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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of recurrent renal disease after transplantation is dependent on an accurate and complete diagnosis of the initial cause of renal failure and a similar determination of the cause of graft failure. To be classified as recurrent, the disease in the renal graft must be identical to that seen in the native kidneys. Recurrence of disease accounts for less than 2% of all graft failures, but the overall incidence of recurrent disease is probably 5 to 10 times more common. The most frequent cause of recurrent disease is glomerulonephritis, which was first recognized to recur soon after renal transplantation was introduced. It was then recognized that a variety of metabolic disorders would recur, but it has taken 25 years of experience for a clear picture to emerge of recurrence in most conditions. No initial cause of renal failure poses a contraindication to at least one attempt at transplantation, although with Fabry's disease and oxalosis, a special assessment of the risks for the individual recipient is warranted. In some patients, experience has shown the need for a delay in the commitment to transplantation (eg, in those with anti-glomerular basement membrane [GBM] antibody glomerulonephritis or Henoch Schonlein purpura), the need for the choice of a particular immunosuppressive regimen (eg, in hemolytic uremic syndrome [HUS]), the need for avoidance of primary nonfunction (eg, in oxalosis), and the desirability of avoiding live kidney donation (eg, in heterozygote donors in Fabry's disease, high-risk recipients with focal glomerulosclerosis, and in recipients with HUS). Probably all types of glomerulonephritis recur, but with great variation in frequency and severity. In some forms of glomerulonephritis, recurrence may be frequent and definite on histopathological criteria but may only have a minor clinical expression (eg, dense deposit disease, anti-GBM antibody glomerulonephritis, IgA nephropathy), but in others, recurrence is less predictable yet it is clearly associated with premature graft failure (eg, focal glomerulosclerosis, membranous nephropathy). A common theme emerging is that where the initial glomerulonephritis is aggressive and causes kidney failure over a short time, recurrence is more likely, and when present, it will lead to graft failure with an increased frequency. Clinical manifestations, the frequency of recurrence, and the prognosis of the graft are now identified for most conditions. Unexpected observations have included the rarity of recurrent systemic lupus erythematosus (SLE), the immediate return of heavy proteinuria in focal glomerulosclerosis, and the predictable return of dense deposit disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Recurrence of disease following renal transplantation. 304 3

To clarify the natural course of gold nephropathy and thereby facilitate its clinical management 21 patients with rheumatoid arthritis who developed proteinuria during treatment with intramuscular sodium aurothiomalate were studied in detail throughout their renal illnesses. Renal biopsies were performed, and creatinine clearance and proteinuria were measured serially for 60 months (range 16-130 months). Ten patients developed proteinuria after six months' treatment, 15 after 12 months, and 18 after 24 months. When treatment was stopped the proteinuria reached a median peak of 2.1 g/day (range 0.7-30.7 g/day) at two months (range 1-13 months) before resolving spontaneously, in eight patients by six months, in 13 by 12 months, and in 18 by 24 months. All patients were free of proteinuria by 39 months, the median duration being 11 months. The median first and last measurements of creatinine clearance showed no significant change (77 ml/minute and 59 ml/minute, respectively), and no patient died from or needed treatment for renal failure. HLA-B8 or DR3 alloantigens, or both, were identified in seven patients. Renal biopsy specimens showed membranous glomerulonephritis in 15 patients, a minimal change nephropathy in two, mesangial electron dense deposits in two, and no appreciable glomerular changes in two. In these 21 patients the proteinuria of gold nephropathy resolved completely when treatment was withdrawn. Renal function did not deteriorate, corticosteroids were unnecessary, and several different renal lesions were seen.
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PMID:The natural course of gold nephropathy: long term study of 21 patients. 311 21

