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Human lymphocyte antigen (HLA)-identical sibling organs offer the best long-term outcomes for recipients of a renal transplant apart from an identical twin. Unlike cadaveric transplants, however, factors that affect long-term survival of these immunologically privileged grafts are not well described. We reviewed 108 HLA-identical transplants performed at our institution between January 1977 and February 1993. Variables chosen for graft survival analysis were: gender, age and ABO blood type of donors and recipients, panel reactivity antibodies (PRA), blood transfusions prior to transplant, pregnancies, and the underlying renal disease. Additionally, incidence of acute rejection (AR), timing of AR, serum creatinine levels at 1 wk and at 1 yr, and presence of hypertension were included in the analysis. Mean follow-up was 130.9 +/- 58.2 months (range 38-250 months). Actual 5-yr patient and graft survivals were 92 and 88%, respectively. Thirty-eight grafts were lost, and 22 recipients died during the observation period. Death was the main cause of graft failure. Cardiac events accounted for the majority of deaths. AR occurred in 46% and repeated rejections in 11% of recipients. Actuarial graft survival at 10 yr was poorer for patients with any AR (69%), and significantly worse with repeated AR (33%), compared to patients without AR (86%), p = 0.001). Sixty percent of all rejections and 88% of the first rejections occurred in the first 60 d post-transplantation. The first AR that occurred after 60 d was associated with poor graft survival (49 vs. 70%, p = 0.04). Recipients with renal diseases with potential to recur (membranous glomerulonephritis (MGN), membrano-proliferative glomerulonephritis (MPGN), focal and segmental glomerulonephritis (FSGN), polyarteritis nodosa (PAN), rapid progressive glomerulonephritis (RPGN), Henoch-Schoenlein purpura (HSP), diabetes mellitus (DM), interstitial nephritis, systemic lupus erythematosus (SLE) and chronic glomerulonephritis (CGN)) faired worse as a group than recipients with hypertensive nephrosclerosis (HTN), autosomal dominant polycystic kidney disease (ADPKD), Alport's, reflux or congenital dysplasia (68 vs. 96% at 10 yr, p = 0.0009). Poor patient survival was seen in diabetics (71 vs. 88% at 10 yr, p = 0.01). There was a trend to poorer graft survival in diabetic recipients when compared to non-diabetics (65 vs. 81% at 10 yr, p = 0.054). Elevated creatinine at 1 yr was associated with worse graft survival. Likewise, the magnitude of creatinine increase during the first year directly correlated with the risk of graft loss. Hypertensive patients were more likely to lose their grafts than normotensive recipients (72 vs. 86%, p = 0.04). Pre-transplant blood transfusion, pregnancy, and PRA level were not associated with increased graft failure or AR. Graft survival was not affected by gender, age, or ABO blood type of donors or recipients. In conclusion, better prevention and treatment of AR, hypertension, and cardiac disease should improve graft and patient survival. Close attention to recurrence of disease and subtle changes in the creatinine level during the first year might dictate early diagnostic and, hopefully, therapeutic interventions.
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PMID:HLA-identical sibling renal transplantation--a 21-yr single-center experience. 1020 12

Membranous nephropathy is a frequent cause of nephrotic syndrome in adults, and in one third of these patients, it leads to end-stage renal disease. Based on an extensive critical review of the literature, the following recommendations are offered. Oral high-dose corticosteroids are ineffective in producing either a sustained remission of nephrotic syndrome or in preserving renal function in patients with membranous nephropathy, and should not be used as the sole therapy (grade A recommendation). The use of azathioprine is not associated with any significant benefits, so its use is not justified (grade C). The alkylating agents cyclophosphamide and chlorambucil are both effective in the management of membranous nephropathy. Because of growing concern about long-term toxicity, especially with cyclophosphamide, these drugs should be reserved for patients who exhibit clinical features, such as severe or prolonged nephrosis, renal insufficiency, or hypertension, that predict a high likelihood of progression to end-stage renal disease. Chlorambucil in conjunction with oral steroids is the drug of first choice (grade A). Cyclophosphamide and oral steroids are alternatives (grade B). Cyclosporine may, in the future, become the agent of choice for membranous nephropathy. Currently, it is recommended (grade B) that cyclosporine use be considered in patients at high risk for progression in membranous nephropathy or if alkylating agents are contraindicated or ineffective.
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PMID:Management of idiopathic membranous nephropathy: evidence-based recommendations. 1036 95

