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IGA Nephropathy. Bethesda, MD: National Kidney and Urologic Diseases Information Clearinghouse. 2008. 4 p.
This fact sheet describes IgA nephropathy, a kidney disorder that occurs when IgA, a protein that helps fight infections, settles in the kidneys. After many years, IgA deposits may cause the kidneys to leak blood and sometimes protein into the urine. About 25 percent of adults with IgA nephropathy eventually development total kidney failure. Written in a question-and-answer format, the fact sheet reviews the symptoms of IgA nephropathy, risk factors, the causes of IgA nephropathy, diagnostic tests used to confirm the condition, and treatment options, including treatment for the concomitant high blood pressure and high cholesterol levels. A final section briefly reviews current research programs in this area. The fact sheet includes the contact details for five resource organizations through which readers can get more information and a description of the goals and activities of the National Kidney and Urologic Diseases Information Clearinghouse.
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Management of Dialysis Patients with Celiac Disease. Practical Gastroenterology. 31(6): 70-72, 77-80, 82. July 2007.
This article considers the management of dialysis patients who also have celiac disease, a condition of gluten intolerance. The author notes that these two diseases are not often reported in the same patient, but celiac disease is sometimes listed as one of the associated diseases of IgA nephropathy. There are no written guidelines for managing these combined diseases, because of the rarity of their co-occurrence, or perhaps because they are underdiagnosed. Celiac disease is characterized by inflammation of the small intestine and malabsorption after the ingestion of gluten; thus, celiac disease is managed by life-long avoidance of gluten in the diet. Kidney disease is manifested by fluid and electrolyte imbalance, which also involves life-long dietary restrictions. This article reviews the renal dietary guidelines and provides suggestions on how to combine those guidelines with the required changes to manage celiac disease. Specific topics include malnutrition, potassium, fluid and sodium, renal bone osteodystrophy, phosphorus, common medications of dialysis patients, and socioeconomic considerations. One table provides a renal and gluten-free diet in a chart format. 4 tables. 9 references.
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Chronic Nephritis in Children: With Emphasis on IGA Nephropathy. IN: Hogg, R., ed. Kidney Disorders in Children and Adolescents: A Global Perspective of Clinical Practice. New York, NY: Informa Healthcare USA. 2006. pp 103-116.
This chapter about chronic nephritis is from a textbook that presents a global perspective of clinical practice regarding kidney disorders in children and adolescents. The authors define chronic nephritis as a slow but persistent form of renal disease that is often accompanied by proteinuria, hematuria, and/or hypertension. The most common form of chronic nephritis that results in end-stage renal disease (ESRD) in both children and adult patients around the world is IgA nephropathy, which is the primary focus of this chapter. The authors discuss epidemiology, pathology, etiology, pathogenesis, predisposing genetic factors, the mechanism of progression of disease in the kidneys, light microscopy findings, clinical features, laboratory studies for chronic nephritis, differential diagnosis, and treatment of IgA nephropathy. The authors conclude that there are multiple factors to consider when deciding whether to treat a child with IgA nephropathy or some other form of chronic nephritis; thus, primary care physicians should seek pediatric nephrology consultation. Because of this complexity, specific treatment options are not discussed in this text. The chapter includes black-and-white illustrations and photographs and concludes with an extensive list of references. 9 figures. 2 tables. 61 references.
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Glomerular Diseases. Bethesda, MD: National Kidney and Urologic Diseases Information Clearinghouse. 2006. 12 p.
This fact sheet reviews glomerular diseases, which involve problems with the glomeruli, the tiny units within the kidney where blood is cleaned. The fact sheet focuses on glomerulonephritis, defined as inflammation of the membrane tissue in the kidney; and glomerulosclerosis, the scarring or hardening of the tiny blood vessels within the kidney. Written in a question-and-answer format, the fact sheet covers the anatomy and function of the kidneys, how glomerular diseases interfere with kidney function, the symptoms of glomerular disease, diagnostic tests used to confirm glomerular disease, the causes of glomerular disease, renal failure, and end-stage renal disease (ESRD). Specific diseases covered include systemic lupus erythematosus (SLE), Goodpasture's syndrome, IgA nephropathy, Alport syndrome, infection-related glomerular disease, bacterial endocarditis, diabetic nephropathy, focal segmental glomerulosclerosis, and minimal change disease (MCD). The booklet summarizes the points covered, provides a brief glossary of terms, lists resource organizations for readers seeking additional information, and a briefly describes the goals and activities of the National Kidney and Urologic Diseases Information Clearinghouse. 2 figures.
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Kidney Disorders in Children and Adolescents: A Global Perspective of Clinical Practice. New York, NY: Informa Healthcare USA. 2006. 266 p.
