Biomedical subjects
Publications and source records attributed to M Sindjić.
Moraxella bovis was repeatedly isolated from cerebrospinal fluid in a girl with two episodes of shunt nephritis. Clinical remission of nephritis was achieved only after shunt replacement. A list of about 20 infectious agents reported to date in patients with shunt nephritis is given. M. bovis is yet another agent previously not reported in patients with shunt nephritis.
Between October 1987 and October 1992 110 biopsies of transplanted kidney. Histologic examination showed 36 cases of acute rejection (Ac), 19 cases of chronic rejection (Chr), 16 cases of acute tubular necrosis (ATN) and 39 cases of cyclosporin nephrotoxicity. Sonographic characteristics as: hyperechogenicity of the cortex, hypoechogenicity of central pyelovascular zone, large and sonolucent pyramids, spherical configuration of renal allograft, were coelating with histologic and relevant clinic sings of disease. The results show statistically significant correlation with sonographic sings of acute rejection and relevant histologic and clinical findings. There was no correlations in other groups of diseases. These results confirm ultrasound as the primary imaging tool and an invaluable diagnostic modality in the renal transplant patient.
Between October 1987. and October 1992. 289 biopsies of the kidney in patients with glomerular diseases were performed. Pathohistologic analysis showed 218 cases with primary and 71 cases with secondary glomerular diseases. In all patients kidneys were measured by ultrasound examinations. The results showed significant difference in longitudinal diameter of kidneys in patients with primary from those with secondary glomerular diseases. These results can help a nephrologist to diagnose glomerular disease.
Jeune's syndrome or asphyxiating thoracic dystrophy is an autosomal recessive osteochondrodysplasia with multisystem involvement. In patients who survive neonatal period in the main clinical feature progressive renal failure is. Renal lesions are variable but is familial juvenile nephronophtisis the most frequent one. We present three patients with Jeune's syndrome phenotype and chronic tubulointerstitial disease. All patients developed terminal renal failure in the eyrly childhood. Renal histology, examined in two cases, was consistent with juvenile nephronophtisis in one case and with renal dysplasia in other case. All our patients had hepatic fibrosis and two of them had pigmentary retinophaty. We want to underline the importance of regular check-up of children with typical phenotype by pediatrician-nephrologist as wel as possibility of prenatal diagnosis of Jeune's syndrome.
We investigated 12 patents with idiopathic membranoproliferative glomerulonephritis. Discriminatory analysis was used for structural functional relationship in order to determine discriminatory power of certain clinical and pathohistological parameters. Semiquantitatively were determined pathohistological parameters: glomerular index in range 0-10, vascular index 1-4, interstitial fibrosis 0-10, interstitial infiltration 0-3, tubular atrophy 0-3. Nephrotic syndrome (symbolic value), quantitative proteinuria and creatinine clearance (continual variable) were used as clinical parameters. Discriminatory power was determined as a degree of decreasing Shennon's entropy dy distinction of patients according to value of creatinine clearance at the time of biopsy. Discriminatory power was measured in the information measurement units (bit). The most powerful was glomerular index (discriminatory power 0.29) in moderately reduced glomerular filtration rate (creatinine clearance 80 ml/min) at the time of biopsy. In severely reduced glomerular filtration rate (creatinine clearance 40 ml/min) vascular index had the greatest discriminatory power (0.24) while interstitial infiltration and interstitial fibrosis had less powerful discriminatory power (0.13). Negative predictive value of reduced glomerular filtration rate at the time of biopsy in membranoproliferative glomerulonephritis has been confirmed in other studies.