The diagnosis of diabetic nephropathy (DN) is almost always based on clinical grounds. The diagnosis is supported by a long history of diabetes, evidence of target organ damage and proteinuria preceding azotemia. The validity of this clinical approach is well established in insulin dependent diabetes mellitus but not in non-insulin dependent diabetes mellitus (NIDDM). It is thus important to determine which patients with NIDDM accompanied by non-diabetic renal disease (NDRD) should have a biopsy. However, factors clinically associated with NDRD in patients with NIDDM remain unclear. Therefore we reviewed clinical data, laboratory data and renal biopsies from 22 NIDDM patients who underwent renal biopsy between 1992 and 1998 in Wonju Christian Hospital. From this data, we identified important features that would discriminate between DN and NDRD. There were 8 women and 14 men. Age ranged from 33 to 68 (51.2 +/- 10.7) years. The duration of diabetes at biopsy ranged from 0 to 13 (4.2 +/- 4.2) years. Nephrotic syndrome was present in 13 patients. The patients with NDRD (n = 14) and DN (n = 8) had comparable 24-hour proteinuria, 24-hour albuminuria, creatinine clearance, serum creatinine, albumin, as well as incidences of neuropathy and hypertension. The significant factors that predict the NDRD included a short duration of the diabetes mellitus, the presence of dysmorphic red blood cells in urine, the absence of retinopathy and HbA1c below 9% (p < 0.05, respectively). NDRD included IgA nephropathy (n = 6), minimal change disease (n = 3), membranous nephropathy (n = 3), membranous lupus nephritis (n = 1) and acute interstitial nephritis (n = 1). Multiple logistic regression analysis revealed that the short duration of DM and the absence of retinopathy were factors significantly associated with NDRD. In summary, when there is a short duration of diabetes mellitus, or an absence of retinopathy seen in patients with NIDDM, then renal biopsy in diabetic patients aids in the detection of NDRD.
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PMID:Non-diabetic renal disease in patients with non-insulin dependent diabetes mellitus. 1048 33

Many important aspects of the therapeutic approach to patients with idiopathic membranous nephropathy are still controversial. There are several reports that the effectiveness of therapy depends on histological staging and severity of interstitial mononuclear cell infiltration. We used several different treatments in 39 patients with stage II to III primary membranous nephropathy with proteinuria more than 2.5 g/d, without hypertension and chronic renal failure at biopsy. Ten patients were not treated, 13 were treated with only steroids, 13 with alternate use of steroids and chlorambucil, and three with cyclosporine A. The follow-up period was 5 to 10 years. Statistics included Kruskall-Wallis and one-way ANOVA analysis. A significant decrease in proteinuria was noted in patients treated with steroids (P < 0.01), from 8.45 +/- 1.04 g/d (mean +/- SEM) to 1. 42 +/- 0.45 g/d after follow-up of 5 years and in patients treated with steroids and chlorambucil (12.9 +/- 2.4 g/d [mean +/- SEM] to 2. 46 +/- 1.38 g/d). Compared with patients treated with steroids (15. 3%) and patients treated with steroids and chlorambucil (15.3%), untreated patients had a high frequency of chronic renal failure after 5 years of follow-up (70%) and had a significant increase in mean serum creatinine (P = 0.008). We conclude that steroid therapy alone, or associated with chlorambucil, is effective in patients with stage II to III membranous nephropathy. Patients responded with a decrease of proteinuria and stable renal function during the long-term follow-up period. The group of patients treated with cyclosporine A was too small to analyze.
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PMID:Treatment and long-term follow-up of patients with stage II to III idiopathic membranous nephropathy. 1056 Nov 49

In children, systemic lupus erythematosus (SLE) is often more severe than in adults. Renal disease is very common in SLE, with clinical symptoms of renal involvement occurring in 30%-70% of patients. In the absence of appropriate treatment the child may die from the disease or progress rapidly to renal failure. However, aggressive treatment regimens, in particular corticosteroids, carry the risk of growth retardation, accelerated atherosclerosis, and severe infectious complications. Lupus nephritis is classified into six groups depending on the severity of the histological lesions. The most-appropriate treatment for optimal efficacy with minimal side-effects depends on the disease severity. Mild lesions (class I or II) require only careful follow-up to identify any disease progression. Patients with class III nephropathy (focal and segmental glomerulonephritis) may have mild clinical symptoms, in which case no specific therapy is indicated, or more-severe symptoms of the nephrotic syndrome, hypertension, and sometimes moderate renal insufficiency. These patients require the same aggressive therapy as those with class IV disease (diffuse proliferative glomerulonephritis). Our current protocol starts with three methylprednisolone pulses followed by 1.5 mg/kg per day oral prednisone and six monthly pulses of cyclophosphamide. After a second renal biopsy the patient may be maintained on azathioprine while the prednisone dosage is slowly tapered. In children with milder disease we use lower doses of oral prednisone (1-1.5 mg/kg per day). Patients with membranous glomerulonephritis (class V) require no specific therapy if they have pure membranous nephropathy, but require aggressive therapy if they have the nephrotic syndrome. In those patients who progress to end-stage renal disease, clinical and serological remission is common and renal transplantation can be performed, as recurrence in the transplant is very rare.
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PMID:Treatment of lupus nephritis in children. 1068 69

