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Bela Ivanyi

Publications and source records attributed to Bela Ivanyi.

6 recordsLinked to original sources
PubMed2006

Primer: Histopathology of calcineurin-inhibitor toxicity in renal allografts.

Calcineurin inhibitors (ciclosporin and tacrolimus) can cause acute and chronic nephrotoxicity. The serum levels of these drugs do not correlate well with the extent of renal damage caused, and the clinical manifestation is nonspecific. Renal biopsy is a reliable tool with which to diagnose calcineurin-inhibitor-induced nephrotoxicity. Ciclosporin and tacrolimus produce identical lesions, which are focal in nature and can be overlooked, necessitating the evaluation of serial tissue sections. Acute toxicity is characterized histologically by necrosis and early hyalinosis of individual smooth muscle cells in the afferent arterioles, and/or isometric vacuolation of the proximal straight tubules; thrombotic microangiopathy is a rare manifestation. In chronic toxicity, the damaged media smooth muscle cells in afferent arterioles are replaced by beaded medial hyaline deposits that bulge into the adventitia; the interstitium displays striped fibrosis and tubular atrophy. As maintenance doses of calcineurin inhibitors in renal transplant recipients have been lowered during the past decade, the incidence of acute toxicity has decreased markedly. Chronic toxicity, however, is still prevalent, and causes chronic allograft damage.

Calcineurin Inhibitors↗
PubMed2006

Primer: histopathology of polyomavirus-associated nephropathy in renal allografts.

The BK polyomavirus exhibits tropism for the renal tubular epithelium, where it establishes latent infection. Vigorous immunosuppression of renal allograft recipients can lead to reactivation of the infection and the development of polyomavirus-associated nephropathy (PVAN). Clinically, gradually decreasing renal function, viremia and viruria are observed several months after transplantation; allograft failure occurs in 1-10% of patients. Definitive diagnosis requires an allograft biopsy. Histologically, viral replication results in tubular epithelial cell enlargement, karyomegaly and nuclear inclusion bodies. The cytopathic changes are often associated with lysis of tubular epithelial cells, denudation of the basement membrane and an interstitial inflammatory response. The involvement is multifocal; distal nephron segments are more severely affected than proximal segments. Changes observed during light microscopy are suggestive but not pathognomonic for PVAN, and the diagnosis must be confirmed by adjunct studies. Adjunct studies consist of immunohistochemistry on paraffin sections using an antibody to the SV40 large T antigen, or electron microscopy of infected tubular epithelial cells (virions 40 nm in diameter). PVAN manifests in three histologic patterns: pattern A, viral cytopathic changes with no or only minimal inflammation; pattern B, cytopathic and cytolytic lesions with interstitial inflammation; or pattern C, predominantly interstitial fibrosis and tubular atrophy, with variable cytopathic and inflammatory changes. These patterns correlate with clinical outcomes.

BK Virus↗
PubMed2006

Thin basement membrane nephropathy: diffuse and segmental types.

CONTEXT: Diffuse thinning of the glomerular basement membrane (GBM) is the ultrastructural diagnostic criterion of thin basement membrane nephropathy (TBMN). However, there is no consensus regarding what diagnosis should be made if the attenuation is segmental. OBJECTIVE: To develop a diagnostic approach to TBMN in cases with segmental GBM thinning. DESIGN: We compared the diagnostic sensitivities of 2 methods used for the quantitative expression of GBM width in a consecutive series of renal biopsies from 26 patients (median age, 36 years; range, 15 to 59 years) with dysmorphic hematuria (a variable degree of proteinuria in 19 patients), a thin GBM, and absence of other renal disease. The harmonic GBM width was determined from orthogonal intercepts, and the actual width in the thinnest loops was obtained by direct measurement. The GBM attenuation was categorized into diffuse or segmental types by conventional inspection. RESULTS: Segmental TBMN accounted for one third of the series. In neither type did the male patients have a higher harmonic mean GBM width than the female patients. Focal-global glomerulosclerosis was more common in diffuse TBMN. The laborious orthogonal intercept method proved insensitive for the verification of segmental TBMN, whereas the much simpler direct measurement technique captured all the cases. CONCLUSIONS: A considerable number of patients with TBMN display segmental GBM attenuation. Because the routine criterion excludes these cases from the diagnosis, we propose to define TBMN as a clinicopathologic entity of dysmorphic hematuria and a diffusely or segmentally thinned GBM confirmed by the direct measurement technique.

Adolescent↗
PubMed2002

L-carnitine ameliorates gentamicin-induced renal injury in rats.

BACKGROUND: This study examined whether administration of L-carnitine ameliorates gentamicin-induced renal injury in rats. METHODS: Male Sprague-Dawley rats were assigned to one of seven treatment groups: group A (control) rats were given normal saline injections daily for 8 consecutive days; group B, C and D rats were given gentamicin injections, 50 mg/kg body weight/day daily for 8 consecutive days; and group E, F and G rats were given gentamicin injections, 80 mg/kg/day daily for 8 consecutive days. Starting 4 days before these injections, all groups were given additional injections, for 12 consecutive days, of normal saline (groups A, B and E) or L-carnitine at 40 mg/kg (groups C and F) or 200 mg/kg (groups D and G). Histological scoring of renal cortical pathology was performed after day 12. RESULTS: Among rats injected with gentamicin 50 mg/kg/day, those given either 40 or 200 mg/kg/day of L-carnitine had higher creatinine clearances at day 12 than the rats not given carnitine. In the rats given 80 mg/kg gentamicin and no carnitine, renal function tended to be lower than in controls. At day 12, the rats given gentamicin 80 mg/kg and L-carnitine 200 mg/kg/day, compared with rats given gentamicin 80 mg/kg and no carnitine, displayed lower serum urea and probably creatinine concentrations, and higher creatinine clearances, and their serum urea was not different from control (group A) rats. Both doses of gentamicin induced renal cortical histopathology. Changes were milder with gentamicin 50 mg/kg/day, and L-carnitine, particularly at 200 mg/kg/day, ameliorated the severity of renal pathology induced by both gentamicin doses. In rats given gentamicin 80 mg/kg/day, the animals treated with carnitine 200 mg/kg/day had significantly less severe proximal tubular necrosis and significantly greater mild proximal tubular necrosis compared with rats receiving L-carnitine 40 mg/kg/day or no carnitine. CONCLUSIONS: In rats receiving gentamicin, daily L-carnitine injections, particularly at 200 mg/kg/day, ameliorate the severity of renal cortical proximal tubular necrosis and maintain greater renal function.

Animals↗