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20 years or more of follow-up of living kidney donors.

https://arctichealth.org/en/permalink/ahliterature222923
Source
Lancet. 1992 Oct 3;340(8823):807-10
Publication Type
Article
Date
Oct-3-1992
Author
J S Najarian
B M Chavers
L E McHugh
A J Matas
Author Affiliation
Department of Surgery, University of Minnesota, Minneapolis 55455.
Source
Lancet. 1992 Oct 3;340(8823):807-10
Date
Oct-3-1992
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Albuminuria - urine
Blood Pressure - physiology
Blood Urea Nitrogen
Canada - epidemiology
Cause of Death
Creatinine - blood - urine
Female
Follow-Up Studies
Humans
Hypertension - etiology
Kidney - physiology
Kidney Transplantation
Male
Middle Aged
Nephrectomy - adverse effects - mortality
Proteinuria - etiology
Pulmonary Embolism - mortality
Tissue Donors
United States - epidemiology
Abstract
The perioperative and long-term risks for living kidney donors are of concern. We have studied donors at the University of Minnesota 20 years or more (mean 23.7) after donation by comparing renal function, blood pressure, and proteinuria in donors with siblings. In 57 donors (mean age 61 [SE 1]), mean serum creatinine is 1.1 (0.01) mg/dl, blood urea nitrogen 17 (0.5) mg/dl, creatinine clearance 82 (2) ml/min, and blood pressure 134 (2)/80 (1) mm Hg. 32% of the donors are taking antihypertensive drugs and 23% have proteinuria. The 65 siblings (mean age 58 [1.3]) do not significantly differ from the donors in any of these variables: 1.1 (0.03) mg/dl, 17 (1.2) mg/dl, 89 (3.3) ml/min, and 130 (3)/80 (1.5) mm Hg, respectively. 44% of the siblings are taking antihypertensives and 22% have proteinuria. To assess perioperative mortality, we surveyed all members of the American Society of Transplant Surgeons about donor mortality at their institutions. We documented 17 perioperative deaths in the USA and Canada after living donation, and estimate mortality to be 0.03%. We conclude that perioperative mortality in the USA and Canada after living-donor nephrectomy is low. In long-term follow-up of our living donors, we found no evidence of progressive renal deterioration or other serious disorders.
Notes
Comment In: Lancet. 1992 Nov 28;340(8831):1354-51360068
PubMed ID
1357243 View in PubMed
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An Acadian variant of Fanconi syndrome.

https://arctichealth.org/en/permalink/ahliterature161951
Source
Pediatr Nephrol. 2007 Oct;22(10):1711-5
Publication Type
Article
Date
Oct-2007
Author
Philip Wornell
John Crocker
Andrew Wade
Jason Dixon
Philip Acott
Author Affiliation
Department of Pediatrics, IWK Health Centre, Dalhouise University, 5850/5980 University Avenue, PO Box 9700, Halifax, Nova Scotia, B3K 6R8, Canada. phil_wornell@yahoo.ca
Source
Pediatr Nephrol. 2007 Oct;22(10):1711-5
Date
Oct-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Birth weight
Body Weight
Canada
Child
Child, Preschool
Fanconi Anemia - genetics
Genetic Variation
Humans
Proteinuria - etiology
Rickets - epidemiology
Abstract
The Acadians were French settlers to Nova Scotia in the seventeenth century. In 1755, they were expelled by the British to various sites in the Americas, including Louisiana, where they are referred to as Cajuns. Many later migrated back to the Maritime Provinces of Canada. The objective of this study was to describe a series of pediatric patients representing an Acadian variant of Fanconi syndrome (AVFS). Nineteen children were diagnosed with AVFS between 1971 and 2006 and followed regularly. Data concerning demographics, growth, bone disease, and renal function at presentation and last observation were collected. The commonest reason for referral was assessment of genu valgum at 8.5 +/- 4.2 years (mean +/- SD) with hypophosphatemic rickets confirmed in all patients. Small-body habitus and short stature were confirmed in all patients. Therapy consisting of alkali replacement and phosphate and vitamin D supplements resulted in improvement of rickets and leg alignment but not stature (median height Z-score at presentation -2.05, range -3.6 to 0.21, vs. -2.05 at last observation, range -3.36 to 0.47). Creatinine clearance decreased (65.4 +/- 24.6 vs. 48.0 +/- 36.0 ml/min per 1.73 m(2), P
PubMed ID
17690917 View in PubMed
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Clinical features, therapeutic interventions and long-term aspects of hemolytic-uremic syndrome in Norwegian children: a nationwide retrospective study from 1999-2008.

