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Persistent Proteinuria (persistent + proteinuria)
Selected AbstractsUnchanged incidence of diabetic nephropathy in Type 1 diabetes: a nation-wide study in IcelandDIABETIC MEDICINE, Issue 2 2005G. Tryggvason Abstract Aims Diabetic nephropathy is an uncommon cause of end-stage renal disease in Iceland in contrast to most industrialized countries. The aim of this study was to examine the incidence of diabetic nephropathy in Iceland. Methods All patients diagnosed with Type 1 diabetes in Iceland before 1992 were studied retrospectively. Patients diagnosed before age 30, who were insulin dependent from the onset, were defined as having Type 1 diabetes. Diabetic nephropathy was defined as persistent proteinuria measured with a dipstick test (Albustix) on three consecutive clinic visits at least 2 months apart. Patients were followed to the end of year 1998, to their last recorded outpatient visit, or until death. The cumulative incidence of diabetic nephropathy was calculated with the Kaplan,Meier method and presented according to the duration of diabetes divided into 5-year intervals. Results A total of 343 patients with Type 1 diabetes were identified. The mean follow-up period was 20.2 ± 11.4 (mean ± sd) years. Only 9.3% of patients were lost to follow-up. Sixty-five patients developed diabetic nephropathy. The cumulative incidence was 22.6% at 20 years and levelled off at 40.3% after approximately 35 years of diabetes duration. No significant changes in cumulative incidence were observed over time. Mean glycated haemoglobin was 8.4% in patients with proteinuria and 7.8% in a group of patients without proteinuria that was matched for age, gender and duration of diabetes (P = 0.04). Conclusions The cumulative incidence of diabetic nephropathy in Iceland is comparable with previously reported cumulative incidence rates and has remained unchanged. Glycaemic control was significantly better in patients without proteinuria. [source] Prediction of diagnosis of immunoglobulin a nephropathy prior to renal biopsy and correlation with urinary sediment findings and prognostic gradingJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 2 2008Kazutaka Nakayama Abstract Several clinical markers correlate well with the diagnosis and prognosis of IgA nephropathy (IgAN). In the present study, we re-evaluated the usefulness of these four clinical markers for prediction of the diagnosis of patients with IgAN through a comparison between many more patients with IgAN and those with other types of renal diseases. 364 patients with IgAN and 289 with other types of renal disease were examined. An analysis was performed prior to renal biopsy, using clinical markers including, serum IgA, serum IgA/C3 ratio, number of red blood cells in urinary sediments, and urinary protein. Patients with IgAN were divided into four groups according to histopathological findings. Presence of microscopic hematuria, persistent proteinuria, high serum IgA levels, and the serum IgA/C3 ratios are useful for prediction of diagnosis of IgAN and distinguishing it from other renal diseases. Blood pressure, urinary protein, serum uric acid, renal function, and urinary sediment findings may be useful for prediction of prognostic grading in patients with IgAN. J. Clin. Lab. Anal. 22:114,118, 2008. © 2008 Wiley-Liss, Inc. [source] Short-term follow-up of patients with sickle cell disease and albuminuriaPEDIATRIC BLOOD & CANCER, Issue 6 2008Ofelia Alvarez MD Abstract Background Albuminuria with normal serum creatinine occurs frequently in patients with sickle cell disease (SCD), but the rate of progression to more advanced chronic renal disease is unknown. The purpose of this study was to investigate the rate of progression of children and young adults with SCD and albuminuria over time. Procedure Urine albumin/creatinine (A/C) ratios and serum creatinine were obtained serially. Serum cystatin C levels were determined in a subgroup of 20 patients. Results Of 38 patients with SCD who had albuminuria (30 with microalbuminuria and 8 with proteinuria), 10.5% had progressive disease during follow-up of 20,±,12 months. Progressive disease was observed in 2 of 30 patients with MA because MA worsened to either intermittent proteinuria (1 patient), or persistent proteinuria after 7 months follow-up (1 patient). Two of eight patients with proteinuria worsened to nephrotic-range after 8 and 17 months with elevations of serum creatinine. All eight patients with proteinuria were treated with angiotensin blockade and/or hydroxyurea. Of those, six patients responded to treatment with decreased albuminuria and no changes in serum creatinine. Serum cystatin C level trended to increase before serum creatinine in patients with proteinuria. Conclusions Patients with rapid progression to nephrotic-range proteinuria showed decreased kidney function. Therefore, patients with albuminuria should be monitored closely for progression, and therapy with hydroxyurea and/or angiotensin blockade should be considered for patients who develop proteinuria. Serum cystatin C appears more sensitive than serum creatinine to detect early decrease in kidney function. Pediatr Blood Cancer 2008;50:1236,1239. © 2008 Wiley-Liss, Inc. [source] Rituximab (B-cell depleting antibody) associated lung injury (RALI): A pediatric case and systematic review of the literaturePEDIATRIC PULMONOLOGY, Issue 9 2009Martin Bitzan MD Abstract Introduction Pulmonary toxicity