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D Adu

Publications and source records attributed to D Adu.

At least 109 records · Page 6Linked to original sources
PubMed1989

Reactive oxygen products in heterologous anti-glomerular basement membrane nephritis in rats.

The effect of 'scavengers' of reactive oxygen products (ROPs) was studied in the heterologous phase of anti-glomerular basement (anti-GBM) nephritis induced in rats. Glomerulonephritis was induced by the intravenous administration of sheep anti-GBM antibody (5 mg/100 g) to rats on day 0. The intraperitoneal administration of superoxide dismutase (SOD) 30 mg/kg/day or 150 mg/kg/day leads to a significant reduction in proteinuria on day 1 and also on day 3 in animals given SOD 30 mg/kg/day. Proteinuria was not significantly reduced by the intraperitoneal administration of inactivated SOD (150 mg/kg/day). In rats given polyethylene glycol coupled catalase (PEG-catalase) intraperitoneally at a dose of 10,000 iu/kg/day and 100,000 iu/kg/day proteinuria was lower than in rats with unmodified anti-GBM nephritis. These differences were significant on day 1 (P less than 0.05) in rats given PEG-catalase 100,000 iu/kg/day and on days 3 and 5 in rats treated with either dose of PEG-catalase (P less than 0.01). These data suggest a role for superoxide anion and hydrogen peroxide, or a product of their interaction such as hydroxyl radical, in glomerular injury induced by anti-GBM antibody.

Animals↗
PubMed1988

Does cyclosporin A adversely affect Pneumocystis carinii infection?

Fourteen immunosuppressed patients with Pneumocystis carinii infection presented in two clusters that were separated by 2 years. The diagnosis in all cases was made early by alveolar lavage with cytology. The first group of seven patients was immunosuppressed with cyclophosphamide or azathioprine and prednisolone. All recovered with high dose co-trimoxazole. The second group of seven patients was on prednisolone and cyclosporin A. Despite identical treatment three patients died and a further two who survived lost their grafts from rejection. Our data suggest that cyclosporin A adversely affects the prognosis from Pneumocystis carinii infection and raises the question of prophylactic co-trimoxazole in these patients. The clustering of Pneumocystis carinii infection suggests the possibility of nosocomial transmission although in this study we were unable to implicate person-to-person spread of infection.

Adult↗
PubMed1988

Hypogammaglobulinaemia in nephrotic rats is attributable to hypercatabolism of IgG.

The effect of the nephrotic syndrome induced by puromycin aminonucleoside (PA) in rats on specific antibody responses to 2,4 dinitrophenyl (DNP) conjugated to either spider crab haemocyanin (MSH), a T cell-dependent antigen, or hydroxyethyl starch (HES), a T cell-independent type 2 antigen were studied. The serum IgG anti-DNP levels following immunization with both antigens were reduced in nephrotic animals compared with controls while IgM anti-DNP antibody titres were higher. The half-life of IgG anti-DNP antibodies passively transferred into non-immunized nephrotic rats was markedly reduced while the half-life of anti-DNP antibodies of the IgM class was comparable to that in controls. Low serum IgG and elevated IgM levels were seen in nephrotic animals compared to controls. Antibody-forming cells specific for DNP were demonstrated by immunohistology on rat spleens and the numbers of both IgG and IgM-producing cells were found to be significantly increased (P less than 0.05) in nephrotic animals in response to both DNP-HES and DNP-MSH. These data indicate that in nephrotic rats the alteration seen in the serum immunoglobulin levels is not attributable to reduced antibody production but increased catabolism of serum IgG antibodies.

Agammaglobulinemia↗
PubMed1988

Cyclosporin A and anti-glomerular basement membrane antibody glomerulonephritis in rats.

In a telescoped model of antiglomerular basement membrane (GBM) antibody induced nephritis, Lewis strain rats were injected in the footpad with rabbit IgG on day 0 and then given a single intravenous injection of rabbit anti-rat GBM antibody on day 5. Proteinuria developed within 24 h and renal histology 7 days later showed a focal or diffuse proliferative glomerulonephritis. In this study rats treated as above were given Cyclosporin A (CyA) 20 mg/kg daily by intraperitoneal injection from day 0 or from day 5. Rats given CyA plus anti-GBM antibody developed extensive glomerular infiltration with polymorphs and glomerular thrombosis, lesions not seen with unmodified anti-GBM nephritis or in rats who received CyA alone. The mechanism by which CyA given prior to or at the onset of immunological insult in this model worsens glomerular injury is unclear.