This textbook presents a global perspective of clinical practice regarding kidney disorders in children and adolescents. The book emphasizes diagnosis and treatment, rather than etiology, pathology, and pathogenesis, which are covered in other textbooks. The text includes 22 chapters: normal kidney function and development and the choice of laboratory studies in children; radiographic studies in children with kidney disorders; congenital abnormalities of the kidney and urinary tract; neonatal kidney problems; mass screening for kidney disease in children; hematuria and proteinuria; the nephrotic syndrome; acute nephritis; chronic nephritis in children, particularly IgA nephropathy; the evaluation, monitoring, and therapy of hypertension; cardiovascular disease in patients with kidney disorders in childhood and adolescence; urinary tract infections and vesicoureteral reflux in children; nocturnal enuresis and voiding disorders; renal tubular disorders; acute renal failure and hemolytic uremic syndrome; chronic renal failure and dialysis options; the effects of kidney disorders on the endocrine system; nutritional and growth aspects of the care of children with kidney disease; immunization and anti-microbial therapy for children with chronic kidney disease (CKD); the social and developmental consequences of chronic kidney disease in children; renal transplantation in childhood; and the transition of children with renal diseases into adulthood. Each chapter includes black-and-white illustrations and photographs and concludes with an extensive list of references. The textbook begins with a section of full-color plates and concludes with a detailed subject index.
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Oculorenal Manifestations in Systematic Autoimmune Diseases. American Journal of Kidney Diseases. 43(2): 209-222. February 2004.
Vasculitides form a heterogeneous group of diseases characterized by blood-vessel inflammation and necrosis (tissue death). Systemic necrotizing vasculitis is characterized by inflammation of blood vessels, which often affects the eyes and kidneys. Vasculitides have a wide spectrum of manifestations because of the involvement of arteries and other vessels of various sizes and locations. Early diagnosis and prompt treatment may decrease the morbidity and mortality associated with systemic autoimmune diseases. In addition, the eyes and kidneys can provide clues to the diagnosis of many systemic diseases and many important complications of these diseases occur in the eye. Therefore, examination of the eyes and kidneys should be a routine and important part of a general examination in systemic diseases. This article reviews the major types of oculorenal manifestations in systemic autoimmune diseases. Diseases discussed include giant cell (temporal) arteritis, polyarteritis nodosa, Kawasaki disease, Wegener's granulomatosis and microscopic polyarteritis, Goodpasture's syndrome, IgA nephropathy and Henoch-Schonlein purpura nephritis, Churg-Strauss syndrome, Behcet's disease, systemic lupus erythematosus, primary antiphospholipid syndrome (APS), sarcoidosis, Sjogren's syndrome, cryoglobulinemia, and tubulointerstitial nephritis and uveitis syndrome. 6 figures. 124 references.
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Renal Risks of an Emerging 'Epidemic' of Obesity: The Role of Adipocyte-Derived Factors. Dialysis and Transplantation. 33(1): 11-21. January 2004.
Obesity has reached epidemic proportions in the affluent societies of the world, especially during the last two decades. Recently, there has been growing awareness and concern regarding rapidly emerging renal (kidney) complications of obesity. Obesity appears to play a central contributory role in the genesis of systemic hypertension (high blood pressure), nephrotic-range proteinuria (protein in the urine) with focal segmental glomerulosclerosis (FSGS) and renal cell carcinoma (kidney cancer), apart from the likely impact that the obesity has on the outcomes of patients on long-term dialysis and those with renal transplants. This article explores the renal risks of this emerging epidemic of obesity, focusing on the role of adipocyte-derived factors. Obesity-related FSGS has characteristic clinicopathological features, i.e., minimal clinical edema and more or less normal levels of serum albumin, cholesterol, and blood pressure. FSGS may progress to end stage renal disease (ESRD) in about 50 percent of cases. In addition, severe obesity may enhance the progression to ESRD of preexisting nephropathies such as IgA nephropathy. Strategies such as weight reduction early in the course of the disease, in conjunction with the judicious use of ACE inhibitors and possibly statins, might improve the outcome of obesity-related hypertension and nephropathy. 2 figures. 1 table. 90 references.
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Tacrolimus Therapy in Pediatric Patients with Treatment-Resistant Nephrotic Syndrome. Pediatric Nephrology. 19(3): 281-287. March 2004.
