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Query: UMLS:C0033687 (
proteinuria
)
24,015
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor, was given to 14 patients with unremittent nephrotic syndrome (heavy
proteinuria
with hyperlipidaemia) for 6 months. Treatment was started at an initial dose of 20 mg/day, increasing to a maximum of 80 mg/day. Treatment was well tolerated except in two patients: one developed rhabdomyolysis and one severe hypertriglyceridaemia requiring an additional antihyperlipidaemic agent. Lovastatin was effective in reducing serum cholesterol, LDL-C and apolipoprotein B in the remaining 12 patients. Cholesterol was reduced by 31% from 8.24 +/- 0.49 mmol/l (mean +/- SEM) to 5.7 +/- 0.18 mmol/l after 6 months (P less than 0.001). LDL-C was normalized to 3.26 +/- 0.21 mmol/l from a pretreatment value of 5.76 +/- 0.48 mmol/l (P less than 0.001), a decrease of 43%. Serum apolipoprotein B was also normalized to 1.11 +/- 0.09 g/l from a basal level of 1.51 +/- 0.10 g/l (P less than 0.05). Triglyceride, HDL-C and apolipoprotein A1 concentrations were unchanged.
Proteinuria
as well as renal albumin clearance were unchanged. GFR by plasma radioisotope Cr-EDTA clearance for the whole group was unaltered by treatment. However, among those with relatively good pretreatment renal function (GFR greater than 70 ml/min per 1.73 m2), GFR increased at the end of 6 months' treatment (118.2 +/- 15 ml/min per 1.73 m2 versus 77.6 +/- 8.4 ml/min per 1.73 m2 in wash-out phase).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol
Dial
Transplant 1992
PMID:Lovastatin in glomerulonephritis patients with hyperlipidaemia and heavy proteinuria. 131 86
We have studied glomerular basal laminar thickness in biopsy material, using a simple technique involving 16 selected measurements per case. Twenty-nine biopsied cases of adult glomerular haematuria were examined together with 'diseased' controls represented by a variety of glomerulopathies including minimal-change disease and IgA nephropathy. 'Normal' control populations were provided by 13 patients with acute-onset renal failure of non-glomerular origin and nine patients undergoing nephrectomy. Analysis of groups determined by the presence or absence of haematuria, the degree of
proteinuria
and presence or absence of a diagnostically characteristic immunofluorescence pattern showed that the nine patients with haematuria and
proteinuria
of less than 200 mg/24 h represented a distinct subpopulation with a mean membrane thickness of 225 nm compared to the control mean of 343 nm (P less than 0.0001). All members of this subpopulation had mean values below an arbitrary cut-off value of 270 nm. Within other specific disease categories, sporadic cases had mean membrane thicknesses below this critical value, indicative of an overlap of pathologies. On short-term follow-up there is no evidence that the 'pure' thin-membrane population are subject to any deterioration in renal function. It is of further interest that eight of nine thin-membrane 'syndrome' cases were O Rh positive. This finding may provide a starting point for investigation of a specific genetic defect.
Nephrol
Dial
Transplant 1992
PMID:Glomerular basement membrane thinning in adults: clinicopathological correlations of a new diagnostic approach. 131 88
Diagnostic criteria of analgesic nephropathy with well-defined sensitivity and specificity are not available. During a 2-year period all new patients (n = 273) starting renal replacement therapy in 13 Belgian dialysis units were investigated aiming to select diagnostic criteria of analgesic nephropathy with acceptable performance. Using several interview techniques, a history of analgesic abuse was found in 31% of the patients. Analgesic abusers presenting a clear non-analgesic-related renal diagnosis were excluded from analysis (n = 25). Comparing the remaining abusers (n = 60) and patients without a history of analgesic abuse (n = 188) it was found that renal imaging investigations (sonography plus tomography), showing a decrease in length combined with bumpy contours of both kidneys, presented a sensitivity of 90% and a specificity of 95%. The additional finding of signs of renal papillary necrosis resulted in an overall sensitivity of 72% and a specificity of 97%, giving a positive predictive value of 92%. Other signs frequently mentioned in the literature (hypertension, anaemia, sterile pyuria, bacteriuria,
proteinuria
) showed insufficient sensitivity and/or specificity to be of help for diagnosing analgesic nephropathy in end-stage renal failure (ESRF) patients starting renal replacement therapy.
