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Biomedical subjects

C Svalander

Publications and source records attributed to C Svalander.

At least 19 recordsLinked to original sources
PubMed2005

Characterization of the humoral immune response in two paediatric patients transplanted with split livers from ABO-incompatible living-related donors: appearance of cytomegalovirus-induced ABO antibodies.

Two blood group O paediatric patients, 12 and 6 months old, were transplanted with liver segments from their blood group A2Le (a(-)b+) Se and blood group A1Le (a(-)b+) Se fathers, respectively. Recipient anti-A antibody titres were reduced prior to transplantation by blood exchange. Both patients had rejection episodes in the post-transplant period that were reversed by anti-rejection therapy. No anti-A antibody titre rise occurred concomitant with these rejections. Postoperatively both patients had cytomegalovirus (CMV) infections, and simultaneous with these infections, a strong increase in anti-A antibody titres was seen, but no rejection occurred. The anti-A antibody titre increase seemed to be specific for A antigens, because the anti-B and anti-alphaGal (anti-pig) antibody titres did not show any changes. CMV infection is a serious cause of morbidity and mortality in immunosuppressed patients, and the virus can influence glycosylation of infected cells. Whether this can explain the importance of the infection in relation to the increase in titre remains to be elucidated.

ABO Blood-Group System↗
PubMed1999

Clinical risk factors for recurrence of IgA nephropathy.

No clinical risk factors for recurrence of immunoglobulin A (IgA) nephropathy in kidney transplants have been defined. This is a single-centre retrospect analysis of recurrence in 104 first kidney transplant patients with biopsy-verified IgA nephropathy. Fifty patients had living donors. All but an identical twin were treated with cyclosporin A. The median follow-up time was 5 yr. Graft biopsies had been obtained from 35 grafts later than 6 months after transplantation, due to deteriorating graft function or gross proteinuria. Thirteen biopsies showed mesangial glomerulopathy proliferative in eleven cases with IgA deposits. Recurrence caused failure of six grafts. Eleven grafts with recurrence were from living donors (p = 0.005). No specific human leukocyte antigen (HLA) was identified as a risk factor. Known duration of original disease until end-stage renal failure was significantly shorter in patients with recurrence (median 5 yr, range 0-25 yr) compared with those without (median of 10 yr, range of 0-37 yr) (p = 0.015). Cumulative graft survival was not reduced in living versus cadaveric donor recipients.

Adolescent↗
PubMed1999

Cadmium, mercury, and lead in kidney cortex of the general Swedish population: a study of biopsies from living kidney donors.

Cadmium, mercury, and lead concentrations were determined in deep-frozen kidney cortex biopsies taken from 36 living, healthy Swedish kidney donors (18 males and 18 females), who were 30-71 (mean 53) years of age. Information about occupation, smoking, the presence of dental amalgam, and fish consumption could be obtained for 27 of the donors. The samples (median dry weight 0.74 mg) were analyzed using inductively coupled plasma mass spectrometry, and the results were transformed to wet-weight concentrations. The median kidney Cd was 17 micrograms/g (95% confidence interval, 14-23 micrograms/g), which was similar in males and females. In 10 active smokers, the median kidney Cd was 24 micrograms/g, and in 12 who never smoked, it was 17 micrograms/g. The median kidney Hg was 0.29 micrograms/g, with higher levels in females (median 0.54 micrograms/g) than in males (median 0.16 micrograms/g). Subjects with amalgam fillings had higher kidney Hg (median 0.47 micrograms/g, n = 20) than those without dental amalgam (median 0.15 micrograms;g/g, n = 6), but kidney Hg was below the detection limit in some samples. Nearly half of the samples had kidney Pb below the detection limit. The median kidney Pb was estimated as 0. 14 micrograms/g. This is the first study of heavy metals in kidney cortex of living, healthy subjects, and the results are relatively similar to those of a few previous autopsy studies, indicating that results from autopsy cases are not seriously biased in relation to kidney metal concentrations in the general population. Cd concentrations in those who never smoked were relatively high, indicating considerable Cd intake from the diet in Sweden. The effect of dental amalgam on kidney Hg was as expected, although the reason for the difference in Hg levels between males and females is unclear.

