Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0035078 (
renal failure
)
31,970
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The clinicopathological picture of 'isolated C3 mesangial nephritis' was studied in our case records. Focal and segmental or generalised deposits of C3 in the mesangium were found in 12 of 157 (7.6%) patients with primary glomerulonephritis. The clinical picture, similar to Berger's disease, was characterised by episodes of gross haematuria and/or persistent or recurrent microhaematuria and/or proteinuria. Arterial hypertension and mild
renal failure
were observed in one case. Light-microscopy showed minor glomerular changes such as focal and segmental increase of mesangial matrix and mesangial hyperplasia. During the short-term follow-up (median 25.5 months) no deterioration of renal function was observed. The clinical course and short-term prognosis suggest that this form of glomerulonephritis is benign.
Nephrol
Dial
Transplant 1990
PMID:Clinicopathological features in patients with isolated C3 mesangial proliferative glomerulonephritis. 212 68
The present study was undertaken to evaluate three factors which may contribute to the myocardial deposition of calcium oxalate in 5/6 nephrectomised rats: (1) increased plasma oxalate, (2) elevated plasma ionised calcium, and (3) local myocardial tissue damage. A simple increase in plasma oxalate concentrations produced by injection of sodium oxalate did not cause deposits in the heart. Increased plasma ionised calcium combined with elevated plasma oxalate for 60 days was likewise unimportant with regard to cardiac deposits. However, when local tissue damage was added by heterotopic cardiac transplantation, deposition of crystals was seen in four or five allografts damaged by rejection. In this model the rat's own heart was not affected. Although an increase in plasma oxalate values is not without significance, the present findings suggest that local tissue damage is a more important factor in the myocardial deposition of oxalate crystals in
renal failure
.
Nephrol
Dial
Transplant 1990
PMID:Oxalate crystal deposits in the heart in chronic renal failure: an experimental study. 213 Feb 93
In the past, cardiac changes in
renal failure
have commonly been ascribed to hypertension and poorly specified toxic effects ('uraemic cardiomyopathy'). Our recent experimental and clinical studies suggest (a) that cardiac hypertrophy can be dissociated from hypertension and that blood pressures may have only a permissive role, (b) that experimental uraemia is associated with specific activation of pericytes and intermyocardiocytic fibrosis. Cardiac hypertrophy not correlated with elevated blood pressure, and intermyocardiocytic fibrosis not observed in similarly hypertensive non-uraemic patients, have recently been documented in dialysis patients. The implications of these findings may be (a) electrical instability and predisposition to a sudden cardiac death and (b) diastolic cardiac malfunction with impaired LV filling and predisposition to dialysis hypotension. Some evidence for the latter possibility is provided.
Nephrol
Dial
Transplant 1990
PMID:Cardiac changes in uraemia and their possible relationship to cardiovascular instability on dialysis. 215 43
Serum low-molecular-weight proteins, beta-2-microglobulin and alpha-1-microglobulin, were measured in 34 patients undergoing maintenance haemodialysis. There was a strong positive correlation between beta 2M and alpha 1M and predialysis serum creatinine and strong negative correlations between these proteins and 24-h urine volume and creatinine clearance. Good correlation was also demonstrated with total duration of haemodialysis, which also correlated with residual renal function. It is suggested that the elevated beta 2M and alpha 1M in haemodialysis patients merely reflect the severity of
renal failure
and are not directly influenced by the duration of dialysis or type of dialysis membrane.
Nephrol
Dial
Transplant 1988
PMID:Serum low-molecular-weight proteins in haemodialysis patients: effect of residual renal function. 245 34
A 26-year-old female was on continuous ambulatory peritoneal dialysis (CAPD) because of diabetic end-stage
renal failure
. She developed an acute peritonitis that relapsed repeatedly despite appropriate antibiotic treatment. Investigations showed the presence of a splenic abscess, and splenectomy and peritoneal cannula removal were required. The patient died of myocardial infarction two weeks postoperatively. This is the first recorded case of peritonitis secondary to splenic abscess in a CAPD patient. Autopsy findings suggest that the abscess developed from infection of a splenic infarct.