This article reports on a retrospective analysis of 16 children started on tacrolimus with various types of treatment-resistant nephrotic syndrome. In the group, there are 13 patients with focal glomerulosclerosis, 1 minimal change disease, and 2 IgA nephropathy with nephrosis. The mean age of the children was 11.4 years (range 3.5 to 18.1 years) with a mean age at diagnosis of 5.6 years (range 1.6 to 13.3 years). All patients initially received prednisone 2 milligrams per kilogram per day. Other therapies for 15 of 16 included cyclosporine (n = 15), chlorambucil (n = 5), mycophenolate mofetil (n = 5), levamisole (n = 3), i.v. methylprednisolone (n = 3), and cyclophosphamide (n = 2). The major indication for the initiation of tacrolimus included treatment resistance or dependence (n = 15) and intolerable side effects from other therapies (n = 1). The average time from the diagnosis to initiation of tacrolimus was 5.3 years. Thirteen patients (81 percent) went into a complete remission within an average of 2 months, with 3 patients relapsing while on treatment. Three patients did not respond. Of these, 2 had partial remissions (13 percent) and 1 failed to respond. Adverse events included anemia (n = 1), seizure (n = 1), worsening or new-onset hypertension (n = 5), and sepsis (n = 1). All patients remained on tacrolimus. The authors conclude that tacrolimus is an effective, well-tolerated medication for treatment-resistant forms of nephrotic syndrome in children, with a complete remission rate of 81 percent and a partial remission rate of 13 percent. 1 figure. 3 tables. 37 references.
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'Evidence-Based' Survey of Therapeutic Options for IgA Nephropathy: Assessment and Criticism. American Journal of Kidney Disease. 41(6): 1129-1139. June 2003.
Immunoglobulin A (IgA) nephropathy is a worldwide disease that causes end stage renal (kidney) disease (ESRD) in 15 to 20 percent of patients within 10 years of the apparent onset of disease and in 30 to 40 percent of individuals within 20 years. Severity of renal lesions, serum creatinine level, and severe proteinuria (protein in the urine) are adverse prognostic indicators. No specific treatment has been established, but several approaches have been tried. This review article evaluates the quality of published randomized trials and the quality of their reporting. Meta-analyses of 10 randomized trials on the efficacy of steroid treatment, cytotoxic agents, and fish oils on the outcome of renal function and daily proteinuria in patients with IgA nephropathy were performed. The authors conclude that the quality of the 10 trials was very poor and a limited amount of data was reported. Cytotoxic agents seem beneficial on both renal function and daily proteinuria in patients with moderate to severe renal damage; steroids act mainly on proteinuria; and fish oils do not impart a particular benefit. These conclusions are based on the very limited and poor available published evidence. 9 figures. 3 tables. 17 references.
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Outcomes Research in Glomerulonephritis. Seminars in Nephrology. 23(4): 340-354. July 2003.
Glomerulonephritis remains the second or third most common primary renal (kidney) disease type to progress to end stage renal disease (ESRD). This disease type is particularly important because its focus is limited to the kidney and its reversal or stabilization ensures a return to a normal quality of life for the individual. Also, because its highest incidence rate is in childhood and early adulthood, the implications of effective therapy in terms of preventing ESRD costs benefits not only the individual but also society. In this article, the author describes three of the most common variants that progress to ESRD: membranous nephropathy, focal segmental glomerulosclerosis, and IgA nephropathy. Together, these three diseases represent approximately 80 percent of the primary glomerular diseases known to progress to ESRD. The author discusses the outcome studies published over the past decade in these disorders that permit the best insight into specific immunotherapy. The data is presented in an evidence-based model so the reader can appreciate the strengths or weaknesses of the therapies discussed. A framework for clinical management is also provided. 1 figure. 6 tables. 59 references.
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Renal Biopsy 2-9 Years After Henoch Schonlein Purpura. Pediatric Nephrology. 18(5): 471-473. May 2003.
This article reports on a study of 12 children and adolescents with classical Henoch-Schonlein purpura (HSP) who underwent kidney (renal) biopsy 2 to 9 years later. The clinical course was favorable in 10 of the patients who received only supportive treatment. Two patients with a prolonged course, characterized by marked hematuria (blood in the urine) and proteinuria (protein in the urine), were given steroids and azathioprine first and mycophenolate mofetil later. At the time of biopsy, 4 patients did not have any urinary abnormalities, 6 had hematuria and or mild proteinuria, and 2 had proteinuria greater than 1 gram per 24 hours. Renal histology showed mild lesions on light microscopy. Immunohistochemistry disclosed mesangial IgA in 8 of the 12 patients. In this small series of selected former HSP patients, the majority had IgA nephropathy years after the initial vasculitis episode. This indicates that some patients with apparently completely healed HSP have a chronic glomerular condition that possibly means protracted disease and certainly indicates the need for careful follow-up. 2 tables. 9 references.
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IgA Nephropathy. New England Journal of Medicine. 347(10): 738-748. September 5, 2002.
