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A Háber

Publications and source records attributed to A Háber.

4 recordsLinked to original sources

Altered humoral immunity against cytomegalovirus and Epstein-Barr virus without detectable virus antigens and virus-DNA in the glomeruli of patients with IGA nephropathy in remission phase.

Herpes viruses, such as cytomegalovirus (CMV) and Epstein-Barr virus (EBV), very often occur in the nasopharynx. A pathogenetic role of these viruses in immunoglobulin A nephropathy (IgA NP) is a challenging hypothesis, since upper respiratory tract infections are frequently and closely related in time to the acute episodes of IgA NP. However, conflicting reports have been published in this field. We compared the IgA and IgG antibody (AB) titres against cytomegalovirus (CMV) in sera of 41 IgANP patients with 80 healthy controls. The prevalence rates of CMV-IgA and CMV-IgG AB were significantly higher in patients with IgA NP than in healthy controls (CMV-IgA, titre > = 8, p < 0.001; CMV-IgG, titre > = 16, p < 0.05). There was also a significant difference in the concentration of CMV-IgA AB between IgANP patients and controls (IgA NP: 0.34 +/- 0.66, healthy controls: 0.06 +/- 0.33, mean +/- SD, p = < 0.002), but not in the concentration of CMV-IgG AB between NP patients and controls. While examining 60 patients with IgA NP and 75 healthy controls a significantly elevated prevalence rate of IgA AB against EBV capsid antigen (EBV-VCA) was also detected in the sera of IgA NP patients vs controls (titre > = 16; p < 0.05). There was no significant difference in the prevalence of IgG AB to EBV-VCA between patients with IgA NP and healthy controls, except at titre = 1024 (p < 0.05). At a follow-up, CMV-IgA persisted in 4 of 5, and EBV-VCA-IgA in 8 of 12 seropositive patients with IgA NP. We could not detect virus antigens or virus deoxyribonucleic acid (DNA) in the glomeruli of NP patients either with immunohistology using a monoclonal antibody or with the DNA in situ hybridization technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Long-term phenytoin (Diphedan) therapy leading to IgA nephropathy].

A single case of IgA nephropathy with a concomitant tubulointerstitial nephritis, developing during a long-term phenytoin therapy is reported. The prolonged phenytoin therapy did neither prevent the transitional increases of serum IgA level nor ward off deterioration of the histological alterations. This case suggests that acute tubulointerstitial nephritis may have played a role in the mesangial trapping of IgA immunocomplexes.

Adult↗

Hyperperfusion injury in IgA nephropathy.

The authors have found morphological alterations identical with hyperfiltration glomerular injury in the renal biopsies of 23 out of 100 patients with IgA nephropathy. In 15 of them the lesions were similar to the different stages of segmental glomerular hyalinosis and sclerosis with deposition of IgM and C3. At the time of renal biopsy, the serum creatinine of all except 8 patients was normal (maximally 170 mumol/1), only 13 had hypertension, and all except 2 were proteinuric. During the follow-up period (mean +/- 2Sd = 138 +/- 76 months) all of them became hypertensive. In 10 patients end-stage renal failure developed, and in another 10, serum creatinine also became elevated (range 124 - 504 mumol/1). On the basis of these data the development of focal segmental hyalinosis and sclerosis should be interpreted as a bad prognostic sign in IgA nephropathy.

Adult↗

Hyperperfusion injury in IgA nephropathy.

The authors have found morphological alterations identical with hyperfiltration glomerular injury in the renal biopsies of 23 out of 100 patients with IgA nephropathy. In 15 of them the lesions were similar to the different stages of segmental glomerular hyalinosis and sclerosis with deposition of IgM and C3. At the time of renal biopsy, the serum creatinine of all except 8 patients was normal (maximally 170 mumol/1), only 13 had hypertension, and all except 2 were proteinuric. During the follow-up period (mean +/- 2Sd = 138 +/- 76 months) all of them became hypertensive. In 10 patients end-stage renal failure developed, and in another 10, serum creatinine also became elevated (range 124 - 504 mumol/1). On the basis of these data the development of focal segmental hyalinosis and sclerosis should be interpreted as a bad prognostic sign in IgA nephropathy.

Adult↗