Perit
Dial
Int 1989
PMID:Splenic abscess and peritonitis in a continuous ambulatory peritoneal dialysis (CAPD) patient. 248 87
Glycosylated and carbamylated haemoglobin were determined in patients with uraemia and/or diabetes mellitus. Glycosylated haemoglobin measured by ion-exchange chromatography (HbA1, HbA1c, HbA1a + b) was elevated in non-diabetic uraemic patients, while colorimetrically determined glycosylated haemoglobin was similar to controls. Patients with diabetes mellitus and normal renal function had similar glycosylated haemoglobin concentrations to those with
renal failure
. Both methods showed an excellent correlation, independent of renal function, in patients with diabetes mellitus. The HbA1c component was more influenced by diabetes and the HbA1a + b component was relatively more dependent on renal function. Carbamylated haemoglobin was detected in all subjects, but was grossly elevated in uraemia. Carbamylated haemoglobin significantly correlated with renal function and chromatographically determined glycosylated haemoglobin. Data from this study strongly suggests that the apparent elevation of chromatographically determined glycosylated haemoglobin in uraemia is due to the increased formation of carbamylated haemoglobin. However, in patients with diabetes mellitus, independent of renal function, both the chromatographic and colorimetric methods of determining glycosylated haemoglobin are equally valuable and reliable. The non-enzymatic formation of carbamylated haemoglobin in uraemia has several similarities to glycosylated haemoglobin in patients with diabetes mellitus. Carbamylated haemoglobin may have a clinical role as a marker of uraemia and may also have a pathophysiological relevance.
Nephrol
Dial
Transplant 1989
PMID:Glycosylated and carbamylated haemoglobin in uraemia. 249 61
The effect of pulse intravenous methylprednisolone therapy followed by oral immunosuppression was evaluated in ten patients with idiopathic membranous glomerulonephritis who had developed progressive
renal failure
--a group generally considered to have a poor prognosis. The patients (six male, four female, mean age 50 years) were monitored over 9-30 months during which time creatinine clearance reduced from (mean +/- SEM) 83 +/- 10 to 29 +/- 6 ml/min, and plasma creatinine increased from 135 +/- 22 to 297 +/- 35 mumol/l. All patient were nephrotic with mean 24-h urinary protein excretion ranging from 5.8 to 19.6 g. Treatment administered was pulse intravenous methyl-prednisolone 1 g X 3 then oral prednisolone 30 mg and azathioprine 50 mg (nine patients) or cyclophosphamide 50 mg (one patient). Mean prednisolone dosage was 25 mg at 3 months, 16 mg at 6, and 10 mg at 12 months. Patients have been followed up for between 12 and 57 months on therapy. Creatinine clearance increased to 39 +/- 6, 47 +/- 5 and 48 +/- 18 ml/min after 3, 6 and 12 months treatment with a fall in proteinuria to 6.2 +/- 1.7, 5.7 +/- 1.4, and 3.1 +/- 1.1 g/24h. The deterioration of renal function was reversed in six patients (associated with a reduction in proteinuria to less than 1 g/24 hours in five), slowed in three (with a significant reduction in proteinuria in two), and only one patient with more advanced
renal failure
before treatment progressed to end-stage failure without any retardation of the rate of deterioration or change in proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol
Dial
Transplant 1989
PMID:Immunosuppression can arrest progressive renal failure due to idiopathic membranous glomerulonephritis. 249 75
Rapidly progressive glomerulonephritis frequently leads to death or dialysis. In 21 cases treated by plasma exchange and immunosuppression we observed seven deaths, with 12 others progressing to chronic renal failure within 3 months. Patients who died were older than those who survived (57.5 +/- 17.7 vs 40.5 +/- 16.5 years, mean +/- SD, P = 0.05), but had similar clinical symptoms (hypertension, haematuria, proteinuria, extrarenal signs) and biochemical presentation (initial creatininaemia). They required the same degree of haemodialysis, of plasma exchanges and of bolus methylprednisolone. The causes of death were infection (three cases), cardiac arrhythmia (two cases) and gastrointestinal bleeding (two cases). Among the 14 remaining patients, only two recovered normal renal function. Twelve had chronic renal failure, six of them requiring chronic dialysis or transplantation. Severe
renal failure
at entry and anuria were more frequently observed in patients whose renal function did not improve during treatment. Plasma exchange and steroid bolus infusions also seemed to have a beneficial effect on renal function.