https://arctichealth.org/en/permalink/ahliterature284010
Source
BMC Infect Dis. 2016 Jun 13;16:285
Publication Type
Article
Date
Jun-13-2016
Author
Gaute Reier Jenssen
Line Vold
Eirik Hovland
Hans-Jacob Bangstad
Karin Nygård
Anna Bjerre
Source
BMC Infect Dis. 2016 Jun 13;16:285
Date
Jun-13-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Anti-Bacterial Agents - therapeutic use
Blood Transfusion
Child
Child, Preschool
Diarrhea - etiology
Escherichia coli Infections - complications - physiopathology - therapy
Female
Heart Diseases - etiology
Hemolytic-Uremic Syndrome - complications - physiopathology - therapy
Humans
Hypertension - etiology
Infant
Kidney
Kidney Failure, Chronic - etiology
Kidney Transplantation
Male
Nervous System Diseases - etiology
Norway
Plasmapheresis
Proteinuria - etiology
Renal Dialysis
Renal Insufficiency, Chronic - etiology
Renal Replacement Therapy
Respiration, Artificial
Respiratory Tract Diseases - etiology
Retrospective Studies
Sepsis - etiology
Shiga-Toxigenic Escherichia coli
Abstract
Hemolytic-uremic syndrome (HUS) is a clinical triad of microangiopathic hemolytic anemia, impaired renal function and thrombocytopenia, primarily affecting pre-school-aged children. HUS can be classified into diarrhea-associated HUS (D(+)HUS), usually caused by Shiga toxin-producing Escherichia coli (STEC), and non-diarrhea-associated HUS (D(-)HUS), both with potentially serious acute and long-term complications. Few data exists on the clinical features and long-term outcome of HUS in Norway. The aim of this paper was to describe these aspects of HUS in children over a 10-year period.
We retrospectively collected data on clinical features, therapeutic interventions and long-term aspects directly from medical records of all identified HUS cases
Notes
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PubMed ID
27297224 View in PubMed
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Source
Am J Dis Child. 1991 Oct;145(10):1181-3
Publication Type
Article
Date
Oct-1991
Author
P. Lautala
M. Uhari
Author Affiliation
Department of Pediatrics, University of Oulu, Finland.
Source
Am J Dis Child. 1991 Oct;145(10):1181-3
Date
Oct-1991
Language
English
Publication Type
Article
Keywords
Alanine Transaminase - blood
Aspartate Aminotransferases - blood
C-Reactive Protein - chemistry
Child
Creatinine - blood
Diagnosis, Differential
Finland - epidemiology
Hemorrhagic Fever with Renal Syndrome - complications - diagnosis - epidemiology
Humans
Incidence
Nephritis, Interstitial - complications - diagnosis - epidemiology
Prognosis
Proteinuria - etiology - urine
Seasons
Sodium - blood
Thrombocytopenia - blood - etiology
Abstract
Epidemic nephropathy, a form of hemorrhagic fever with renal syndrome, caused by the Puumala serotype of hantaviruses and occurring endemically in northern Scandinavia, was studied in 13 children. The clinical symptoms and signs were somewhat different from those reported in adults; none of our patients had hemorrhagic manifestations despite low thrombocyte counts. The most common presenting symptoms were fever, abdominal pain, and renal tenderness with oliguria followed by polyuria. The predominant laboratory findings were proteinuria and/or hematuria and elevated serum creatinine levels. Thrombocytopenia was a constant finding in the children in whom thrombocyte count was obtained. Most children had a decreased serum sodium concentration during the oliguric phase of the disease. All the children recovered, with no long-term renal disease. Epidemic nephropathy is an important alternative for differential diagnosis in children with findings suggesting nephritis, especially in endemic areas. An awareness and knowledge of this syndrome and an ability to diagnose it by means of a specific antibody measurement will probably improve our understanding of its epidemiologic features in children.
PubMed ID
1681724 View in PubMed
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Henoch-Schoenlein nephritis in adults-clinical features and outcomes in Finnish patients.

