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Biomedical subjects

L Grcevska

Publications and source records attributed to L Grcevska.

At least 37 records · Page 2Linked to original sources

Plasmapheresis in treatment of acute oligoanuria in crescentic glomerulonephritis.

Plasmapheresis therapy can provide an approach in the treatment of crescentic glomerulonephritis by mechanically removing nephritogenic factors from the circulation, both antiglomerular basement membrane antibodies and circulating immune complexes as well as antineutrophil cytoplasmic antibodies (ANCAs). We present our experience with plasmapheresis treatment in patients with acute oligoanuria caused by crescentic glomerulonephritis. We used membrane plasmapheresis to treat 11 patients with crescentic glomerulonephritis with more than 80% crescent formation on biopsy and with acute onset of the disease and acute oligoanuria. The immune complex form of the disease was documented in 7, the antiglomerular basement membrane antibodies mediated (anti-GBM) form in 2, the ANCA-associated form in 1 case, and the recurrent anti-GBM form in 1 patient. Plasmapheresis was performed 2-3 times weekly using Bellco BL 500 and Gambro 2000 PF plasma filters. The total number of plasma exchanges (2,000-2,200 ml each) for each patient was 5-9. The treatment was associated with steroids and cyclophosphamide. The improvement of renal function with the start of diuresis and significant decrease of creatinine from the range of 786-1,301 microM at the start of the treatment was noted in 5 of the 11 patients. The duration of remission without hemodialysis was 6-12 months. Treatment with plasmapheresis in cases with recurrent anuria was without benefit. We can conclude that plasmapheresis can delay end-stage renal failure in cases with acute onset of crescentic glomerulonephritis.

Acute Disease↗

Adult familial nephrotic syndrome--Balkan variant of congenital nephrotic syndrome.

We report on two families from the southern part of Former Yugoslav Republic of Macedonia (close to Mediterranean area) with autosomal dominant inherited nephrotic syndrome, documented with renal biopsy in three family members. Histopathological examination confirmed microcystic tubular changes and focal segmental glomerulosclerosis. In biopsied patients proteinuria was noted in the first decade, or second, but it was quantitatively documented as nephrotic in the second and third decade. The prognosis of the patients was poor: one patient died because of intracranial hemorrhage before developing end stage renal disease; the other two cases developed end stage chronic renal failure in the third and fourth decade.

Adolescent↗

Acute renal failure with severe tubulointerstitial changes in a patient with minimal change nephrotic syndrome treated with enalapril.

A 35-year-old nephrotic man developed acute renal failure with serum creatinine to 1543 micromol/l after a month of therapy with enalapril. Renal biopsy demonstrated minimal glomerular changes with fusion of podocytes, tubular necrosis with regeneration of tubular epithelial cells, interstitial edema with focal interstitial fibrosis, and interstitial infiltration with neutrophils, eosinophils, plasma cells and mononuclear cells. Three hemodialyses were performed in the patient during the oliguric phase of the disease. Renal function was restored after withdrawal of enalapril and initiation of steroid therapy. Steroids also contributed to the improvement of the nephrotic syndrome and proteinuria decreased from maximal ranges of 27 g/l to 2.2 g/l after six months of the follow-up. Similar cases were previously described associated with captopril treatment, but not with enalapril.

Acute Kidney Injury↗

[Disorders of renal function in patients with minimal change glomerulopathy].

We report a group of 27 patients with minimal-change nephrotic syndrome who experienced complete recovery from the nephrotic syndrome and the other clinical signs during follow-up. At the start of the examination elevated serum urea was found in 10 (37%) and serum creatinine in 4 (15%) patients. Creatinine clearance was decreased in 10 (37%), systolic blood pressure was elevated in 8 (29%) and diastolic in 11 (41%). Interstitial oedema was found in 3, tubular parenchymal degeneration in 4, slight interstitial mononuclear infiltration in 6 and slight interstitial fibrosis in one patient. Complete recovery of renal function was seen in all patients.

Adolescent↗

Hantaan virus infection with acute renal failure.

