Oxford Medicine Online
You are looking at 31-40 of 49 items for: evidence-based AND medicine oxford_clinical_nephrology_series
Clinical manifestations of lupus nephritis Mary Anne Dooley Print Publication Year: 2010 Published Online: Nov 2012 Publisher: Oxford University Press ISBN: 9780199568055 eISBN: 9780191753374 DOI: 10.1093/med/9780199568055.003.0001 Item type: chapter
Thus, systemic lupus with nephritis presents with features falling within the usual spectrum of renal syndromes, almost always with added features of a systemic disease. Today, with treatment graded to the severity of the disease (see Chapter 7), the prognostic value of the different clinical presentations has been all but eliminated, but this is another way of saying that the presence of, for example, a full nephrotic syndrome, renal dysfunction, and hypertension are indications for aggressive treatment. Nevertheless, each of these renal symptoms and signs needs to be dissected carefully, particularly in relation to histology (Chapter 8) if the most effective treatment, individualized for the particular patient under consideration, is to be achieved.
Rheumatic complications of HIV infection Ulrich A. Walker Print Publication Year: 2012 Published Online: Feb 2013 ISBN: 9780199579655 eISBN: 9780191763472 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199579655.003.0128
1. Autoimmune phenomena in terms of laboratory abnormalities without an associated rheumatic condition are highly prevalent in HIV-infected persons. 2. Bacterial, fungal or opportunistic pathogens may be recovered from virtually every structure of the musculoskeletal system. 3. The wide spectrum of articular complaints includes nonspecific arthralgia, HIV-associated arthritis, Reiter's syndrome and psoriatic arthritis. 4. Myopathic problems consist of rhabdomyolysis, polymyositis and zidovudine myopathy. 5. Vasculitis may present as cryoglobulinaemia, large vessel vasculitis, cerebral angiitis and polyarteritis nodosa, among other entities. 6. SLE has many features of HIV infection and may also induce false positive HIV serology. 7. Bones are subject to a high prevalence of osteonecrosis and osteoporosis, the latter of which is of multi-factorial origin and induces fractures. The contribution of HIV infection itself and ART to bone mineral loss is currently the focus of intense research. 8. Some rheumatic conditions require the use of immunosuppressive drugs.
Lupus nephritisHistopathology David J. Cimbaluk and Melvin M. Schwartz Print Publication Year: 2012 Published Online: Feb 2013 ISBN: 9780199579655 eISBN: 9780191763472 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199579655.003.0013
1. Is renal dysfunction caused by lupus or a non-SLE renal lesion? Renal insufficiency in SLE may be caused by SLE-related glomerular pathology, tubulo-interstitial or vascular pathology, or non-SLE pathogenic mechanisms such as prerenal hemodynamic factors or a drug-related tubulo-interstitial nephritis. In general, if the biopsy shows active lupus nephritis (Class III or IV), renal insufficiency should be attributed to the glomerular disease. If the biopsy shows one of the less inflammatory forms or glomerular involvement (Class I, II, or V), and there is acute tubulo-interstitial nephritis, a non-lupus aetiology should be excluded, clinically. The presence of both lupus GN and tubulo-interstitial damage requires treatment of the glomerular lesion and removal of potentially damaging drugs from the therapeutic regimen. 2. How severe is the glomerular pathology? The renal biopsy documents the presence and distribution of pathology among the glomeruli. Using these observations, the pathologist makes a diagnosis based upon the ISN/RPS classification. The prognosis (and severity) of the lesion is implicit in the class of the glomerular pathology. 3. Is the pathology reversible? Whether the pathology seen on renal biopsy is reversible depends on the relative contribution of lesions that can be expected to heal with and without scarring. By its nature, lupus nephritis can heal with scarring, and a glomerular scar implies a loss of function. Although the extent of glomerular scarring does not correlate well with function, the associated tubular atrophy and interstitial fibrosis directly correlate with the creatinine clearance. Thus, the pathology indicates reversibility of the lesion by describing the nature and the extent of glomerular inflammation (potentially reversible in the absence of necrosis) and the extent of glomerular scarring, interstitial fibrosis and tubular atrophy (irreversible lesions). 4. How should the patient be treated? The renal pathology makes a major contribution to the answer of this critical question. Once it has been determined that the patient has lupus nephritis, the biopsy is placed into one of the ISN/RPS classes. The glomerular pathology of Class I and II lesions receives limited treatment in the absence of systemic disease activity. The lesion-specific treatment of proliferative (Classes III and IV) and membranous (Class V) forms of lupus nephritis has been recently reviewed. When renal insufficiency results from extensive, irreversible lesions (ISN/RPS Class VI), the renal biopsy may be used to support a decision not to treat.