Nephrol
Dial
Transplant 1992
PMID:Diagnostic criteria of analgesic nephropathy in patients with end-stage renal failure: results of the Belgian study. 132 Feb 26
In this retrospective study we have analysed the rate of progression of renal insufficiency, ascertained from the slopes of the plot of inverse serum creatinine against time, of 102 patients with moderate to severe chronic renal failure (CRF). We have applied 'breakpoint' analysis of the slopes to identify changes in the rate of progression and attempted to determine the factors associated with these changes. Seventy-one patients were found to have progressive CRF, while the remaining 31 had stable or improving renal function. Of the parameters studied, using weighted least-squares analysis,
proteinuria
was the most significant predictor of progression (regression coefficient: -0.1775, P = 0.0075, adjusted r2 = 0.1059). A positive correlation was observed between
proteinuria
and diastolic blood pressure (DBP) (r = 0.336, P = 0.0054). Once the predictive value of
proteinuria
was taken into account, there was no difference in the progression rate between diagnostic groups, other than those patients with polycystic kidney disease who had a significantly faster rate of progression (P = 0.0037). In 49 patients, there was at least one change in the rate of progression with time. There was an inverse correlation between change in slope and a change in DBP (r = -0.352, P = 0.003). We conclude that changes in DBP are often associated with the frequent changes in the rate of progression of CRF. However, a causal link could not be established as in a large number of cases the two changes appeared to occur simultaneously in the absence of changes in antihypertensive therapy.
Nephrol
Dial
Transplant 1992
PMID:Natural history of chronic renal failure: a reappraisal. 132 71
The results of renal transplantation in patients with juvenile-onset diabetes mellitus were compared to those of a well-matched control group of non-diabetic patients. All transplantations were performed between 1977 and 1988. In the diabetic group hypertension (72 versus 41%), coronary artery disease (17 versus 0%), and peripheral vascular disease (19 versus 0%) had been significantly more frequent pretransplantation. Fewer diabetic patients had previously been treated with dialysis therapy (69 versus 97%). Graft function measured by creatinine clearance after 1 year follow-up, and incidence of
proteinuria
were not significantly different. The overall graft survival was significantly worse in the diabetic group compared to the control group: 42 versus 69% after 60 months and 21 versus 62% after 90 months. This was caused by a significantly worse patient survival in the diabetic group after 105 months: 28 versus 78% in the control group. The graft survival following exclusion of the patients who died with a functioning graft did not differ significantly between the groups after 60 and 90 months: 62 and 31% in the diabetic group and 69 and 62% in the control group. The existence of any vascular disease before transplantation, especially pre-existing peripheral vascular disease, had a significant effect on mortality in diabetic patients (P = 0.0003). After transplantation, diabetic patients had significantly more cerebrovascular accidents (23 versus 3%), peripheral vascular disease (31 versus 3%), and number of infections (1.9 versus 1.2). Retransplantation was carried out in each group to the same extent, with the same success rate.
Nephrol
Dial
Transplant 1992
PMID:Increased morbidity and mortality in patients with diabetes mellitus after kidney transplantation as compared with non-diabetic patients. 132 80
The use of 24-h urine protein collections for the assessment of
proteinuria
in renal transplant patients has been compared with the protein creatinine index (PCI) obtained from spot urine samples. Paired data from 148 patients showed a correlation of 0.77 (P less than 0.001) between 24-h protein excretion and the PCI. A PCI of 750 identified
proteinuria
of greater than 1.0 g/24 h with a sensitivity of 89% and a specificity of 93%. The predictive value of a positive test was 81% and that of a negative test 96%. Similar performance was observed for the detection of
proteinuria
of differing severities ranging from 0.5 g/24 h to 2.0 g/24 h. The use of spot testing was popular with both patients and staff, and reduced the sample handling cost to 15% of that of 24-h urine collection. We recommend that PCI be adopted as the standard outpatient test for the assessment of
proteinuria
following renal transplantation.