https://arctichealth.org/en/permalink/ahliterature189239
Source
Clin Nephrol. 2002 Jul;58(1):1-8
Publication Type
Article
Date
Jul-2002
Author
V. Rauta
T. Törnroth
C. Grönhagen-Riska
Author Affiliation
Department of Medicine, Helsinki University Central Hospital, Finland.
Source
Clin Nephrol. 2002 Jul;58(1):1-8
Date
Jul-2002
Language
English
Publication Type
Article
Keywords
Adult
Disease Progression
Female
Finland
Follow-Up Studies
Hematuria - etiology
Humans
Kidney - pathology
Male
Proteinuria - etiology
Purpura, Schoenlein-Henoch - classification - complications - pathology
Renal Insufficiency - etiology
Abstract
Henoch-Schoenlein purpura (HSP) is a small vessel vasculitis that often involves the kidneys. It affects many more children than adults. Few studies on HSP nephritis (HSN) in adult patients have been reported. One aim of the study described here was to determine clinical features in adults diagnosed at a single center as suffering from HSN. Other aims were to record outcomes of the disease and factors associated with its progression.
Between 1980 and 1995, 42 adults attending our clinic were diagnosed consecutively, by means of renal biopsy, as suffering from HSN. Data on 38 patients with a follow-up period of at least a year were subsequently analyzed to determine whether any clinical, laboratory or histopathological variable was associated with the progression of HSN.
The mean age of the patients on biopsy was 42.0 years (SD 16.5). Eighteen of the 38 patients were male. Eleven of the 38 patients had isolated hematuria as an indication for renal biopsy and 25 had Ccr > or = 85 ml/min on diagnosis. Eight patients exhibited progression of HSN, 3 to end-stage renal failure (ESRF), during a mean follow-up time of 6.1 years (SD 4.3). Renal survival 10 years after renal biopsy was 91%. No histopathological findings were associated with poor outcome. The only factor statistically significantly related to the progression of HSN was a level of proteinuria greater than 1.0 g/24 h (p
PubMed ID
12141401 View in PubMed
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Histopathologic features aid in predicting risk for progression of IgA nephropathy.

https://arctichealth.org/en/permalink/ahliterature145966
Source
Clin J Am Soc Nephrol. 2010 Mar;5(3):425-30
Publication Type
Article
Date
Mar-2010
Author
Michael Walsh
Aylin Sar
Diane Lee
Serdar Yilmaz
Hallgrimur Benediktsson
Braden Manns
Brenda Hemmelgarn
Author Affiliation
Division of Nephrology, Foothills Medical Centre, Calgary, AB, T2N 0L9, Canada. mwwalsh@ucalgary.ca
Source
Clin J Am Soc Nephrol. 2010 Mar;5(3):425-30
Date
Mar-2010
Language
English
Publication Type
Article
Keywords
Adult
Alberta
Atrophy
Biological Markers - blood
Biopsy
Chi-Square Distribution
Creatinine - blood
Disease Progression
Female
Fibrosis
Glomerulonephritis, IGA - blood - complications - diagnosis - mortality - pathology
Humans
Hypertension - complications - pathology
Kidney Failure, Chronic - blood - etiology - mortality - pathology
Kidney Glomerulus - pathology
Male
Middle Aged
Predictive value of tests
Proportional Hazards Models
Proteinuria - etiology - pathology
Retrospective Studies
Risk assessment
Risk factors
Sclerosis
Time Factors
Abstract
IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide. Accurately identifying patients who are at risk for progressive disease is challenging. The extent to which histopathologic features improves prognostication is uncertain.
We studied a retrospective cohort with biopsy-proven IgAN in Calgary, Canada. Renal biopsies were reviewed by a nephropathologist with histopathologic data abstracted using a standardized form. The primary outcome was the composite of doubling of serum creatinine, ESRD, or death. Spline models defined significant levels of interstitial fibrosis, glomerulosclerosis, hypertension, proteinuria, and creatinine. The prognostic significances of clinical and histopathologic parameters were determined using Cox proportional hazards models.
Data from 146 cases were available for analysis with a median follow-up of 5.8 years. Greater than 25% interstitial fibrosis, >40% glomerular sclerosis, and a systolic BP >150 mmHg were risk thresholds. In univariable analyses, baseline creatinine, proteinuria, systolic BP, glomerular sclerosis, interstitial fibrosis, and crescentic disease were predictors of the primary outcome. In multivariable models adjusted for clinical characteristics, interstitial fibrosis (hazard ratio [HR]2.7; 95% confidence interval [CI] 1.2 to 6.0), glomerular sclerosis (HR 2.6; 95% CI 1.2 to 4.5), and crescents (HR 2.4; 95% CI 1.2 to 5.1) remained independent predictors of the primary outcome and significantly improved model fit compared with clinical characteristics alone.
Baseline histopathologic parameters are independent predictors of adverse outcomes in IgAN even after taking into consideration clinical characteristics. Relatively small degrees of interstitial fibrosis confer an increased risk for progressive IgAN.
Notes
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PubMed ID
20089495 View in PubMed
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How are hypertensive children evaluated and managed? A survey of North American pediatric nephrologists.