Nephrotoxicity of chemotherapy agents and chemotherapy administration in patients with renal disease Carlos D. Flombaum Print Publication Year: 2010 Published Online: Nov 2012 Publisher: Oxford University Press ISBN: 9780199580194 eISBN: 9780191753404 DOI: 10.1093/med/9780199580194.003.0005 Item type: chapter
The kidneys normally receive 20% of the cardiac output. Drugs are filtered and/or secreted and then progressively concentrated in the urine. Therefore, these organs are especially vulnerable to the toxic effects of many drugs, including chemotherapy agents. Nephrotoxicity is often a dose-limiting adverse effect of chemotherapy. Chemotherapy agents can affect the microvasculature, the glomerulus, or the tubules. Depending on the site of the nephron more adversely affected, the clinical manifestations may vary from a hemolytic process resembling the hemolytic uremic syndrome (HUS) or a tubular-interstitial injury causing asymptomatic decreases in the glomerular filtration rate (GFR), overt renal failure requiring dialysis, or a variety of electrolyte disorders. Because the kidneys are one of the major routes of elimination of many drugs, nephrotoxicity is a serious complication in patients undergoing chemotherapy. The dose of renally eliminated drugs has to be adjusted in order to prevent systemic toxicity, and the administration of other potentially nephrotoxic drugs, such as chemotherapy agents or antibiotics, may have to be interrupted, making management of the patient more difficult. This section will review the nephrotoxic effects of different chemotherapy agents and some preventive measures to avoid their nephrotoxicity. The metabolism of those chemotherapy agents that are predominantly renally excreted and the recommended dose modifications in patients with renal insufficiency will be reviewed in the second part of this chapter. The most common methods utilized to estimate GFR are the creatinine clearance (CrCl) or the clearance of radiolabeled compounds. The creatinine clearance can be determined from a 24-hour urine collection or based on formulas which use the plasma creatinine concentration (like the Cockcroft–Gault equation). More recently, clinical laboratories are using the Modification of Diet in Renal Disease (MDRD) equation to report GFR, but it needs to be stressed that up to now, the vast majority of pharmacokinetic studies in oncology did not use this formula and were performed by measuring CrCl or estimating it by the Cockcroft–Gault equation. For practical purposes and because they are close to each other in absolute value, creatinine clearance and GFR are used interchangeably throughout this chapter.
Bone histomorphometry in renal osteodystrophy Arnold J Felsenfeld and Armando Torres Print Publication Year: 2010 Published Online: Nov 2012 Publisher: Oxford University Press ISBN: 9780199559176 eISBN: 9780191753350 DOI: 10.1093/med/9780199559176.003.010 Item type: chapter
of bone turnover. However, less well appreciated is that several factors may alter the bone response to PTH. Several studies of bone histology in dialysis patients have shown that the bone response to PTH as measured by the osteoblast surface and bone formation rate, decreases after age 45 or 50 years. Older patients also eat less protein resulting in a decreased phosphate load that, in turn, reduces the stimulus for PTH secretion. There is also increasing evidence that the bone response to PTH, as determined by bone turnover in histological studies, is decreased in black CKD patients. Attempts to use non-invasive means of assessing bone turnover, such as PTH values and bone alkaline phosphatase, have lacked sensitivity at intermediate PTH values between 150 and 450pg/ml. Finally, variability in PTH assays and problems associated with the collection of PTH samples have further complicated the ability to make therapeutic decisions based on PTH measurements.
Other primary glomerular diseases Claudio Ponticelli and Richard Glassock Print Publication Year: 2009 Published Online: Nov 2012 Publisher: Oxford University Press ISBN: 9780199552887 eISBN: 9780191753282 DOI: 10.1093/med/9780199552887.003.0011 Item type: chapter
Fibrillary glomerulonephritis (FGN) and immunotactoid glomerulopathy (ITG) are both glomerular diseases characterized histologically by a diffuse increase in mesangial matrix due to deposits having a fibrillary structure by electron microscopy, which are negative for Congo-red stains but positive for immunoglobulin deposition. Most patients present with proteinuria, often in a nephrotic range, microhematuria, and hypertension. Almost half of patients have a reduced renal function at presentation. Although FGN and ITG have quite similar light microscopical and clinical features the current opinion is that they represent two separate diseases. FGN is an idiopathic (primary) condition characterized by polyclonal immune deposits with restricted gamma isotypes. Most patients present with significant renal insufficiency and have a poor outcome despite immunosuppressive therapy. By contrast, ITG very often contains monoclonal IgG deposits and has a significant association with underlying monoclonal paraproteinemia and hypocomplementemia. ITG is more properly classified as a mono-clonal immunoglobulin deposition disease (MIDD). Differentiation of FGN from the much more rare entity ITG appears justified on immunopathologic, ultrastructural, and clinical grounds (Fogo et al., 1993; Bridoux et al., 2002; Rosenstock et al., 2003). Both will be discussed together, although only FGN should be regarded as a primary glomerular disease, as defined in this monograph.