We report on 10 patients with acute renal involvement in Hantaan virus infection observed at the Department of Nephrology, Faculty of Medicine, Skopje, Republic of Macedonia, during a period of 3 years (October 1987-July 1990). Eight patients were male and 2 were female, aged 37.5 +/- 4.8 years. The diagnosis of Hantaan virus infection was proven by an indirect immunofluorescent and ELISA test with a significant increase of the titer after a week to ranges from 1:512 to 1:2,048. Percutaneous renal biopsy was performed in 3 cases using standard procedures for optical and immunofluorescent microscopy. Fever, weakness, headache, conjunctival injection, hematuria, and lumbar pain were clinical features all patients had in common. Complete anuria was noted in 7 out of 10 and oliguria in the other 3 of the 10 cases with serum levels of creatinine 967 +/- 152.6 mumol/L. Other following laboratory findings were leukocytosis in 10 out of 10 patients, with neutrophylia, and reduction of serum sodium and potassium in 8 out of 10, and a decrease in serum complement C3 in 3 out of 10 patients. Percutaneous renal biopsy confirmed interstitionephritis in 2 out of 3 biopsied patients and acute diffuse proliferative glomerulonephritis in the third. Interstitial mononuclear infiltration with dominant T cells proven with monoclonal antisera (direct immunoperoxidase method) was present in all 3 cases. The outcome of the disease was good in 8 of the 10 patients with a development of polyuric phase and complete recovery of renal function later. One patient with interstitial lesions on biopsy developed chronic renal failure, and the other with a concomitant brucellosis died during the polyuric phase of the disease.

Acute Kidney Injury↗

Crescentic glomerulonephritis as renal cause of acute renal failure.

Over a period of 5 years, we observed 28 patients with biopsy-proven crescentic glomerulonephritis. Four of these patients were ANCA associated (pauci immune), 1 had anti-glomerular basement membrane antibodies (anti-GBM), and the other 23 cases had immune complex form (22 poststreptococcal and 1 poststaphylococcal). Acute renal failure as a main clinical feature was found in 11/28 (35.7%), all with more than 80% crescents, including all ANCA-associated cases, anti-GBM form, and the patient with poststaphylococcal form. Using "pulse" therapy with methylprednisolone, cyclophosphamide, and plasmapheresis, renal function was improved in 5/11 (45.4%), diuresis started, and end-stage renal disease was delayed. The therapy was continued orally with steroids and cyclophosphamide. The second attach of oligoanuria developed after a period of 6-12 months without improvement after the therapy used previously (during the first attack), and it was necessary to begin chronic hemodialysis treatment.

Acute Kidney Injury↗

Development of renal failure in IgA nephropathy: the importance of interstitial infiltration and deposition of fibrinogen.

We analyzed renal biopsy specimens of 60 patients with IgA nephropathy, 34 male and 26 female, aged 32, 8 +/- 9, 1. Patients were divided into 5 classes according to the morphological classification proposed on the basis of WHO criteria: 1, minimal lesions; 2, minor changes; 3, focal and segmental glomerulonephritis; 4, diffuse mesangial proliferation; and 5, sclerotic changes. Interstitial infiltration on optical microscopy and fibrinogen deposition on immunofluorescent microscopy were graded using a semiquantitative score. Clinical features (hypertension, proteinuria, erythruria/hematuria, renal function) were taken into consideration. The Mann-Whitney test was used for comparison of results between different classes. Classes 1 and 2 were younger (p < 0.01) and had significantly better renal function than classes 3 and 4. Proteinuria was significantly higher in classes 2 and 3 (p < 0.001) than the others. Macroscopic hematuria was more frequent in classes 1 and 2. Hypertension was absent in class 1 and correlated with the severity of histologic changes. Interstitial infiltration was absent in class 1 and also correlated with the degree of histological changes, but in contrast, fibrinogen deposits were more severe in earlier histological classes.

Adult↗

The importance of the clinico-pathological presentations in the evaluation of the survival of patients with IgA nephropathy.

The authors analyzed renal biopsy specimens, clinical data (erythruria/hematuria, severity of proteinuria, occurrence of hypertension and renal failure) and survival (using the original method by Cutler and Ederer) in 60 patients with IgA nephropathy, 34 were male and 26 female aged between 15 and 56 years (32.8 +/- 9.1). The authors divided all cases in 5 classes taking into consideration glomerular changes: class 1 disease-minimal lesions, class 2-minor changes, classes 3-focal and segmental lesions, class 4-diffuse proliferation and class 5 disease-diffuse sclerotic changes. The authors found that: class 1 was younger than the others; macroscopic hematuria was more frequent in classes 1 and 2; proteinuria was significantly higher in classes and 3; and hypertension was absent in class 1 correlating with the severity of glomerular changes. Development of chronic renal failure and occurrence of kidney death also correlated directly with the severity of histologic glomerular classes.

Adolescent↗