Nephrol
Dial
Transplant 1992
PMID:Use of the urinary protein creatinine index to assess proteinuria in renal transplant patients. 132 84
Lipoprotein(a) (Lp(a)) has recently been recognized to be a risk factor for coronary heart disease. Lp(a) median values in the absence of renal disease are around 10 mg/dl. Higher levels (greater than or equal to 30 mg/dl) correlate with the occurrence of coronary heart disease, particularly in the presence of elevated cholesterol. We have studied Lp(a) in 76 adults with
proteinuria
. Fifty had glomerular diseases and 26 non-glomerular diseases, with renal function varying from normal to advanced chronic renal failure. Lp(a) values were shifted to the right, with a median of 21.0 mg/dl, and 25% of patients had values of 30 mg/dl or more. Lp(a) did not correlate with cholesterol, age, lipoprotein subclasses, apoproteins A-I or B-100, albumin, creatinine, or creatinine clearance. Median Lp(a) values did not differ significantly comparing men versus women, or glomerular versus non-glomerular disease. Lp(a) may inhibit fibrinolysis, and is deposited in atherosclerotic lesions. Although the cause of these elevated Lp(a) levels is uncertain, we propose that they contribute to the increased risk of coronary heart disease in the nephrotic syndrome, and may play a role in progressive renal disease.
Nephrol
Dial
Transplant 1992
PMID:Lipoprotein(a) in patients with proteinuria. 132 68
Patients with heavy
proteinuria
have an increased incidence of venous thrombosis and coronary heart disease (CHD). They also exhibit perturbations in lipoprotein metabolism. Lipoprotein (a) (Lp(a)) predisposes to CHD; it may also promote intravascular thrombosis since it contains apolipoprotein (a), which could act as a competitive inhibitor of plasminogen activation. We have measured the concentration of serum Lp(a) in 10 men with
proteinuria
due to idiopathic membranous nephropathy (IMN), in eight men with a similar diagnosis but who were in remission, and in 103 healthy men. Serum Lp(a) levels were significantly elevated in the men with active IMN, having a median value of 31.3 (range 3.2-75.0) mg/dl, whereas they were 8.4 (3.4-31.5) mg/dl in the patients in remission, which was similar to the value of 11.3 (< 0.8-87.4) mg/dl found in the healthy controls. Lp(a) is unique in containing an apolipoprotein which is a giant mutant of plasminogen and it is thus possible that the high circulating levels of Lp(a) contribute to the vascular morbidity associated with
proteinuria
by promoting thrombosis or atherogenesis or both.
Nephrol
Dial
Transplant 1992
PMID:Serum lipoprotein (a) in men with proteinuria due to idiopathic membranous nephropathy. 133 76
Membranous nephropathy is a histological appearance which indicates a particular immunopathogenesis, but may have many basic aetiologies and is probably not a single disease. It is predominantly an appearance seen in middle-aged and elderly individuals, and in general has a slow progression over years or even decades towards remission or renal impairment in almost equal proportions. An aggressive search for associated disease is worthwhile, and one should wait to see what the evolution of
proteinuria
and renal function may be. If a progressive course becomes evident, then a trial of treatment with corticosteroids is worthwhile, but if this is ineffective, a more aggressive approach involving the use of alkylating agents may be justified. Cyclosporin does not appear to have a major effect in the majority of patients, and intravenous gammaglobulin is under evaluation at the moment with some encouraging results. The best treatment regime remains to be determined.
Nephrol
Dial
Transplant 1992
PMID:Membranous nephropathy and its treatment. 133 86
To assess the significance of remissions and relapses in idiopathic nephrotic syndrome the outcome of 169 patients was reviewed of them III had either a complete or partial remission. The probability of obtaining a complete remission within 5 years was 44% for the whole group, being significantly higher (P = 0.015) for those patients who had been treated with steroids plus cytotoxic drugs. Of the 74 patients who had complete remission only two showed renal function deterioration over time. Relapse of non-nephrotic
proteinuria
occurred in 22 patients. Of these, 12 again entered complete remission spontaneously, which persisted in nine until the last observation. Relapse of nephrotic syndrome occurred in 42 of III patients. Six patients showed a moderate renal function deterioration. Of 27 untreated patients, 17 had again a partial or complete remission that persisted in 13 until the last observation. All the 15 patients submitted to treatment again entered remission, which persisted in nine of 11 patients given prednisolone and chlorambucil and only in one of four given steroids alone. In conclusion, (a) the development of complete remission is a good marker of an excellent renal outcome, (b) patients with relapse of non-nephrotic
proteinuria
usually carry a good prognosis, (c) about half of patients with relapse of nephrotic syndrome show a spontaneous remission, and (d) the chances of a stable remission may be increased by treatment with steroids and cytotoxic agents.
Nephrol
Dial
Transplant 1992
PMID:Remissions and relapses in idiopathic membranous nephropathy. 133 88
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