https://arctichealth.org/en/permalink/ahliterature175424
Source
Pediatr Nephrol. 2005 Jun;20(6):791-7
Publication Type
Article
Date
Jun-2005
Author
Robert P Woroniecki
Joseph T Flynn
Author Affiliation
Division of Pediatric Nephrology, Montefiore Medical Center, Bronx, NY 10467, USA.
Source
Pediatr Nephrol. 2005 Jun;20(6):791-7
Date
Jun-2005
Language
English
Publication Type
Article
Keywords
Antihypertensive Agents - therapeutic use
Blood Pressure Determination
Canada
Child
Goals
Humans
Hypertension - complications - diagnosis - drug therapy
Nephrology - methods
Pediatrics - methods
Professional Practice
Proteinuria - etiology
Questionnaires
Renal Insufficiency - etiology
United States
Abstract
To assess how children with hypertension are currently evaluated and managed, we surveyed 438 North American pediatric nephrologists on how they measure blood pressure (BP), BP goals used in pharmacologically treated patients, and antihypertensive drug choices. 190 replies were received (43% response rate), and 185 were analyzable. Oscillometric and aneroid sphygmomanometers were the most commonly used devices for office BP measurement (74.8% of respondents). Ambulatory blood pressure monitoring was used by 63% of respondents. Goal BP in pharmacologically treated patients was set at the 95th percentile by 39% of respondents, and at the 90th percentile by 59%. Only 37% used a different goal BP in children with hypertension and renal disease; of these, 85% used a lower goal and 15% a higher goal. For hypertensive children with diabetes, 47% used a different goal; 99% lower and 1% higher. Whereas angiotensin-converting enzyme inhibitors (ACEI) and calcium-channel blockers (CCB) were chosen by similar proportions of respondents as initial agents for treatment of primary hypertension, most (84%) chose ACEI as their initial agent for hypertension in children with renal disease. Although most pediatric nephrologists treat hypertensive children to a BP goal below the 90th percentile, most do not use lower goals for patients with renal disease or diabetes, in contrast with current recommendations for treatment of adults with these conditions. These findings highlight the need for further studies to determine whether recommendations for treatment of hypertension in adults should be followed in children.
PubMed ID
15809834 View in PubMed
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Late failure or human renal transplants. An analysis of transplant disease and graft failure among 125 recipients surviving for one to eight years.

https://arctichealth.org/en/permalink/ahliterature28040
Source
Medicine (Baltimore). 1975 Jan;54(1):45-71
Publication Type
Article
Date
Jan-1975
Author
V P Petersen
T S Olsen
F. Kissmeyer-Nielsen
S O Bohman
H E Hansen
E S Hansen
P E Skov
K. Solling
Source
Medicine (Baltimore). 1975 Jan;54(1):45-71
Date
Jan-1975
Language
English
Publication Type
Article
Keywords
Adult
Anemia, Hemolytic - complications
Biopsy, Needle
Denmark
Female
Follow-Up Studies
Glomerulonephritis - physiopathology
Graft Rejection - complications
Graft vs Host Reaction
Histocompatibility testing
Humans
Kidney Failure, Chronic - surgery
Kidney Glomerulus - pathology
Kidney Transplantation
Male
Microscopy, Fluorescence
Middle Aged
Nephritis, Interstitial - complications
Nephrosclerosis - complications
Proteinuria - etiology
Serum Albumin
Transplantation, Homologous
Abstract
The purpose of the present paper was to study clinical, morphological and immunological aspects of late rejection of renal allotransplants. We have, therefore, analyzed the occurrence and nature of renal transplant disease and graft failure among 125 recipients surviving for 1 to more than 8 years after transplantation. In this population transplant disease as defined by the appearance of heavy proteinuria and/or steadily declining graft function occurred in 22 patients. At the closure date of the study on December 31, 1972 complete graft failure had occurred in 12 of these 22 patients and 4 of these have died. In addition two patients died in the presence of normal graft function, due to chronic hepatitis and metastatic cancer respectively. As based on clinical findings, pathophysiological features and renal lesions the patients with late transplant disease were classified into two groups and described accordingly. Group A, termed glomerular transplant disease, included a majority of 16 patients, constituting a rather homogenous idsease entity in relation to course of disease, clinical findings and renal lesions as studied by light-, immunofluorescence- and electron microscopy. All these patients presented with heavy proteinuria, which was non-selective in all but two, resulting eventually in complete loss of graft function in eight cases. All these patients developed hypoalbuminemia and hypercholesterolemia, and one half manifested a classical nephrotic syndrome. Arterial hypertension occurred in all patients except two. Glomerular structure as studied by light microscopy revealed a number of lesions of a rather polymorphous pattern in all patients in group A. Endomesangial proliferation, hyperplasia and segmental proliferation of epithelial cells and thickening of capillary walls were prominent features, although the degree of severity, extension and type of lesion occurred in such varying proportions that classification into any well characterized category of glomerulonephritis was not possible. All cases in group A revealed immune deposits, most frequently containing IgG, IgM, complement and fibrinogen. IgA, IgD and IgE were also demonstrated in a lesser proportion of cases in this group. The immunofluorescent pattern was a mixed granular and linear, and in no case strictly linear or granular alone. The ultrastructural investigation contains a detailed analysis of the
PubMed ID
235063 View in PubMed
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19 records – page 1 of 2.