[Causes of perinatal hypoxia. Clinical and pathomorphologic studies].
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Asphyxia Neonatorum↗
Biomedical subjects
M Sindjić
Publications and source records attributed to M Sindjić.
[IgA nephropathy in children with various clinico-histologic features and therapy].
Clinical and hystological features of IgA nephropathy were evaluated in 17 children (age range 6 to 14 years). Hematuria was present in all patients (macroscopic hematuria in 10 patients, microscopic hematuria in 7). Mild to moderate proteinuria was present in 10, nephrotic syndrome in two cases. The majority of renal biopsy showed normal picture of mild mesangial proliferation, with crescents in only one patient. Transient impairment of renal function developed in two patients. One of patients progressed to chronic renal failure. Four patients were treated (two with persistent proteinuria, one with nephrotic syndrome, one with nephritic syndrome). Corticosteroid treatment resulted in aggravation of proteinuria in two patients with persistent proteinuria. Patient with nephrotic syndrome demonstrated only diminution of proteinuria during different treatments: corticosteroids, ciclophosphamid and Ciclosporin A. Ciclophosphamid was beneficial in patient with nephritic syndrome.
Adolescent↗
[Functional and histologic changes in the kidney in copper poisoning in rats].
The acute intoxication (by intraperitoneal way) and chronic intoxication (by inhalation, during one year) were carried out with pure copper. On the basis of experimental studies, it was established that the kidney was a critical organ in copper intoxication. On all rats acutely intoxicated damages of the function (similar to Fanconi's syndrome in Wilson's disease), diffuse pathologic lesions and presence of fine copper particles in protoplasm of proximal tubule epithelial cells, were found. By chronic intoxication it was proved that the organism could be loaded with copper through inhalation of copper particles. In chronic intoxication damages of renal functions were insignificant, but very heavy pathohistologic lesions were only focal and they influenced glomerules, proximal tubules, initial parts of Henle's loop and interstice. Copper was found in the form of strip-like deposits in glomerules and proximal tubule basal membrane, then in the form of fine and coarse granules in protoplasm of proximal tubule epithelial cells.
Animals↗
[Shunt nephritis. 2 case reports and a review of the literature].
Two cases of glomerulonephritis associated with colonization of cerebrospinal fluid shunts inserted for the treatment of hydrocephalus (shunt nephritis) are described and additional 113 cases reported in world literature, are reviewed. Both of our patients were affected by two episodes of shunt nephritis. Complete clinical remission of renal disease followed antibiotic treatment in one patient, and shunt replacement combined with antibiotic therapy in the other. In the 115 cases of shunt nephritis reported to date, the causative organisms, clinical features, pathogenesis, renal histology, treatment, and outcome are discussed in detail. The importance of regular observation for early recognition of this reversible form of glomerulonephritis, is emphasized.
Cerebrospinal Fluid Shunts↗
Therapy of rapidly progressive glomerulonephritis with immunosuppressive agents.
Rapidly progressive glomerulonephritis is a kidney disease leading to sudden and definitive damages of the renal parenchyma and progressive impairment of its function until the complete failure. Histological findings of the changes are characterized with dominant glomerular lesions with crescentic formations. Early and intensive immunosuppressive therapy with pulse doses of steroids (Solumedrol 1.5 to 2.5 g), followed by Prednisolone 1 mg/kg every other day and cytostatic drugs (cyclophosphamide 1-2 mg-kg/every other day) discontinues the processes of specific and non-specific inflammation in the kidney and could enable regeneration of the kidney tissues with favorable outcome of the disease. Immunosuppressive therapy should be gradually lowered after two months, and applied for at least three to six months.
Acute Kidney Injury↗