This article reviews the medical progress in the area of IgA nephropathy (kidney disease). Primary IgA nephropathy is an immune-complex mediated glomerulonephritis (inflammation of the kidney's filtering capillaries) defined by the presence of IgA deposits in the glomeruli, accompanied by a variety of histopathologic lesions. Although primary IgA nephropathy was considered a benign condition for many years, it is now clear that a large number of cases eventually progress to renal (kidney) failure. The authors review the demographic features, incidence, causes (etiology) and genetic factors, pathogenesis (development), pathology, clinical features, outcome, treatment, renal transplantation, and differential diagnosis of IgA nephropathy. There is no cure for the disease, but recent trials have shown that corticosteroids, with an without immunosuppressive agents, and n-3 fatty acids have favorable effects on the progression of renal disease. Renal transplantation is the treatment of choice for patients in whom end stage renal disease (ESRD) develops. 3 figures. 2 tables. 110 references.
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Glomerulonephritis Recurrence in the Renal Graft. JASN. Journal of the American Society of Nephrology. 12(2): 394-402. February 2001.
Although kidney transplantation may return renal (kidney) function to the recipient, it does not necessarily remove the cause of the recipient's original kidney disease. Glomerulonephritis is the cause of renal failure for 20 to 40 percent of those who receive a transplant; for these recipients, the threat of recurrent disease is very real. This article discusses recurrent glomerulonephritis. The author first reviews the epidemiology of recurrence in a general sense, then addresses recurrence of specific forms of the disease. The incidence of recurrence and recurrence leading to graft failure is examined, and risk factors for disease recurrence are assessed. Where available, data on the pathogenesis and management of recurrent glomerulonephritis is also presented. The typical features of recurrent glomerulonephritis are those of nephritis involving the native kidney, including proteinuria (protein in the urine), hematuria (blood in the urine), and deterioration in renal function. When the diagnosis of recurrence is suspected, renal biopsy is essential. The author discusses IgA nephropathy and Henoch Schonlein purpura; antineutrophil cytoplasmic antibody associated vasculitis, Wegener's granulomatosis, microscopic polyangiitis, and idiopathic necrotizing crescentic glomerulonephritis; anti GBM disease; hemolytic uremic syndrome (HUS); focal and segmental glomerulosclerosis; membranous glomerulonephritis; mesangiocapillary glomerulonephritis; lupus nephritis; systemic sclerosis and scleroderma; and fibrillary glomerulonephritis and immunotactoid glomerulonephritis. Strong data have emerged on patterns of recurrence, risk factors for recurrence, and the implications for patient and graft outcomes after recurrence of the most common glomerulopathies. However, data available on recurrence of the less common nephropathies are inadequate and make treatment and prevention more difficult. 1 figure. 1 table. 60 references.
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Outcome of Renal Transplants in Patients with IgA Nephropathy. Transplantation Proceedings. 33(7-8): 3429-3430. November 2001.
Immunoglobulin A nephropathy (IgAN) is the most common type of glomerulonephritis (inflammation of the filtering units of the kidney) worldwide, with 20 percent of patients progressing to end stage renal (kidney) failure. IgAN also has a strong tendency to recur in the graft after a patient receives a kidney transplant. Short term graft survival in patients with recurrent IgAN suggested excellent results, but the long term followup has noted more severe clinical courses, with nephrotic syndrome and higher rates of graft loss. This article reports on a study that evaluated the long term outcome, in terms of recurrence and graft survival, in patients with IgAN. Between December 1979 and December 2000, 38 patients (32 males), mean age at transplantation 37.6 years (range 20 to 57 years), whose original renal disease was biopsy proven IgAN, received 40 renal allografts (28 cadaveric, 12 living-related) and have been followed for an average of 68.4 months (range 3 to 280 months). Recurrence of IgAN was diagnosed by certain laboratory criteria or when graft biopsy disclosed histologic recurrence. IgAN recurred in 16 allografts (incidence of 40 percent) in 15 patients, 38.6 months (range 3 to 144) after kidney transplantation, in 6 living and 10 cadaveric grafts, and in one patient with two consecutive grafts. Followup after recurrence (mean time 48.8 months, range 2 to 138) revealed 10 patients with stable graft function and 5 patients with a significant loss of graft function. Graft failure was the consequence not only of recurrent IgAN but also poorly controlled hypertension (high blood pressure), rejection episodes, and noncompliance. The authors conclude that histologic recurrence of IgAN depends largely on the timing of renal biopsy, being approximately 50 percent at 2 to 5 years but approaching 100 percent at 10 to 20 years after renal transplantation. The risk of recurrence is similar for recipients of living related donor and cadaveric renal allografts. Hematuria (blood in the urine) and low grade proteinuria (protein in the urine) are characteristic of recurrence. 12 references.
