1/52. Fibrillary glomerulonephritis in a renal allograft.Fibrillary glomerulonephritis is an uncommon disease seen in approximately 1% of all native kidney biopsy specimens. We present here a case of a 40-year-old white woman with the rapid loss of graft function secondary to fibrillary glomerulonephritis within 7 days of receiving a living-related renal allograft. This case emphasizes the values of combining urinalysis with prompt allograft kidney biopsy in recipients with an elevated serum creatinine posttransplantation. When one encounters rapidly progressing glomerulonephritis or a pulmonary-renal syndrome in the immediate posttransplantation period, fibrillary glomerulonephritis must be considered in the differential diagnosis. Because of a high recurrence rate and no available treatment to modify a potentially malignant course of this disease, we recommend caution when considering these patients for transplantation.- - - - - - - - - - ranking = 1keywords = kidney (Clic here for more details about this article) |
2/52. nephrotic syndrome with mesangial proliferative glomerulonephritis induced by multiple wasp stings.We report the case of a young male who developed severe nephrotic syndrome within 2-3 weeks after being stung by 3 wasps. A percutaneous kidney biopsy specimen revealed mesangioproliferative glomerulonephritis with occasional subepithelial deposits suggestive of early membranous nephropathy. The patient was treated with oral prednisone 60 mg/day with no significant clinical response after 4 weeks, at which point he was started on oral cyclophosphamide, 100 mg/day, while the prednisone dose was tapered to 20 mg every other day over a 2-week period. Six months after initiation of cyclophosphamide, he still has severe nephrotic syndrome. We also briefly review the literature on hymenoptera sting associated nephrotic syndrome.- - - - - - - - - - ranking = 0.5keywords = kidney (Clic here for more details about this article) |
3/52. Membranoproliferative glomerulonephritis with subendothelial deposits (type 1) associated with hepatitis G virus infection in a renal transplant recipient.BACKGROUND: infection with hepatitis b virus (HBV) or hepatitis c virus (HCV) is a well-known etiology for membranoproliferative glomerulonephritis (MPGN) with subendothelial deposits (MPGN type 1). MATERIAL AND methods: The newly discovered hepatitis G virus (HGV) is currently under active investigation. We report the first case of de novo MPGN type 1 associated with HGV infection in a young male renal transplant recipient who manifested glomerulonephritis (GN) with proteinuria 7 years after transplant, and whose original disease was chronic obstructive pyelonephritis secondary to nephrolithiasis. RESULTS: serum markers for HBV and HCV infections were negative. HGV infection was detected by specific double-nested reverse transcriptase-polymerase chain reaction (RT-PCR) in sera (positive HGV viremia) 2.5 years after renal transplantation. By specific in situ RT-PCR, the presence of the HGV genome was detected in peripheral blood mononuclear cells and in the kidney biopsy (glomeruli and tubules), but not in the liver. CONCLUSION: This report adds new information on the role of HGV infection in the occurrence of de novo GN (MPGN type 1) in renal transplantation.- - - - - - - - - - ranking = 0.5keywords = kidney (Clic here for more details about this article) |
4/52. Low serum C3, leukopenia, and thrombocytopenia: unusual features of henoch-schonlein purpura.Henoch-Schonlein purpura (HSP) affects predominantly the skin, joints, gastrointestinal tract and kidney. Although the pathogenesis is probably of immune origin and complement activation is thought to play a role, laboratory findings including the serum level of the complement components are usually normal. We present a patient with a severe form of HSP nephritis who had unusual laboratory findings of a low level of C3, mild leukopenia and thrombocytopenia. These findings may further support the importance of complement activation in the pathogenesis of HSP.- - - - - - - - - - ranking = 0.5keywords = kidney (Clic here for more details about this article) |