To elucidate the natural course of the nephropathy associated with penicillamine and thereby facilitate its clinical management 33 patients with rheumatoid arthritis who developed proteinuria during treatment with oral penicillamine were studied in detail throughout their renal illness. Renal biopsies were performed, and creatinine clearance and proteinuria were measured serially for 74 months (range 16-148 months). Fourteen patients developed proteinuria within six months after the start of treatment and 27 within 12 months. When treatment was stopped the proteinuria reached a median peak of 4.2 g/24 h (range 0.3-15.0 g/24 h) at one month (range 0-7 months) before resolving spontaneously by six months (12 patients), 12 months (21), or 18 months (29). In all patients but one, who developed carcinoma of the renal pelvis, proteinuria resolved by 21 months and its median duration was eight months. The median first and last measurements of creatinine clearance showed no appreciable change (80 ml/min and 78 ml/min), and no patient died from or needed treatment for renal failure. The HLA-B8 or HLA-DR3 alloantigen, or both, were identified in 10 patients. Renal biopsy specimens showed membranous glomerulonephritis in 29 patients, minimal change nephropathy in two, and electron dense deposits in the mesangial regions in two. In all the patients whose nephropathy was due solely to treatment with penicillamine the proteinuria resolved completely when the drug was withdrawn; renal function did not deteriorate, and corticosteroids were unnecessary.
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PMID:Natural course of penicillamine nephropathy: a long term study of 33 patients. 313 18

The clinical presentation and natural history of 428 patients with biopsy-proven primary glomerulonephritis were reviewed. Minimal change glomerulonephritis presented with the nephrotic syndrome and followed a benign course. Membranous glomerulonephritis took a slow downhill course. HBs antigenaemia was present in 30% of patients with membranous glomerulonephritis. Mesangiocapillary glomerulonephritis often presented with mixed nephritic-nephrotic syndrome and had a bad prognosis. No type II variant was detected. Mesangial IgA glomerulonephritis commonly presented with abnormal urinary sediments although 2.5% of adults presenting with the nephrotic syndrome without glomerular insufficiency had mesangial IgA disease. Mesangial IgA glomerulonephritis was an important cause of end-stage renal failure in Hong Kong.
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PMID:Primary glomerulonephritis in Hong Kong. 317 Jan 12

Four elderly patients developed nephrotic syndrome while receiving sulindac. Sulindac treatment had commenced 4-12 months prior to presentation with the nephrotic syndrome. Two patients also developed oliguric renal failure. Renal biopsy in one showed minimal change nephropathy and in three cases membranous nephropathy. Interstitial nephritis was present on renal biopsy in all cases. The nephrotic syndrome and renal failure resolved in all cases after withdrawal of sulindac. Two patients received steroid therapy and improvement in renal function and disappearance of proteinuria seemed to be temporarily related to steroid therapy in both cases. Despite the fact that sulindac is less likely to cause renal failure due to inhibition of renal prostaglandin secretion this report shows that sulindac treatment can be associated with renal failure and the nephrotic syndrome.
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PMID:Renal failure and nephrotic syndrome associated with sulindac. 320 59

The clinical course of 139 patients (77 male, 62 female) with idiopathic membranous glomerulonephritis is reviewed. The median duration of follow-up was 52 months; 45% and 25% were followed for more than 5 and 10 years respectively. The median age at presentation was 36. Fifty-four percent of patients had the nephrotic syndrome at presentation. Half of the patients were treated at some stage with cyclophosphamide or corticosteroids. During the course of follow-up some deterioration in renal function occurred in only 20% of patients. The patients who suffered deterioration in renal function were mainly male and had significantly worse renal function and a higher incidence of the nephrotic syndrome than the other patients at presentation. Only 7 male patients (5%) developed terminal renal failure during follow-up and one female presented in terminal renal failure. Survival was 88% and 81% at 5 and 10 years. The median predicted (or actual) time for development of terminal renal failure in patients with progressive deterioration was 7.3 years. These data are in accord with other recently published series which have described a relatively benign prognosis for idiopathic membranous glomerulonephritis.
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PMID:Idiopathic membranous glomerulonephritis: long-term follow-up in 139 cases. 321 63