Animals↗
PubMed1987

The role of superoxide anion and hydrogen peroxide in glomerular injury induced by puromycin aminonucleoside in rats.

1. The nephrotic syndrome was induced in inbred female Wistar rats by the intravenous injection of puromycin aminonucleoside (PA) (5 mg/100 g body weight). 2. One group (n = 12) received superoxide dismutase (SOD) (15 mg/kg body weight), a second group (n = 12) received polyethylene glycol coupled catalase (PEG-catalase) (5000 i.u./kg body weight) and the third (n = 9) saline (150 mmol/l NaCl) via the intraperitoneal route, in addition to the PA. 3. SOD and PEG-catalase reduced the 24 h urine protein on days 8 and 15 compared with unmodified puromycin treated animals and this difference was significant on day 15 for SOD (P less than 0.05) and for PEG-catalase (P less than 0.01). Glomerular filtration rate, as measured by the creatinine clearance, was lower in the PEG-catalase group but did not differ significantly from the saline treated group. 4. These data suggest that superoxide anion and hydrogen peroxide, or their reaction products, are involved in the glomerular injury of puromycin nephropathy.

Animals↗
PubMed1987

Rheumatoid arthritis and IgA nephropathy.

We describe four patients with seropositive rheumatoid arthritis who developed proteinuria and microscopic haematuria. Renal biopsy demonstrated a mesangial proliferative glomerulonephritis with mesangial deposits of IgA. These data suggest a possible causal relationship between rheumatoid arthritis and IgA nephropathy.

Adult↗
PubMed1987

Amyloidosis in continuous ambulatory peritoneal dialysis.

We report a 53 year old man with chronic renal failure on continuous ambulatory peritoneal dialysis. Following eight episodes of severe peritonitis over a 2 year period, he died and was found to have widespread AA amyloid at post-mortem.

Amyloidosis↗
PubMed1987

Polyarteritis and the kidney.

We report data on 43 patients with polyarteritis affecting the kidneys. The majority (41 patients) had renal histological evidence of microscopic polyarteritis. Although most patients (30 of 43) had significant renal impairment at the time of diagnosis (serum creatinine greater than 250 mumol/l) only five had a symptom, macroscopic haematuria, that directed attention to the kidneys. In the majority of patients in whom data was available there was rapid deterioration in renal function between presentation and diagnosis. Renal function at diagnosis was worse in patients aged over 50 of whom 20 out of 29 had a serum creatinine greater than 500 mumol/l compared with only four of 14 patients aged less than 50. The prognosis was worse in patients over 50 (41 per cent died), in patients with a serum creatinine higher than 500 mumol/l (54 per cent died) and in patients treated with intravenous methylprednisolone, (four also had intravenous cyclophosphamide) (38 per cent died). The major cause of death was sepsis and the actuarial one-year survival was 62 per cent. These results suggest that our approach to treatment should be modified towards lessening immunosuppression in older patients and in patients with renal failure at diagnosis.

Adult↗
PubMed1987

Changing pattern of acute renal failure.

During the four-year period 1981-1984, 250 patients with severe acute renal failure were treated at one centre. There were seven obstetric cases (2.8 per cent) 118 'surgical' cases (47.2 per cent) and 125 medical cases (50 per cent). This is a different pattern from that seen in the majority of earlier reports. In 60 of the 125 medical patients the aetiology of the acute renal failure could only be determined by renal biopsy. This series suggests that with changing medical practice (particularly the improvement in resuscitation) and an ageing population, the pattern of causes of acute renal failure is altering. It also highlights the value of renal histology as a guide to diagnosis and treatment in patients with unexplained acute renal failure.

Acute Kidney Injury↗
PubMed1987

The glomerular tip lesion: a steroid responsive nephrotic syndrome.

The glomerular tip nephropathy is a cause of the nephrotic syndrome and has distinct pathological features. Glomerular tufts appear normal on light microscopy except for a segmental lesion invariably present in all glomeruli at the origin of the proximal tubule. Data on twenty adults whose renal biopsies demonstrated this lesion and who were followed for a mean of 7.4 years are analyzed. Eighteen patients were treated with steroids; ten of these had complete remission of proteinuria and seven a significant reduction of their proteinuria. Ten patients had moderately impaired renal function (serum creatinine greater than 120 mumol/l) at presentation, eight received steroids and achieved a reduction in serum creatinine. The prognosis was good, with no patient developing chronic renal failure requiring dialysis.

Adult↗