We investigated 28 patients with IgA nephropathy. Discriminatory analysis was the method used to determine discriminatory power of certain clinical and pathohistological parameters. Semiquantitatively were determined pathohistological parameters: glomerular index in range 0-10, vascular index 1-4, interstitial fibrosis 0-10, interstitial infiltration 0-3, tubular atrophy 0-3. Nephrotic syndrome (symbolic value), quantitative proteinuria and creatinine clearance at the time of biopsy and year after (continual variable) were used as clinical parameters. Discriminatory power was determined as a degree of decreasing Shennon's entropy by distinction of patients according to value of creatinine clearance at the time of biopsy, and a year after biopsy. Discriminatory power was measured in he information measurement units (bit). Based on discriminatory-predictive analysis we determined that glomerula changes and interstitial fibrosis had an equal effect (discriminatory power) on renal function at the time of biopsy and a year latter, as well as predictive value of these histological parameters and creatinine clearance at the time of biopsy.
Recent data have shown the protective effect of thiol groups on the progression of adriamycin-induced experimental nephropathy, in which reactive oxygen metabolites have been postulated to play an important role. To gain greater insight in the role of glutathione (GSH) in adriamycin-induced nephrosis, we studied changes in reduced GSH level and its associated enzymes in kidney tissue of rats undergoing chronic renal failure produced by i.v. infections of adriamycin (2 x 2 mg/kg b.w.). Kidney damage was characterized by increases in relative kidney weight and BUN levels. The results obtained revealed a 15% drop in renal GSH level in adriamycin-treated animals associated by a similar decrease in the gamma-glutamylcysteine synthetase activity. The activities of kidney glutathione reductase (GR) and glutathione peroxiase (GSH-Px) which are critical constituents of GSH-redox cycle, were significantly decreased (23 an 26%, respectively) in response to adriamycin treatment. Rat kidney glutathione-S transferase and gamma-glutamyl transpeptidase activities were not affected in adriamycin induced nephrosis. We propose that the impairment of renal antioxidant defense, characterized by combined drop in GSH, GR and GSH-Px levels, could permit enhanced free radical induced kidney damage in adriamycin-induced nephropathy.
Cyclosporin A (CyA) was administered at the Clinic of Nephrology, CCS, in treatment of 8 patients with steroid-resistant nephrotic syndrome (NS) caused by focal segmental glomerulosclerosis (FSG), Cyclophosphamide (CP) treatment was attempted in 6 of these cases, but without success. Prior to the onset of CyA therapy, CP treatment was interrupted, and the dose of prednisone was reduced to 0.4 mg/kg/48 h. CyA was applied in the initial dose of 5 mg/kg/bw/24h, and then adjusted so that CyA blood level was 80-120 ng/ml. Although CyA treatment caused proteinuric decrease in most of the patients (from 12.1 g/24 h to 8.2 g/24 h), complete NS remission was achieved in only one patient, the same as the incomplete one. The female patient with a positive response to CyA treatment behaved as "CyA-dependent" and each discontinuation of CyA therapy soon led to recurrent NS. Insignificant CyA effect on NS or renal function was registered in 4 patients, and the therapy was interrupted in two cases due to renal function impairment. Apart from nephrotoxicity, other CyA side effects were absent.
We report the clinical and morphological features of a distinctive hepatorenal disorder in four patients and review the five similar patients in the literature. The main clinical characteristics were early onset of cholestatic liver disease and progressive tubulointerstitial nephritis leading to renal death in early childhood. Liver histology showed disturbed architecture with nodular and acinar formations and portal fibrosis and bile duct proliferation. Histological abnormalities in the kidney were severe interstitial fibrosis and tubular atrophy and dilatation, while the typical features of nephronophthisis were lacking. These clinical and morphological characteristics distinguish our patients from the majority described, as having nephronophthisis and congenital hepatic fibrosis or any other known syndrome with concomitant hepatorenal involvement. We suggest that the association of cholestatic liver disease and progressive tubulointerstitial nephritis represents a new syndrome.
A boy who developed haemolytic-uraemic syndrome (HUS) at 8 years 6 months of age had four further episodes of the disease during the next 3 years. No renal abnormalities were detected between the attacks nor in the 2.5 years after the last recurrence. Reduced levels of serum complement were found during four of the episodes and in two intervening periods.
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