Membranous nephropathy remains the most common cause of the nephrotic syndrome in adults. Most patients do well with long-term natural history studies reporting a 10-year renal survival of 70% to 90% but the remainder progress to end stage renal failure. This plus the associated morbidity of those with persistent high grade proteinuria makes the decision about the timing and type of treatment difficult. Models have been developed to help predict at an early stage of the disease those at the highest risk of progression and their use is encouraged. The use of nonspecific, nontoxic therapy, ie, angiotensin-converting enzyme inhibitor (ACEI), for both hypertension control and their renoprotective effect is supported by evidence from high-quality studies. Modest dietary protein restriction may be of use but its effect is more controversial. If subnephrotic proteinuria plus normal renal function is present or inducible, conservative therapy and ongoing observation is probably all that is warranted. If high-grade proteinuria (>3.5 g/d) persists then the Italian regime consisting of cytotoxic therapy alternating monthly with prednisone treatment for three cycles has shown the best evidence of long-term induction of remission of proteinuria and preservation of renal function. If this fails or is judged too toxic then a 6- to 12-month course of cyclosporine seems warranted, especially if renal function is deteriorating. Introduction of treatment for risk reduction of both secondary effects of the disease and for modification of the adverse effects of immunosuppressive drugs should be considered in cases with high-grade persistent proteinuria.
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PMID:The treatment of idiopathic membranous nephropathy. 1085 40

Previous reports have clarified that focal and segmental glomerulosclerosis(FSGS) appearing in membranous nephropathy(MN) is associated with a poorer prognosis than that of MN without FSGS. However, the etiology and pathogenesis of such FSGS lesions may show substantial individual differences. In some patients, hemodynamic alterations secondary to hypertension and vascular disorders seem to play a crucial role in the development of such FSGS lesions. In such instances, steady regulation of blood pressure might slow down further progression of FSGS lesions. Here we describe two cases of biopsy-proven MN with FSGS. Case I was a 44-year-old man who had shown massive proteinuria with hematuria at the age of 39 years. Renal biopsy specimens obtained at the age of 40 and 41 years showed MN without FSGS and MN with FSGS, respectively. His blood pressure control was fairly good throughout the course. Although he was on a steroid, an immunosuppressant, a low protein diet, and an ACE inhibitor, his renal function declined in 5 years. Case 2 was a 61-year-old woman who showed nephrotic syndrome at the age of 39 years. A renal biopsy specimen obtained at the age of 58 years showed MN with FSGS and remarkable atherosclerotic changes of the interlobular arteries. Her blood pressure control was rather poor throughout the course. Her renal function gradually declined over 22 years. Since parts of the FSGS lesions of the second case may have been caused by hypertension, it is tempting to speculate that day-to-day control of blood pressure could improve the long-term prognosis. We believe that, at least in some patients of MN with FSGS, careful management may lead to a more favorable course of decline in renal function.
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PMID:[Two cases of idiopathic membranous nephropathy with focal and segmental glomerulosclerotic lesions in which renal function progressively deteriorated]. 1099 19