5/52. Recurrent type I membranoproliferative glomerulonephritis in a renal allograft: successful treatment with plasmapheresis.Recurrent disease is increasingly recognized as a cause of renal allograft dysfunction and failure. We describe a patient with type I membranoproliferative glomerulonephritis not associated with hepatitis c. The glomerular disease recurred in the renal allograft within 1 month of transplantation, leading to acute allograft dysfunction and nephrotic syndrome. Aggressive treatment with prednisone and plasmapheresis resulted in improvement in kidney function, improvement of the light microscopic picture, and removal of immune complexes from the glomerular subendothelial space.- - - - - - - - - - ranking = 0.5keywords = kidney (Clic here for more details about this article) |
6/52. Type I membranoproliferative glomerulonephritis in a renal allograft: A recurrence induced by a cytomegalovirus infection?A 40-year-old white woman with end-stage renal disease from idiopathic type I membranoproliferative glomerulonephritis (MPGN) developed proteinuria and renal dysfunction 7 weeks after cadaveric donor renal transplantation. At the same time, a primary cytomegalovirus (CMV) infection was diagnosed. Complement levels were low. A renal biopsy disclosed an acute exudative proliferative glomerulonephritis with influx of polymorphonuclear granulocytes (PMNs), with granular deposits of C3, C1q, IgG, and IgM. The immunofluorescence (IF) and electron microscopy (EM) findings were compatible with an early stage of a type I MPGN. CMV could not be detected in the glomeruli nor elsewhere in the kidney by IF or EM. The patient was treated with ganciclovir. In a renal biopsy 3 weeks later, the exudative lesions had disappeared, and some glomeruli now showed the characteristic lesions of a type I MPGN with an increase of mesangial cells and matrix, and reduplication of the glomerular basement membrane. Over the following period, repeated biopsies were performed. The activity of the glomerular inflammation and immune complex deposits paralleled the waxing and waning of the CMV viral load. After 10.5 months, the graft was removed because of a life-threatening systemic fungal infection. At that time, the CMV infection had cleared, and in the transplantectomy material, the membranoproliferative pattern of injury had disappeared, and in the glomeruli hardly any deposits were found. These data strongly suggest that a primary CMV virus infection can induce an apparent recurrence of type I MPGN.- - - - - - - - - - ranking = 0.5keywords = kidney (Clic here for more details about this article) |
7/52. Unusual presentation of mesangial proliferative glomerulonephritis in hellp syndrome associated with acute renal failure.Acute renal failure in pregnancy is not common in industrialized countries. hellp syndrome (hemolysis, elevated liver enzyme, and low platelets) was one of the causes of acute renal failure in pregnancy, but renal pathological findings in case of acute renal failure had rarely been reported. We reported an unusual case of hellp syndrome with acute renal failure requiring renal replacement therapy and which histopathologic findings of kidney biopsy showed mesangial proliferative glomerulonephritis and her renal function completely recovered after immediate artificial abortion, supportive management, transfusion of blood products, and hemodialysis.- - - - - - - - - - ranking = 0.5keywords = kidney (Clic here for more details about this article) |
8/52. Dramatic worsening of vascular calcifications after kidney transplantation in spite of early parathyroidectomy.vascular calcification is a common feature in chronic dialysis patients, but their clinical significance is debated and the role of kidney transplantation (TP) in the natural history of their development has received scanty attention. We will describe a case of dramatic worsening of vascular calcifications during TP in a young patient in spite of early and successful parathyroidectomy (PTX), and will discuss other causes which might be putatively linked to vascular damage during the time of TP. A 37-year-old man on regular dialytic treatment (RDT) for 11 years, received his first cadaveric transplantation in January 1993. He underwent PTX 6 months after TP because of the lack of decreasing in parathyroid hormone values despite normal graft function. Although PTX was effective, a dramatic worsening was evident in large as well as in medium and small-sized arteries during the following three years of TP. In February 1997, few months after starting dialysis again because of the recurrence of his primary membranoproliferative glomerulonephritis (MPGN), the patient