of delayed onset is a rare complication of B-lymphocyte depleting antibody therapy and has been almost exclusively reported in older patients with B-cell malignancies. Aims To describe a pediatric patient with rituximab-associated lung injury (RALI), to systematically analyze previous reports of pulmonary complications, and to summarize common clinico-pathological features, treatment, and outcome. Results A teenage boy with focal segmental glomerulosclerosis (FSGS) presented with progressive dyspnea, fever, hypoxemia and fatigue 18 days after the completion of a second course of rituximab infusions for calcineurin inhibitor-dependent nephrotic syndrome. Respiratory symptoms started while he received high-dose prednisone for persistent proteinuria. Bilateral, diffuse ground-glass infiltrates corresponded to the presence of inflammatory cells in the bronchioalveolar lavage fluid. Empiric antibiotic treatment including clarithromycin was given, but the microbiological work-up remained negative. Serum IgE, C3, and C4 concentrations were normal. He recovered within 3 weeks after onset. We systematically reviewed 23 reports describing 30 additional cases of rituximab-associated lung disease. Twenty eight patients had received rituximab for B-cell malignancies, one for graft-versus-host disease and one for immune thrombocytopenia. Median age was 64 years (interquartile range [IQR] 58,69 years). Seventy one percent received concomitant chemotherapy. Time to onset from the last rituximab dose was 14 days (IQR 11,22 days). Eleven of 31 patients required mechanical ventilation, and 9 died (29%). Ventilation was a significant predictor of fatal outcome (odds ratio 46.7; confidence interval 9.5,229.9). High dose glucocorticoid therapy did not improve survival or prevent severe lung disease or death. Conclusions With the expanding use of rituximab for novel indications, additional cases of RALI affecting younger age groups are expected to emerge. Mechanical ventilation predicts poor outcome. Glucocorticoids may not be protective. Pediatr Pulmonol. 2009; 44:922,934. © 2009 Wiley-Liss, Inc. [source] Persistent Glomerular Hematuria in Living Kidney Donors Confers a Risk of Progressive Kidney Disease in Donors After HeminephrectomyAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2010R. Kido Although glomerular hematuria is likely a sign of chronic kidney disease that will develop into overt nephropathy after donation, it remains unclear whether prospective donors with hematuria should be excluded. We reviewed the medical records of 242 donors who donated at our institution from 2001 to 2007 and surveyed the prevalence of hematuria pre- and postdonation. We then investigated the association of hematuria with proteinuria postdonation and trends in glomerular filtration rate. Before donation, 8.3% of 242 donors presented with persistent hematuria, a finding that was significantly associated with dysmorphic hematuria before donation. Most cases of predonation persistent hematuria persisted after donation, and the overall prevalence increased to 15.3%. During a median follow-up period of 2.3 years after donation, 8.3% developed persistent proteinuria, with incidence being significantly higher in donors having persistent hematuria with dysmorphic red blood cells (d-RBC) both before and after donation. Postdonation persistent hematuria with d-RBC was also associated with a progressive decline in renal function. These results indicate that persistent glomerular hematuria is strongly associated with a higher incidence of postdonation progressive kidney disease. Potential donors with persistent glomerular hematuria should be excluded, while those with isolated hematuria need to be evaluated with heightened caution. [source] How Do Living Kidney Donors Develop End-Stage Renal Disease?AMERICAN JOURNAL OF TRANSPLANTATION, Issue 11 2009R. Kido The clinical course and risk factors for developing end-stage renal disease (ESRD) after heminephrectomy in living kidney donors have scarcely been investigated. We reviewed medical records and identified eight case donors who developed chronic kidney disease (CKD) stage 5 or ESRD, and subsequently investigated the association between postoperative clinical courses and changes in renal function. To conduct a case-control study, we also selected a control group comprising 24 donors who had maintained stable renal function and were matched for age, sex and follow-up time since donation. Except for one donor who developed ESRD caused by a traffic accident, none of the donors developed progressive renal dysfunction immediately after donation. Their renal functions remained stable for a long period of time, but started to decline after developing new comorbidities, especially risk factors known as progression factors (proteinuria or hypertension) or accelerating factors (cardiovascular [CV] event or infection) of CKD. As compared with the control donors, incidence of postoperative persistent proteinuria, acute CV event, severe infection and hospitalization due to accelerating factors of CKD were significantly higher in the case donors. These results suggest the importance of long-term (more than 10 years) follow-up of donors with special attention on the risk factors of CKD. [source] Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitisCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009J. W. Cohen Tervaert Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible. [source] | ||||||||||