lisinopril and Glomerulonephritis--Membranoproliferative

A 12-year-old boy was admitted in paediatric nephrology unit of Bangabandhu Sheikh Mujib Medical University (BSMMU) with massive proteinuria, hypertension, respiratory distress and anaemia and diagnosed as nephrotic syndrome. Percutaneous needle biopsy was consistent with diffuse endocapillary proliferative glomerulonephritis and initially managed conservatively with injection methyl prednisolone, cyclophosphamide, lisinopril etc. without any improvement. Living-related renal transplantation was done successfully from paternal uncle. Two episodes of acute rejection occurred, one immediately after transplantation and another after one month. These were managed with IV methyl prednisolone for 3 days. At present, he is on oral prednisolone, cyclosporine, azathioprine and antihypertensives with normal haemoglobin and stable serum creatinine level (pre-transplant level 12.5mg/dl to post-transplant level 1.5mg/dl). He has been maintaining his normal life including schooling for last few months. It is concluded that a patient with uncommon presentation of nephrotic syndrome should be confirmed by renal biopsy and renal transplantation may be considered if conservative measures fail.

Topics: Adolescent; Antihypertensive Agents; Azathioprine; Child; Cyclophosphamide; Glomerulonephritis, Membranoproliferative; Glucocorticoids; Graft Rejection; Humans; Immunosuppressive Agents; Kidney Transplantation; Lisinopril; Male; Methylprednisolone; Nephrology

A 44-year-old woman on maintenance hemodialysis was admitted to our hospital because of severe abdominal pain. The patient had been medicated with lisinopril and valsartan for hypertension for one month prior to admission. An abdominal computerized scan (CT) showed a dilated and thickened loop of the small bowel with massive ascites and a small nodule in the jejunum. The patient's abdominal pain was thought to be due to isolated visceral angioneurotic edema induced by lisinopril and/or valsartan, and medication of these two drugs was therefore stopped. Her symptoms resolved and an abdominal CT demonstrated almost complete resolution of ascites and of small bowel edema except for a small nodule in the jejunum. A laparoscopic operation was performed to excise the small nodule of the jejunum, and a histological diagnosis of accessory pancreas of the jejunum was made. This is the first report of isolated visceral angioneurotic edema induced by lisinopril and/or valsartan in a patient on maintenance hemodialysis and, moreover, with the association of accessory pancreas of the jejunum.

Topics: Adult; Angioedema; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Diagnosis, Differential; Female; Glomerulonephritis, Membranoproliferative; Humans; Lisinopril; Renal Dialysis; Tetrazoles; Valine; Valsartan

We evaluated the effect of blocking angiotensin II (AngII) on the development of proteinuria and glomerular injury in antithymocyte serum (ATS) glomerulonephritis. Disease was induced in Sprague-Dawley rats by a single intravenous injection of rabbit ATS. Three groups of rats were considered: group 1 (n = 13), ATS rats with no therapy; group 2 (n = 13), ATS rats treated with angiotensin-converting enzyme inhibitor (40 mg/L lisinopril in the drinking water); and group 3 (n = 13), ATS rats treated with AngII receptor antagonist (50 mg/L L-158,809 in the drinking water). Treatment started 3 hours after ATS injection and lasted 4 days. An additional group of control rats (group 4, n = 13) received preimmune serum. At day 4, ATS rats developed proteinuria (46+/-5 mg/d v control 12+/-1 mg/d; P < 0.01), which was prevented by both lisinopril and L-158,809 (14+/-0.2 mg/d and 15+/-1.6 mg/d, respectively, P < 0.01 v ATS). Systolic blood pressure was comparable in ATS rats and in controls (119+/-4 mm Hg v 120+/-2 mm Hg). Systolic blood pressure values were significantly decreased after either lisinopril or L-158,809 (104+/-3 mm Hg and 101+/-5 mm Hg, respectively; P < 0.01 v ATS). Serum creatinine levels were similar in all groups. Quantitation of proliferating cells and macrophages by analysis of proliferating cell nuclear antigen-positive and ED1-positive cells/glomerular cross-section showed a marked increase in proliferating cell nuclear antigen-positive cells in glomeruli of ATS rats over controls (12.6+/-0.5 cells/glomerular cross-section v 1.9+/-0.2 cells/glomerular cross-section; P < 0.01), which was significantly (P < 0.01) prevented by both treatments (lisinopril, 5.7+/-1.0 cells/glomerular cross-section; L-158,809, 4.8+/-1.5 cells/glomerular cross-section). The increase in ED1-positive cells (10+/-0.7 cells/glomerular cross-section v controls, 1.8+/-0.2 cells/glomerular cross-section; P < 0.01) was also significantly (P < 0.01) reduced by lisinopril and L-158,809 (4.1+/-0.7 cells/glomerular cross-sections and 2.6+/-0.6 cells/glomerular cross-section, respectively). Blocking of AngII activity prevented almost completely the formation of microaneurysms in ATS rats (percent of glomeruli with microaneurysms: ATS, 11.5%+/-3.5%; ATS + lisinopril, 0.4%+/-0.2%; ATS + L-158,809, 0.8%+/-0.8%; controls, 0%). Because AngII is a potent inducer of renal transforming growth factor-beta (TGF-beta), a cytokine involved in the regulation of cell proliferation, matrix deposi

Topics: Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Antilymphocyte Serum; Blood Pressure; Cell Division; Creatinine; Glomerulonephritis, Membranoproliferative; Immunoglobulin G; Kidney; Kidney Glomerulus; Lisinopril; Macrophages; Male; Monocytes; Proteinuria; Rats; Rats, Sprague-Dawley; Transforming Growth Factor beta