Adult↗
PubMed1998

Focal segmental glomerulosclerosis in a kidney transplant population: hereditary and sporadic forms.

Between 1985 and 1993, 16 of 1000 kidney transplant patients in Göteborg had biopsy-verified primary focal segmental glomerulosclerosis (FSGS), and among them they received 23 transplants. Their age range was 19-67 years (median 39 years). Patients were followed for 3-10 years (median 6.5 years). Eight patients were members of seven separate families in which at least one other member had FSGS, while eight cases were sporadic. The patients with hereditary FSGS were younger at onset of symptoms than sporadic cases (median 12.5 vs 26 years, P = 0.041) but not at the time of renal failure. Only one versus five had received immunotherapy. After transplantation, recurrence of FSGS occurred in five grafts, all in sporadic cases, and two of these were lost. In conclusion, it appears that there are at least two forms of FSGS, one hereditary and one sporadic form. The hereditary form does not seem to recur after transplantation, whereas the risk in sporadic cases is very high.

Adult↗
PubMed1998

Patients hospitalized because of small vessel vasculitides with renal involvement in the period 1975-95: organ involvement, anti-neutrophil cytoplasmic antibodies patterns, seasonal attack rates and fluctuation of annual frequencies.

OBJECTIVES: To study organ involvement, anti-neutrophil cytoplasmic antibodies (ANCA) patterns, trends in yearly frequencies and seasonal variations of symptom onset in patients hospitalized because of small vessel vasculitides during a 21 year period (1975-95). DESIGN: A retrospective investigation was conducted of 138 patients hospitalized with a diagnosis of small vessel vasculitides, as defined by the Chapel Hill Consensus Conference, within the County of Orebro, a mixed urban and rural area of central Sweden. SETTING: Orebro Medical Center Hospital, Orebro, Sweden and two district hospitals within the County of Orebro, Sweden. RESULTS: During the studied period there were 19 patients with a diagnosis of Wegener's granulomatosis (WG), 70 patients with microscopic polyangiitis (MPA), 36 patients with renal limited vasculitis (RLV), two with Churge-Strauss vasculitis (C-S), seven with Henoch-Schönleins purpura (HSP) and four with essential cryoglobulinemic vasculitis (ECV). Renal involvement was present in 123 patients (89.1%). A positive c- and/or pANCA was found in nearly 90% of the 111 patients where sera were available. Calculations of frequency data, restricted to the primary catchment area for patients with ANCA associated vasculitis and renal involvement (WG, MPA, RLV) during a 21-year period (1975-95) gave a mean annual frequency of 1.6 per 100,000 adults (95% CI: 1.2-3.1); for this group of patients with the inclusion of those with C-S, HSP and ECV during the last 10 year period (1986-95) gave a mean annual frequency of 2.5 per 100,000 adults (95% CI: 1.7-3.4), for male adults 3 per 100,000 (95% CI: 1.6-4.4), and female adults 1.9 (95% CI: 0.9-2.8). A frequency peak of 6.3 per 100,000 was seen for men aged 55-64. A periodic fluctuation of the frequencies with peaks every 3-4 years was noted for patients with ANCA related vasculitis (WG, MPA, RLV) during the 21-year period 1975-95. Onset of symptoms was predominantly noticed during the winter months (December-February) for patients with a positive cANCA. CONCLUSION: The observed frequencies in our study of patients with small vessel vasculitides were higher than those previously documented. We also showed a periodic fluctuation of the annual frequencies and a seasonal variation of symptom onset.

Adult↗
PubMed1997

Alpha-1-antitrypsin deficiency associated with hepatic cirrhosis and IgA nephritis.

