs) halt CKD progression in patients is weak. Their management is of course likely to include other interventions such as blood pressure control. There is risk to low-protein diets. There is some evidence that high protein intakes are harmful. We therefore recommend moderate protein intake (not low; not high – no protein supplements; around 1g/kg/day). Salt handling is impaired in most patients with CKD, probably even early stages, and hypertension is an early feature, except in salt-losing patients, to whom different rules apply. Salt intake tends to raise blood pressure, worsen proteinuria, and reduce the effects of angiotensin converting enzyme inhibitors on blood pressure and proteinuria. Very low salt intakes are difficult to comply with and limit diet. In early stages of CKD we therefore recommend restriction to moderately low levels (below 6g/day of salt; 100 mmol of sodium). Lower levels may have additional benefits, and these limits may need to be reduced as GFR declines. Potassium is associated with healthy, desirable foods such as fruit and vegetables. It should only be restricted if high serum values make this necessary.

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Jardine, Alan G., and Rajan K. Patel. Lipid disorders of patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0102.

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The risk of developing cardiovascular (CV) disease is increased in patients with chronic kidney disease (CKD) and although dyslipidaemia is a major contributory factor to the development of premature CV disease, the relationship is complex. Changes in lipid fractions are related to glomerular filtration rate and the presence and severity of proteinuria, diabetes, and other confounding factors. The spectrum of CV disease changes from lipid-dependent, atheromatous coronary disease in early CKD to lipid-independent, non-coronary disease, manifesting as heart failure, and sudden cardiac death in advanced and end-stage renal disease. Statin-based lipid-lowering therapy is proven to reduce coronary events across the spectrum of CKD. The relative reduction in overall CV events, however, diminishes as CKD progresses and the proportion of lipid-dependent coronary events declines. There is nevertheless a strong argument for the use of statin-based therapy across the spectrum of CKD. The argument is particularly strong for those patients with progressive renal disease who will eventually require transplantation, in whom preventive therapy should start as early as possible. The SHARP study established the benefits and endorses the use of lipid-lowering therapy in CKD 3-4 but uncertainty about the value of initiation of statin therapy in CKD 5 remains. There is, however, no rationale for stopping agents started earlier in the course of the illness for compelling indications, particularly in those who will ultimately be transplanted. The place of high-density lipoprotein-cholesterol raising and triglyceride lowering therapy needs to be assessed in trials. Modifying dyslipidaemia in CKD has demonstrated that lipid-dependent atheromatous cardiovascular disease is only one component of the burden of CV disease in CKD patients, that this is proportionately less in advanced CKD, and that modification of lipid profiles is only one part of CV risk management.

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