Fifteen patients of idiopathic nephrotic syndrome who failed to respond to 8 weeks of corticosteroid therapy formed the material for this study. There were 10 males and 5 females, age ranging from 4 to 56 years. Three patients had hypertension. Histological lesions were focal and segmental glomerulosclerosis (FSGS) in 8; membranous glomerulonephritis in 3; mesangial proliferative glomerulonephritis in 2 and membranoproliferative glomerulonephritis in 2 patients. Proteinuria ranged from 3.64 to 8.66 g/1.73 m2/day. Serum albumin ranged between 2.2 to 3.3 g/dl. Serum creatinine was elevated > 1.5 mg/dl in 3 cases. After discontinuing steroids, enalapril was started in a dose of 2.5 mg/day and increased by 2.5 mg/day every 3-4 days till the maximum tolerated dose but not exceeding 20 mg/day. Proteinuria, serum albumin and serum creatinine estimations were done every 4 weeks for six months and every three months thereafter. Patients were followed up for 6 to 30 months. Proteinuria decreased to < 1.5 g/1.73 m2/day in 12 patients (80%) and to < 0.5 g/1.73 m2/day in 10 patients (66.7%) by 8 weeks. There was no significant decrease in proteinuria in 3 (20%) patients; two of these were cases of FSGS and one of membranoproliferative glomerulonephritis. Oedema, hypoalbuminaemia and hypercholesterolaemia returned to normal in all patients who had a decrease in the proteinuria. There was no correlation between the histological lesion and response to enalapril. There was no rise in the serum creatinine level above the baseline in any of the patients. Except for cough in one patient, no other significant side effects were observed. We conclude that enalapril is effective in reducing proteinuria and thereby the morbidity in steroid resistant nephrotic syndrome irrespective of the underlying pathology.
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PMID:Efficacy of enalapril in the treatment of steroid resistant idiopathic nephrotic syndrome. 1099 84

In focal segmental glomerulosclerosis (FSGS), a biphasic change in glomerular size is described in which glomeruli are enlarged with early glomerulosclerosis. Hyperperfusion of larger glomeruli is believed to contribute to progressive glomerular injury. This study was undertaken to investigate whether similar alterations in glomerular size can be found in other renal diseases. Volumes of sclerotic and nonsclerotic glomeruli were estimated in renal biopsy specimens using the Weibel and Gomez method (1962). Glomerulosclerosis was graded on individual glomeruli from 0 to 4, with 0 as no sclerosis and 4 as 76% to 100% sclerosis. Primary and secondary FSGS showed a biphasic change in which grade 2 glomeruli were 50% larger than grade 0 glomeruli and grades 3 and 4 glomeruli were solidified and smaller than grade 0 glomeruli. In essential hypertension, no increase in glomerular size was seen with early glomerulosclerosis, and the latter stages consisted of ischemic obsolescence in which collapsed tufts were 50% smaller than solidified glomeruli of FSGS. Grade 0 glomeruli of membranous glomerulonephritis (MGN) were significantly larger than grade 0 glomeruli of FSGS, and no significant difference in size was seen between grades 0 and 2 glomerulosclerosis. Solidified diabetic glomeruli maintained a large size with grades 3 and 4 sclerosis. Glomeruloscleroses of FSGS, hypertension, MGN, and diabetes have stereologically distinct features. A biphasic change in glomerular size is characteristic of primary and secondary FSGS, but not hypertension, in which tuft collapse supports reduced rather than increased perfusion in the pathogenesis of its glomerular obsolescence.
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PMID:Glomerular size and glomerulosclerosis: relationships to disease categories, glomerular solidification, and ischemic obsolescence. 1192 Mar 32

This retrospective study was carried out in patients with membranous glomerulonephritis (MGN) and repeated pregnancies, the aim being to see how one influences the other. Patients with two or more pregnancies after MGN were included in the study. Nine patients underwent 51 pregnancies (range 2-12, mean 5.6) and 30 were post-MGN (range 2-5, mean 3.2). Their ages were 27-44 (32 +/- 5.7) years. The duration of follow-up was 2-10 (5.6 +/- 2.5) years. The pregnancy outcome, i.e., number of full-term deliveries (FT), spontaneous abortion, preterm deliveries (PT), perinatal mortality (PM), low-birth-weight babies (LBW) and cesarean section (CS), was noted. In the pre-MGN group (n = 21), there were 20 (95.2%) live births and 1 (4.7%) abortion; none had PT, PM, LBW or CS. In the post-MGN group (n = 30), there were 27 (90%) live births, 2 (6.6%) PT, 1 (3.3%) abortion, 1 (3.3%) PM, 3 (10.0%) LBW babies and 3 (10.3%) CS. However, in comparison, there was no statistically significant difference in the pregnancy outcome between the two groups (p > 0.05 in all). Comparing the incidence of hypertension, proteinuria and serum creatinine levels between the first and the last post-MGN pregnancies, there was no statistically significant difference between the two groups. Only 1 patient developed renal insufficiency (serum creatinine 220 micromol/l) after undergoing 5 pregnancies and follow-up of 6 years. In conclusion, the outcome of repeated pregnancies in patients with MGN is good with 90% live births. Repeated pregnancies do not influence the course of MGN.
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PMID:Repeated pregnancies in patients with primary membranous glomerulonephritis. 1202 15


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