Clinical presentation and assessment of disease activity in lupus nephritis Venkat Reddy and David Isenberg Print Publication Year: 2012 Published Online: Feb 2013 ISBN: 9780199579655 eISBN: 9780191763472 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199579655.003.0010
factor. 3. Defining whether renal abnormalities are due to activity, damage or a combination of both is important in guiding treatment. 4. General activity indices such as the BILAG or SLEDAI scoring systems, together with more specific indicators (e.g. PCR and the presence of urinary red cells and casts) provide an optimal way of assessing disease activity in a patient with lupus nephritis. 5. Renal biopsy remains an essential ‘tool’ in determining the type of lupus involvement, the degree of activity and damage, and the outcome.
Assessment of disease activity and damage in the ANCA-associated systemic vasculitides Joanna C. Robson, Ravi Suppiah, and Raashid A. Luqmani Print Publication Year: 2012 Published Online: Feb 2013 ISBN: 9780199579655 eISBN: 9780191763472 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199579655.003.0061
1. Currently there is no available gold standard method of assessment of disease activity; inflammatory markers can be non-specifically raised with infection or malignancy, rises in ANCA titre do not reliably predict clinical relapse and imaging modalities such as PET or MRI are not helpful in small vessel vasculitis. 2. In ANCA-associated vasculitis, disease activity and damage are both measured using specific validated clinical tools. 3. Disease activity is measured using the BVAS, which is a formalized assessment of active vasculitis over nine specific organ systems (systemic, cutaneous, mucous membranes/eyes, ENT, chest, cardiovascular, abdominal, renal and nervous systems). 4. Disease damage is measured using the VDI, which includes 64 items over 11 organ systems. Damage can be secondary to the effects of acute vasculitis or its treatment, with items only recorded if they have been present for more than 3 months. 5. Significant impairments in health-related quality of life have been demonstrated in patients with ANCA-associated vasculitis using generic tools such as the SF-36. The OMERACT vasculitis working group have identified the need to develop a vasculitis-specific patient reported outcome.
Symptomatic therapy Richard J. Glassock Print Publication Year: 2009 Published Online: Nov 2012 Publisher: Oxford University Press ISBN: 9780199552887 eISBN: 9780191753282 DOI: 10.1093/med/9780199552887.003.0001 Item type: chapter
and thereby to a reduction in plasma oncotic pressure. Changes in the synthesis, turnover, and plasma concentration of various proteins and lipids develop and can lead to an imbalance of pro-thrombotic and anti-thrombotic factors promoting a ‘thrombophilic’ state (Vaziri, 2003; Crew et al., 2004; Glassock, 2007) Disturbances in the renal handling of sodium chloride (NaCl) and water are often associated with edema formation and/or hypertension (Perico and Remuzzi, 1993; Schrier and Fassett, 1998). Finally, the rapid or slow loss of the glomerular filtration capacity (glomerular filtration rate, GFR) due to damage of single nephrons (perhaps mediated by filtered proteins and their reabsorption) as well as by the ‘drop out’ of functioning nephrons from the overall population of nephrons in the two kidneys is responsible for ultimate progression to end-stage renal disease (ESRD) in many, but not all, of the primary glomerular disorders (Drummond et al., 1994; Remuzzi and Bertani, 1998; Squarer, et al., 1998; Floege and Feehally, 2007). Collectively these abnormalities give rise to ‘syndromes’ of glomerular disease. These ‘syndromes’ can be arbitrarily, but usefully, grouped into five categories which may overlap to some degree; namely, the acute nephritic syndrome, rapidly progressive glomerulonephritis, the nephrotic syndrome, ‘symptomless’, haematuria and/or proteinuria, and slowly progressive ‘chronic’ nephritis (Glassock et al., 1995). The cardinal features of these syndromes and the diseases to which they are most closely associated are discussed in this monograph. This monograph will deal largely with those glomerular diseases which primarily affect the kidneys and in which the extra-renal manifestations are the consequence of the impairment or disturbance of kidney function itself (the so-called primary glomerular diseases).
Acquired cysts and cancer of failing kidneys Isao Ishikawa Print Publication Year: 2010 Published Online: Nov 2012 Publisher: Oxford University Press ISBN: 9780199580194 eISBN: 9780191753404 DOI: 10.1093/med/9780199580194.003.0011 Item type: chapter
and has a good post-operative prognosis, screening for RCC is recommended for selected dialysis patients. In particular, screening for RCC is necessary before renal transplantation. Screening for RCC should be based on the risks of age and gender, and on the general condition of the patient. In 15.4% of dialysis patients with RCC, RCC had metastasized by the time of our surveys. Some hemodialysis patients develop rapidly progressive RCC. Laparoscopic radical nephrectomy is preferred. Sorafenib or sunitinib is also beginning to be used in patients with progressive RCC.