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Primary IgA Nephropathy: Pathophysiology, Diagnosis, and Clinical Management. Nephrology Nursing Journal. 28(2): 151-156. April 2001.
Berger's disease, or IgA nephropathy (kidney disease), initially described in 1968 by Berger and Hinglais, has become recognized as the most prevalent type of glomerulonephritis (inflammation of the filtering glomeruli of the kidneys) worldwide. This article familiarizes nurses with the pathophysiology, diagnosis, and clinical management of primary IgA nephropathy. The exact pathophysiology of IgA nephropathy is unknown. Diagnosis of IgA nephropathy is confirmed by renal (kidney) biopsy findings of mesangial deposition of IgA. The author reviews the differential diagnosis of IgA nephropathy and acute postinfectious glomerulonephritis. There is no specific treatment protocol for IgA nephropathy, but clinicians often use oral glucocorticoids, angiotensin converting enzyme (ACE) inhibitors, or fish oil. Clinical management will continue to be unclear until the exact pathogenesis of IgA nephropathy is known. Hypertension (high blood pressure) and proteinuria (the spilling of protein into the urine) must be treated to prevent or slow progression to end stage renal disease (ESRD) in patients with IgA nephropathy. Ten percent of patients will have sustained remission, and 60 to 70 percent will have a course of recurrent symptoms. Of this latter group, approximately 30 percent will maintain a normal glomerular filtration rate (GFR, a test of kidney function) and another 30 percent will develop ESRD and require dialysis or transplantation. Prognosis is based on the patient's clinical course. Nurses can educate the patient and answer questions that may arise about the pathophysiology and the prescribed regimen. Nurses must also encourage patients to follow the prescribed treatment plan even though immediate results are not evident to the patient. 3 figures. 1 table. 17 references.
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Protean Face of Renal Sarcoidosis. JASN. Journal of the American Society of Nephrology. 12(3): 616-623. March 2001.
This article reviews renal (kidney) sarcoidosis, one manifestation of this multisystem granulomatous disorder of unknown cause. The disease is characterized by the presence of noncaseating epithelioid granulomas in involved organs. The cause of sarcoidosis remains to be determined; an infectious cause has been postulated since the disease was first described but has not been secured convincingly. Clinically important renal involvement is only an occasional problem in sarcoidosis. However, sarcoidosis can be a factor in renal stone disease (abnormal calcium homeostasis, or balance). The chronic hypercalcemia (too much calcium in the blood) and hypercalciuria (too much calcium in the urine) that can accompany sarcoidosis can lead to kidney insufficiency. Also, approximately 20 percent of patients with sarcoidosis show granulomatous inflammation in the kidney. Glomerular (the bundles of filtering nephrons in the kidney) involvement in sarcoidosis is not common, although various problems including membranous glomerulonephritis, IgA nephropathy, and focal segmental sclerosis have all been described. For each of these manifestations, the authors present a brief case report that illustrates the patient presentation and management issues. A final section notes that transplantation is not precluded in patients with sarcoidosis, although the condition may recur. Because lymph nodes throughout the body may enlarge, ureteral obstruction and retroperitoneal fibrosis have been described. The authors conclude that sarcoidosis offers a challenge to the nephrologist. 6 figures. 61 references.
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Tonsillectomy and Steroid Pulse Therapy Significantly Impact on Clinical Remission in Patients with IgA Nephropathy. American Journal of Kidney Diseases. 38(4): 736-743. October 2001.
This article reports on a retrospective investigation of kidney (renal) outcome in 329 patients with immunoglobulin A (IgA) nephropathy (kidney disease) with an observation period longer than 36 months in the authors' renal unit between 1977 and 1995. Clinical remission, renal progression, and the impact of covariates were estimated. In 157 of 329 patients (48 percent), disappearance of urinary abnormalities (clinical remission) was obtained. None of these 157 patients showed progressive deterioration, defined as a 50 percent increase in serum creatinine (Scr) level from baseline, during the observation period. Conversely, in patients without clinical remission, the estimate of probability of progressive deterioration was 21 percent (plus or minus 5 percent) at 10 years. In the multivariate Cox regression model with 13 independent covariates, initial Scr level, histological score, tonsillectomy, and high dose methylprednisolone therapy had a significant impact on clinical remission, whereas proteinuria, age, sex, levels of hematuria, blood pressure, conventional steroid therapy, ACE inhibitor therapy, and cyclophosphamide therapy had no significant effect. These findings indicate that interventions aimed at achieving clinical remission have provided encouraging results applicable to managing patients with IgA nephropathy. 7 figures. 3 tables. 27 references.