Nephrol
Dial
Transplant 1989
PMID:Plasma exchange and immunosuppression for rapidly progressive glomerulonephritis: prognosis and complications. 249 77
Eight patients with end-stage
renal failure
(plasma albumin less than 35 g/l) who were established on glucose CAPD exchanges, were studied for 4-week periods before, and after 12 weeks when 1% amino-acid solution had been used for the morning exchange. Anthropometric, biochemical, clinical and dietary assessments were made every 4 weeks. Dietary intakes of protein and calories were maintained. Studies with amino-acid solutions showed a mean of 13% and 8% amino acids remaining in the dialysate after 6 and 8 h respectively. Plasma amino acids increased to a maximum after 2 h of dialysis; however, fasting concentrations were constant over the 5 months. Osmolality of amino acids decreased comparably with 1.36% glucose during 8-h exchanges although the recovery of fluid was marginally less. Plasma transferrin increased significantly after 8 weeks of amino acids but subsequently decreased in one patient due to infection. No significant changes occurred in albumin, apolipoprotein A, IgG, IgA or prealbumin. Cholesterol and apolipoprotein B decreased in seven patients but increased in one due to rising calorie intake. Increases in urea and decreases in bicarbonate were not clinically significant. Amino-acid-based fluid was well tolerated with modest nutritional benefit and reduction in hyperlipidaemia. Optimal effects of amino acids are likely at higher concentrations using two or more exchanges in patients eating less than 0.9 g protein/kg per day.
Nephrol
Dial
Transplant 1989
PMID:The use of an amino-acid-based CAPD fluid over 12 weeks. 250 36
The single i.v. dose kinetics of a fixed combination of imipenem/cilastatin were investigated in ten critically ill patients treated by continuous arteriovenous haemofiltration (CAVH). Eight patients suffered from acute renal failure and two had normal renal function. Both drugs were measured in plasma and ultrafiltrate by high-performance liquid chromatography. While the pharmacokinetics of both drugs are almost identical in patients with normal renal function, we found the following dissociation of pharmacokinetic parameters in our patients with
renal failure
: for imipenem the total clearance and elimination half-life was 104 +/- 12 ml/min and 2.2 +/- 0.1 h, respectively, and for cilastatin 29 +/- 10 ml/min and 13.8 +/- 4.5 h. The pharmacokinetics of imipenem and cilastatin differ from each other in
renal failure
because imipenem, unlike cilastatin, undergoes marked elimination by non-renal pathways. Our results did not differ from previously reported data in healthy volunteers and patients with impaired renal function. Elimination of imipenem by CAVH was low (7% of the dose). As a consequence of the unsatisfactory non-renal clearance of cilastatin, however, the fraction of the dose removed by CAVH was significantly greater (approximately 30%) than that of imipenem. This did not, however, correct the dissociation of the pharmacokinetic profiles of the two drugs. In conclusion, the dose of imipenem/cilastatin in critically ill patients with
renal failure
treated by CAVH should be modified according to renal function but elimination by CAVH does not need to be considered.
Nephrol
Dial
Transplant 1989
PMID:Single-dose kinetics of imipenem/cilastatin during continuous arteriovenous haemofiltration in intensive care patients. 251 62
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>