The association between alpha1-antitrypsin (A1AT) deficiency and glomerulonephritis has only sporadically been reported, and mostly based upon autopsy findings, as opposed to the more frequent linkage between A1AT deficiency and lung emphysema with or without hepatic cirrhosis. The present case report describes a 30-year-old man with A1AT deficiency, without evidence of lung disease, who developed hepatic cirrhosis in early childhood and IgA glomerulonephritis and hypertension in adult life. The IgA nephritis followed an unusual course, with a sudden deterioration of the renal function, possibly induced by uncontrolled hypertension or the possible occurrence of vasculitis. After 6 months of hemodialysis, the patient successfully underwent living-related-donor kidney transplantation.

Adult↗
PubMed1995

[Alpha 1-antitrypsin deficiency--not only pulmonary and hepatic involvement].

The association between deficiency of alpha-1-antitrypsin (A1AT) and glomerulonephritis has been only sporadically reported on, as opposed to the linkage between A1AT-deficiency and lung emphysema or hepatic cirrhosis. We describe the case of a 30-year-old man with A1AT deficiency who developed hepatic cirrhosis in early childhood, and IgA glomerulonephritis and hypertension in adult life. The IgA nephritis followed an unusual course. After three years of slight elevation of serum creatinine levels, the patient rapidly developed renal failure necessitating acute hemodialysis. The deterioration of the renal function was preceded by eruption of skin lesions, believed to represent a vasculitis. After six months of hemodialysis, the patient successfully received a transplanted kidney from his mother. The literature is reviewed with respect to the association between A1AT-deficiency and renal disease. We discuss possible underlying causes for the rapid deterioration of renal function in this patient.

Adult↗
PubMed1995

Plasmapheresis as a rescue therapy to resolve cardiac rejection with vasculitis and severe heart failure. A report of five cases.

The predominant causes of late graft loss and death after cardiac transplantation are graft rejection and infection. The histopathological classification of acute rejection is based on cellular phenomena such as lymphocytic infiltration and myocyte damage. The adverse prognostic importance of vascular or humoral rejection has been reported, but there is no well-documented treatment available. In our experience, comprising 151 orthotopic transplants, five patients presented with graft rejection characterized by a lymphocytic vasculitis that did not respond to conventional therapy. Because of a deteriorating condition, in spite of vigorous antirejection treatment that included inotropic drugs and circulatory support. plasmapheresis was tried as a last, desperate means to stop the process from developing further. The clinical symptoms rapidly subsided in all five patients after the first couple of plasma exchanges. All of the patients are alive and well after 2-3.5 years of follow-up. Although the mechanism of action is unclear, plasmapheresis was beneficial in these critically ill patients.

Adolescent↗
PubMed1995

Original renal disease in a kidney-transplant population.

Classification of the underlying renal disorder in kidney transplant patients involves some uncertainties. To allow evaluation of the risk of recurrence of renal disease in the transplanted kidney and other characteristics and risks inherent to the specific renal disorder we have investigated the basis for and reevaluated the diagnosis of 1000 consecutive patients who received transplants in Göteborg 1985-1993. In the original registry, 36% of patients had been given the diagnosis chronic glomerulonephritis but the diagnosis was confirmed by biopsy in only half of them, 18% of the total population. Systemic vasculitides and hereditary disorders other than adult polycystic kidney disease which constituted 3% and 6%, respectively, had frequently been overlooked. The term chronic pyelonephritis (15%) covered a variety of conditions including toxic tubulointerstitial disease, but was dominated by those caused by congenital urinary tract formations. Diabetic nephropathy (21%) was the consequence of Type 1 diabetes in 18% and Type 2 or other forms of diabetes in 3%. The proportion of patients with unknown cause of renal failure was 20%. The registry allows identification of small, distinct entities, which may be characterised as regards prerequisites for and consequences of kidney transplantation.

Aged↗
PubMed1995

Spectrum of hereditary renal disease in a kidney transplant population.