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Treating IgA Nephropathy (editorial). JASN. Journal of the American Society of Nephrology. 12(4): 846-847. April 2001.
IgA nephropathy (a kidney disease) may be the most common type of glomerulonephritis; it causes end stage renal disease (ESRD) in 15 to 20 percent of patients within 10 years of onset and in 30 to 35 percent of individuals within 20 years of onset. Proteinuria (protein in the urine), an elevated serum (blood) creatinine concentration, and hypertension (high blood pressure) predict progression of the disease, as can renal biopsy. However, even with these markers, predicting the course of the disease in specific individuals is difficult. This editorial comments on a research trial which explores the benefits of fish oil for treating IgA nephropathy. The author of the editorial notes that questions still remain about fish oil. The author has calculated that there was only a 75 percent probability that fish oil was beneficial. In the recent research, the lack of a dose response effect argues against fish oil being beneficial. In addition, neither the first research trial (in 1994) which showed great benefits associated with fish oil, nor the recent trial demonstrated a significant reduction in proteinuria. Proteinuria is a key therapeutic target because it may, itself, cause renal injury and because its reduction correlates with preservation of renal (kidney) function. The author briefly reviews other therapies for IgA nephropathy, including ACE inhibitors and corticosteroids. The author concludes that compelling evidence favors the ACE inhibitors at this point. 20 references.
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Changing Incidence of Glomerular Diseases in Adults. American Journal of Kidney Diseases. 35(5): 878-883. May 2000.
Studies performed at large metropolitan medical centers have reported an increasing incidence of idiopathic focal segmental glomerulosclerosis (FSGS) in adults. This article reports on a study that reviewed that patient records of all adults who underwent renal biopsies at the authors' institution over the 20 year period from 1974 to 1994. The study was undertaken to determine whether a similar trend occurs in small urban and rural communities (as in the metropolitan areas) and to determine the role of race in these observations. The patients were grouped for analysis in 5 year intervals and for the following diagnoses: FSGS, membranous nephropathy (MN), minimal change nephropathy (MCN), membranoproliferative glomerulonephritis (MPGN), immunoglobulin A (IgA) nephropathy, chronic glomerulonephritis, diabetic nephropathy, hypertensive nephrosclerosis, or chronic interstitial nephritis. Patients with secondary causes for these lesions were excluded. The relative frequency of FSGS increased from 13.7 percent during 1975 to 1979 to 25 percent during 1990 to 1994. The relative frequency of MN decreased from 38.3 percent during 1975 to 1979 to 14.5 percent during 1990 to 1994. There were no changes in the frequencies of the other diagnoses during the 20 year period. However, there was a significant increase in the percentage of blacks with FSGS, from 0 percent in 1975 to 22.6 percent in the last 5 year period (1990 to 1994). There was also an increased percentage of Hispanics with FSGS, from 0 percent in the first 5 year period to 21.3 percent in the last 5 year period. The incidence of MN in blacks and whites decreased over the 20 year period. No changes in age or sex between groups or over time accounted for these results. The authors conclude that FSGS is now diagnosed twice as often as MN and is the most common idiopathic glomerular disease at the authors' hospital. Reasons for this increase include the emergence of FSGS in both Hispanics and blacks, with a modest increase of FSGS in whites. The increase in FSGS in the three most common races in this community suggests that factors other than genetic, perhaps environmental, have a role in the pathogenesis of FSGS. 6 tables. 22 references.
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Characterization of Early IgA Nephropathy. American Journal of Kidney Diseases. 36(4): 703-708. October 2000.
This article reports on a study in which histological grading of 45 patients with clinical early immunoglobulin A (IgA) nephropathy (kidney disease) was correlated with disease progression over a median followup of 123 months. Clinical early IgA nephropathy was defined as a serum creatinine level of 1.3 mg per dL or less, proteinuria (protein in the urine) of 0.4 grams per day or less of protein, and the absence of hypertension (high blood pressure) at the time of renal (kidney) biopsy. Disease progression was related to the occurrence of impaired renal function, increased proteinuria, and hypertension. The authors applied a previously described chronicity based histological grading to the renal biopsy specimen and also assessed acute glomerular lesions. Disease progression was observed in 44 percent of these patients. Forty patients (89 percent) showed glomerular grade 1 (GG1) and five patients (11 percent) showed GG2, but this grading did not correlate with disease progression. However, when GG1 was subdivided into GG1a (mean sclerosis per glomerulus was less than 10 percent) and GG1b (mean sclerosis per glomerulus was 10 to less than 25 percent), GG1a correlated with nonprogressive disease. Tubulointerstitial grade also correlated with disease progression but was associated with a low sensitivity for predicting nonprogressive disease. Hyaline arteriosclerosis and acute glomerular lesions did not correlate with disease progression. The chronicity based histological grading is not only applicable to clinical early IgA nephropathy, but more importantly it characterizes GG1a in a subset of patients with a very low risk for disease progression, which can be regarded as genuine early IgA nephropathy. 4 figures. 3 tables. 17 references.