experienced myocardial infarction followed by aorto-coronary bypass (right coronary artery and anterior descending coronary artery) and leg "claudicatio". Though a role for parathyroid hormone in vascular disease has been commonly accepted, the case here reported clearly shows that blunting parathyroid gland activity may be unable to avoid the worsening of a process of vascular disease during the time of TP. Many other factors--linked to the time of TP--may be involved in vascular diseases, such as nephrotic syndrome, dyslipidemia, hypertension and drugs. In the case of our patient, a clear cut risk factor for his progressive atherosclerosis can be designated hyperlipidema and other disturbancies secondary to a nephrotic syndrome due to relapse of MPGN, together with persistent hypertension. This is the first case report in the English literature which clearly demonstrates that TP may add fuel to the fire of vascular disease also in young people and even in the absence of parathyroid hyperactivity, perhaps on the basis of a favorable genetic background. Furthermore, the history of our patient demonstrates that vascular calcifcation heralds major cardiovascular diseases.- - - - - - - - - - ranking = 2.5keywords = kidney (Clic here for more details about this article) |
9/52. Renal involvement in juvenile rheumatoid arthritis: report of two cases.Renal involvement is a rare occurrence in juvenile rheumatoid arthritis (JRA). We report on two JRA patients with kidney disease. The first was a 14-year-old African-American female with a 12-month history of polyarthritis. On presentation she was found to have an ESR of 127 mm/h and a positive ANA, rheumatoid factor (RF), perinuclear antineutrophil cytoplasmic antibodies (pANCA), haematuria, proteinuria with normal BUN and creatinine. Renal biopsy showed focal segmental glomerulosclerosis. Her renal function deteriorated to end-stage renal failure requiring dialysis within a few months, despite aggressive treatment with steorids and monthly i.v. pulses of cyclophosphamide. The second patient presented with a 6-week history of polyarthritis and intermittent fever, and had a salmon-coloured evanescent rash. On presentation his laboratory evaluation was significant for elevated ESR and negative ANA, RF and ANCA tests. Within 8 months the patient had developed a persistent microscopic haematuria. Renal biopsy showed mild mesangial glomerulonephritis. On low-dose methotrexate therapy his JRA went into remission and his renal function remained normal. The haematuria persisted for 1 year and then resolved spontaneously. This is the first time that focal segmental glomerulosclerosis and mesangial glomerulonephritis have been described in JRA. Although the association may be just coincidental, further studies are needed to define the role of JRA in these renal conditions. In patients with JRA, urinalysis and renal function should be routinely monitored.- - - - - - - - - - ranking = 6.1903111281226keywords = kidney disease, kidney (Clic here for more details about this article) |
10/52. Mesangial proliferative glomerulonephritis with deposits of anti-nicotinic acetylcholine receptor antibody in a patient with myasthenia gravis.A patient with myasthenia gravis developed nephrotic syndrome 3 years after thymectomy. The kidney biopsy specimen revealed mesangial proliferative glomerulonephritis with immune deposits. The glomerular mesangial cells and tubular epithelial cells were sensitive to alpha-bungarotoxin (alpha-BT), a ligand for nicotinic acetylcholine receptor (nAChR), and the binding was inhibited by native alpha-BT, as well as other nAChR ligands, nicotine and d-tubocurarine. In addition, FITC-alpha-BT-neuromuscular junction complexes could also bind to the mesangial cells, and preincubation with unlabeled nAChR inhibited the binding. These findings are consistent with the notion that both nAChR-like protein and anti-nAChR antibody are present in t he mesangial cells of the patient. Although the pathogenetic role of anti-nAChR antibody on the development of glomerulonephritis is unclear, the present observations provide an important insight into the autoimmune-mediated pathophysiological relationship between myasthenia gravis and mesangial proliferative glomerulonephritis.- - - - - - - - - - ranking = 0.5keywords = kidney (Clic here for more details about this article) |
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