Re-evaluation of the underlying renal disease in 1000 consecutive kidney transplant patients revealed 129 cases of adult autosomal dominant polycystic kidney disease and 60 clear and seven suspected cases with other hereditary renal disorders. Twenty-four of 60 patients had cystic/dysplastic disease--10 of these classified as nephronophthisis, five as polycystic disease, and nine with the renal affection as part of a congenital malformation syndrome. Thirteen patients had Alport's syndrome, nine were diagnosed with tubulointerstitial nephritis, and six had an adult form of focal segmental glomerular sclerosis (FSGS). Two had changes classified as nephrosclerosis, but with an autosomal dominant mode of inheritance. Finnish type congenital nephrotic syndrome was present in two children and familial amyloidosis in two adults. Two patients had an unclassified disease. During follow-up, five patients with cystic/dysplastic disorders manifested liver disease. None of the patients with FSGS had recurrence and none of the Alport patients had anti-GBM disease. There were no other complications related to the renal condition. In conclusion, hereditary disorders are underestimated in regular registries of patients with end-stage renal failure. An adult form of FSGS and what seems to be a hereditary form of nephrosclerosis are among those that merit further study.

Adolescent↗
PubMed1994

Long-term renal allograft function.

Long-term function of transplanted kidneys was measured as 51Cr EDTA clearance (GFR). All kidneys transplanted in 1985 with preserved function after 6 months were again studied after 12, 24, 36, and 60 months. Grafts lost due to the patient's death were excluded. There was no significant GFR difference at 6 months between grafts with continued function (median 42 ml/min, range 15-79 ml/min; n = 69) and those that failed later (median 39 ml/min, range 20-87 ml/min; n = 18). Median GFR of surviving grafts remained stable, but individual variations included reductions by 5-49 ml in 29 patients and increases by 5-33 ml in 22 patients. Nine of the failing grafts showed a continuous but rarely linear decline, while eight had initially increased GFR. The long-term GFR changes were not statistically correlated with the dosage of cyclosporin at 6 months or with later dose reductions. In conclusion, renal transplant function may deteriorate in the long-term but can also improve.

Adolescent↗
PubMed1992

Glomerular volume in kidneys transplanted into diabetic and non-diabetic patients.

Biopsies taken at the time of renal transplantation in 12 non-diabetic and 23 diabetic patients were studied by quantitative light- and electron-microscopy. Repeat biopsies were taken at 6 months and/or after 2-3 years in patients who had acceptable graft function. All patients except two received cyclosporin as part of the immunosuppression. Glomerular volume was significantly increased, + 36(95% CI +6 to +65) % (p = 0.03), in the diabetic patients at 6 months which differed from the change of -20 (-50 to +10) % in the non-diabetic patients (p = 0.03). After 2-3 years glomerular volume was equal to the baseline value in the diabetic patients, while the change from baseline in the non-diabetic patients was -21 (-42 to -1) %. Substantial glomerular occlusion was seen in only three diabetic patients after 2-3 years. Total structural volumes per glomerulus in the 2-3-year biopsies showed an increase in basement membrane material of 0.09 x 10(6) microns 3 in the diabetic patients, significantly different from the change in non-diabetic patients (-0.10 x 10(6) microns 3, p = 0.003). No correlation was obtained between the 6-month increase in glomerular volume and the development of diabetic glomerulopathy at 2-3 years. The fact that glomerular hypertrophy was not present in the entire series may be due to the cyclosporin and to rejection. Nevertheless the diabetic group did show an early hypertrophy which did not seem to play a major role in the ensuing development of diabetic glomerulopathy.

Adult↗
PubMed1992

Recurrence of SLE in transplanted kidneys: a follow-up transplant biopsy study.

Renal transplant biopsies were obtained from 16 patients with systemic lupus erythematosus 6 months to 11 years post-transplant. Eight biopsies were taken on clinical grounds while eight were elective. Histopathological findings suggesting recurrent lupus nephritis were found in seven biopsies, five of which were taken on clinical indication. By light-microscopy, five graft biopsies showed proliferative glomerulopathy and two glomerulosclerosis. Immunofluorescence was positive for IgM and C3 in a finely granular pattern in all biopsies, for C1q in three, but for IgG in only two. Electron-dense deposits were found in all seven biopsies with predominantly subendothelial location. All but one patient had clinical signs of renal involvement, but only three had extrarenal symptoms and three had serological signs of active SLE. Upon increased immunosuppressive therapy, renal and serological signs improved but one graft was later lost due to recurrent SLE nephritis.

Adolescent↗