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IgA Nephropathy: Recent Developments. JASN. Journal of the American Society of Nephrology. 11(12): 2395-2403. December 2000.
IgA nephropathy (IgAN, a kidney disease) is a type of glomerulonephritis (inflammation of the filtering bundles in the kidneys). This article reviews recent developments in IgAN, noting that IgAN seems to be a form of Henoch Schonlein purpura (HSP) that is restricted to the kidneys. The authors cover clinical presentation, pathology, diagnosis, pathogenesis, prognosis, treatment strategies, and recurrent IgAN after transplantation. In the great majority of cases, IgAN is an isolated kidney disease with no apparent clinical association; this is called primary IgAN. Secondary IgAN is associated with other clinical contexts, including rheumatoid arthritis, ankylosing spondylitis, and Reiter's syndrome; celiac disease and dermatitis herpetiformis; chronic liver disease (especially alcohol induced); and viral diseases, notably HIV and hepatitis B. Most nephrologists limit the use of biopsy for diagnosis to patients with proteinuria (protein in the urine) of more than 1 gram per 24 hours, because only those patients are candidates for the emerging treatment approaches discussed in this article. Treatment includes general measures such as aggressive therapy of high blood pressure (hypertension), preferably with an ACE inhibitor; corticosteroids; immunosuppressive drugs; fish oil; and anticoagulant and antiplatelet drugs. The authors discuss patient candidacy for each of these options. 3 figures. 1 table. 64 references.
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Kidney Disease and Gastrointestinal Involvement. Dialysis and Transplantation. 29(4): 202-204, 206-207. April 2000.
Some kidney diseases may present with gastrointestinal (GI) manifestations. Conversely, in some GI diseases, renal involvement is present. In addition, some systemic diseases are associated with both kidney and GI involvement. In this review article, the interrelationship between kidney diseases and GI manifestations is addressed. The interrelationship between the kidney and liver diseases is also covered. Patients with chronic renal failure often consult a gastroenterologist first because of anorexia, nausea, vomiting, heartburn, and indigestion of a few month's duration. Patients with acute renal failure may also present with anorexia (lack of appetite), nausea, vomiting, and GI bleeding. Kidney diseases that may cause GI manifestations include acute glomerulonephritis, nephrotic syndrome, reflux nephropathy and pyelonephritis, analgesic (pain medication) nephropathy, acute tubulointerstitial nephritis following administration of NSAIDs, obstructive uropathy, polycystic kidney disease, and GI manifestations in patients on dialysis. GI related causes may contribute to the following kidney diseases: prerenal failure, resulting from fluid losses related to vomiting, diarrhea, hemorrhage, bowel fistula, or bowel obstruction; acute tubular necrosis, resulting from extreme renal ischemia; obstructive uropathy, usually due to active inflammatory GI disease; urinary tract infections, which often result in women from E. coli ascending from the GI tract; postinfectious glomerulonephritis; IgA nephropathy, which is often secondary to chronic liver diseases, celiac disease (gluten intolerance), Crohn's disease, adenocarcinomas of the GI tract; and liver disease. 23 references.
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Kidney Disease and Gastrointestinal Involvement. Dialysis and Transplantation. 29(4): 202-204, 206-207. April 2000.
Some kidney diseases may present with gastrointestinal (GI) manifestations. Conversely, in some gastrointestinal diseases, renal involvement is present. In addition, some systemic diseases are associated with both kidney and GI involvement. In this review article, the interrelationship between kidney diseases and GI manifestations is addressed. The interrelationship between the kidney and liver diseases is also covered. Patients with chronic renal failure (CFR) often consult the gastroenterologist first because of anorexia, nausea, vomiting, heartburn, and indigestion of a few months duration. Patients with acute renal failure (ARF) may also present with anorexia (lack of appetite), nausea, vomiting, and GI bleeding. Kidney diseases that may cause GI manifestations include acute glomerulonephritis, nephrotic syndrome, reflux nephropathy and pyelonephritis, analgesic (pain medication) nephropathy, acute tubulointerstitial nephritis following NSAID administration, obstructive uropathy, polycystic kidney disease (PKD), and GI manifestations in patients on dialysis. Gastrointestinal related causes may contribute to the following kidney diseases: prerenal failure resulting from fluid losses related to vomiting, diarrhea, hemorrhage, bowel fistula, or bowel obstruction; acute tubular necrosis resulting from extreme renal ischemia; obstructive uropathy usually due to active inflammatory GI disease; urinary tract infections, which often result in women from E. coli ascending from the GI tract; postinfectious glomerulonephritis; IgA nephropathy, which is often secondary to chronic liver diseases, celiac disease (gluten intolerance), Crohn's disease, adenocarcinomas of the GI tract, and other diseases such as shistosomiasis. 23 references.