In this article, emphasis is placed on those conditions that appear as the idiopathic nephrotic syndrome but that are more likely to result in progressive renal failure. Four conditions, membranoproliferative glomerulonephritis (mesangiocapillary glomerulonephritis), mesangial proliferative glomerulonephritis, membranous nephropathy, and focal segmental glomerulocosclerosis, account for 12 to 15 per cent of cases of idiopathic nephrotic syndrome during childhood. The further aim of this article is to focus on recent progress in our understanding of these conditions and to remind readers that little is known regarding the etiology and pathogenesis of each, and that effective, clearly proven forms of treatment for each are not apparent currently.
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PMID:Forms of nephrotic syndrome more likely to progress to renal impairment. 329 19

Patients with membranous glomerulonephritis (MGN), impaired renal function and the nephrotic syndrome are at high risk of developing renal failure. Twenty-six such patients were studied with serum creatinine concentrations exceeding 135 microM, and 24-hour urine protein excretion of at least 3.5 g/day to determine the potential benefit of cyclophosphamide therapy. Cyclophosphamide (mean 1.5 mg/kg/day) was given to nine patients for 23 +/- 4 months. These patients were compared with 17 concurrent controls. The two groups did not differ in clinical or laboratory features at the time of biopsy or start of treatment or its equivalent. Six of the nine cyclophosphamide treated patients and 15 of the 17 controls had received prednisone therapy. The total follow-up was 49 +/- 10 months in the treated group and 50 +/- 6 months in the controls. At last observation, serum creatinine values exceeded 400 microM in eight controls (4 on dialysis) and in none of the treated patients. The mean serum creatinine level was significantly lower (P less than 0.02) in the treated group (173 +/- 24 microM) than in controls (433 +/- 71 0.02) in the treated group (173 +/- 24 microM) than in controls (433 +/- 71 microM). The mean serum albumin level and 24-hour urine protein excretion both improved significantly with treatment as compared with controls. There were four complete remissions, five partial remissions and no patient with persistent nephrotic syndrome after treatment. In the controls, there were no complete remissions, six partial remissions and 11 patients had persistent nephrotic syndrome (P less than 0.001). Thus, cyclophosphamide therapy appears to be of benefit in patients with MGN, the nephrotic syndrome and impaired renal function.
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PMID:A controlled trial of cyclophosphamide in patients with membranous glomerulonephritis. 332 96

Twelve HBsAg-negative patients with histologically documented cirrhosis of the liver of either alcoholic (8 of 12) or cryptogenic (4 of 12) origin underwent renal biopsy to investigate proteinuria, hematuria and/or renal failure. Immunofluorescence was positive for IgA in 2 patients with mesangiocapillary glomerulonephritis (MCGN) and could not be performed in 2 additional patients with the same diagnosis. However, in the remaining 8 patients, immunofluorescence was negative for IgA and frequently positive for C3, IgG, IgM and/or fibrinogen. These 8 patients without IgA were classified as follows: MCGN with subendothelial electron-dense deposits (2 cases), IgM-IgG cryoglobulinemia with diffuse endocapillary glomerulonephritis (1 case), membranous nephropathy (1 case), diffuse endocapillary proliferative glomerulonephritis (1 case), vasculitis with focal segmental necrotizing glomerulitis and crescentic glomerulonephritis (2 cases). These results show that cirrhosis of the liver can be associated with a wide variety of glomerular disorders. Contrary to previous belief, IgA is absent in two thirds of patients with cirrhosis and glomerulopathy. Therefore, the pathogenetic importance of IgA in the development of glomerular disease in such patients is doubtful.
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PMID:Glomerular disease in cirrhosis of the liver: low frequency of IgA deposits. 352 93

A case of idiopathic crescentic membranous glomerulonephritis is reported. In addition to the present case, eight cases of this type of glomerulonephritis reported in the literature are reviewed. This is an uncommon form of glomerulonephritis, seen in middle age and in both sexes. Clinical presentation is similar to idiopathic membranous nephropathy. Lupus and antiglomerular-basement membrane nephritis should be excluded by serological tests. Prognosis is grave, resulting in end-stage renal failure (ESRD) within a year in most patients. There is no specific therapy known to alter the course of the disease. In this patient, short courses of high-dose corticosteroids, administered during flares of glomerulonephritis, seemed to improve renal function.
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PMID:Idiopathic crescentic membranous glomerulonephritis. 353 73


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