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Nephropathies of HIV Infection: Pathogenesis and Treatment. Current Opinion in Nephrology and Hypertension. 9(2): 117-122. March 2000.
Several different renal syndromes have been reported in patients with HIV infection. This article reviews the pathogenesis and treatment of the various nephropathies (kidney diseases) associated with HIV infection. The author notes that patient characteristics and a syndrome approach may help the clinician formulate a tentative diagnosis, but a renal biopsy is necessary to make a firm diagnosis in patients with chronic renal disease in the setting of HIV infection. In addition, the pathogenesis of HIV nephropathies (HIVAN) can provide information about the pathophysiology of common renal problems such as IgA nephropathy, immune complex glomerulonephritis, focal segmental glomerulosclerosis, and renal disease associated with diabetes (diabetic nephropathy). HIV associated renal disease may be the result of the interaction of the expression of specific HIV genes in patients with distinct genetic susceptibilities to disease in particular environments. New treatment approaches (including ACE inhibitors and highly active antiretroviral therapy or HAART) have provided hope for patients with classic HIV associated nephropathy. 34 references (17 annotated).
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Rationales for Treating IgA Nephropathies. Renal Failure. 21(1): 1-16. 2000.
This article offers an outline of the pathophysiology of IgA nephropathy in order to emphasize the role of eicosanoids, angiotensin II, and reactive oxygen species. The most typical cases of IgA nephropathies have hematuria (blood in the urine) following upper respiratory infection or tonsillitis. ACE inhibitors and early corticosteroid usage are prime therapies for these patients. Tonsillectomy is to be considered, certainly for individual cases. The other drugs that may be used include thromboxane antagonists, leukotriene antagonists, or PAF antagonist. In theory, there should also be benefits from antioxidants. The author notes that fish oils have not come up to expectation. PDGF aptamers look promising for the prevention of mesangial cell proliferation. The author briefly reports on the use of various other agents that could help reduce decline. 3 figures. 1 table. 116 references.
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Treatment of Glomerulonephritis in the Elderly. Seminars in Nephrology. 20(3): 256-264. May 2000.
With the increasing use of renal biopsy in the elderly, glomerulonephritis (inflammation of the kidney glomerulus) is now known to be a common finding. This article reviews the treatment options for glomerulonephritis in the elderly. In general, the elderly present similarly to the younger population, although there are marked changes in the kidney related to aging which may be exaggerated in the patient with concomitant hypertension and more advanced atherosclerotic (cardiovascular) disease. Whereas membranous glomerulonephritis and minimal change disease are common in younger and older adults, primary amyloidosis and crescentic glomerulonephritis are more common in the elderly. Other glomerulonephritides such as focal segmental glomerulosclerosis or IgA nephropathy are very uncommon in the elderly. Because of the serious consequences of the nephrotic syndrome and acute and chronic renal failure (ARF and CRF, respectively) in the elderly, aggressive treatment with immunosuppression should not be withheld. The authors caution that elderly patients must be monitored carefully, as there is presumed greater morbidity and mortality from such treatment in this population. In all elderly patients with proteinuria, ACE inhibitors should be administered if renal function is not too severely impaired. Diuretics should be given to enhance the antiproteinuric effect of ACE inhibition and to control blood pressure and edema. 57 references.
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Treatment of IgA Nephropathy. Seminars in Nephrology. 20(3): 277-285. May 2000.
IgA nephropathy (Berger's disease) is the most common primary glomerulonephritis (infection of the kidney glomeruli) worldwide and was once equated with benign recurrent hematuria (blood in the urine). This article reviews the patient care management of IgA nephropathy. Of the patient population with IgA nephropathy, 15 to 30 percent progress to end stage renal failure after 20 years of clinical manifestations. Because the pathogenesis remains enigmatic, therapy to slow disease progression cannot be disease specific. Control of blood pressure remains the cornerstone of treatment, as for patients with other types of kidney disease. Several approaches to treatment have generated increasing interest in the last few years, including angiotensin inhibition, glucocorticoids, fish oil, cyclophosphamide, tonsillectomy, and mycophenolate mofetil. For patients reaching end stage renal failure, recurrent disease after transplantation can be a clinically important problem (even in light of continued immunosuppression after the transplantation). 2 figures. 65 references.
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