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Biomedical subjects

J Feehally

Publications and source records attributed to J Feehally.

At least 109 records · Page 6Linked to original sources
PubMed1990

The role of continuous ambulatory peritoneal dialysis in end-stage renal failure due to multiple myeloma.

A study in 10 patients (eight male, two female; mean age 61.9 +/- 10.7 years) suffering from multiple myeloma (MM) and end-stage renal failure (ESRF) is detailed. Continuous ambulatory peritoneal dialysis (CAPD) was the preferred mode of chronic dialysis in all the patients. Survival after diagnosis was 32.2 +/- 23.9 months. Survival after starting dialysis was 24.6 +/- 20.6 months. All patients on CAPD were adequately dialyzed and in good fluid control. Peritonitis was the main problem on CAPD (one episode per 5.6 patient-months). The majority of peritonitis episodes responded to intraperitoneal antibiotic therapy. One patient with Staphylococcus aureus peritonitis, septicemia, and neutropenia secondary to chemotherapy, died. Recommendations for prophylaxis and treatment of peritonitis are given. Three patients were transferred to hemodialysis. The use of subclavian vein catheters during hemodialysis was associated with a high incidence of gram-positive septicemia. Alkylating agent-based chemotherapy resulted in hematological responses in five patients. Survival after diagnosis in those responders was 47.4 +/- 25.6 months, compared with 17.0 +/- 7.2 months in the nonresponders (P less than 0.05). All responders subsequently relapsed. Four patients died with progressive myeloma. Bone marrow suppression resulted in a high blood transfusion requirement, neutropenia, and thrombocytopenia associated with bleeding into the gastrointestinal tract and central nervous system. Uremic myeloma patients can be adequately dialyzed using CAPD. Those patients who do not have an initial hematological response have a poor prognosis.

Adult↗
PubMed1990

Effect of nifedipine on renal haemodynamics in an animal model of cyclosporin A nephrotoxicity.

1. This study investigates the effect of nifedipine on cyclosporin A nephrotoxicity in the spontaneously hypertensive rat. 2. Cyclosporin A, administered daily by subcutaneous injection at 25 mg/kg body weight for 14 days, induced a significant reduction in glomerular filtration rate (35.3%) and effective renal plasma flow (45.0%), and an increase in renal vascular resistance (219%). Using this regimen, tubular, glomerular or vascular morphological damage was not evident on light microscopy. 3. The administration of nifedipine simultaneously with cyclosporin A from day 1 prevented the characteristic decline in renal function and increase in renal vascular resistance. However, the administration of nifedipine to spontaneously hypertensive rats previously exposed to cyclosporin A for 7 days failed to improve renal haemodynamics. 4. This study suggests that the beneficial effect conferred by nifedipine on cyclosporin A nephrotoxicity is present only when treatment is initiated simultaneously with cyclosporin A.

Animals↗
PubMed1990

The effect of nifedipine on renal function in normotensive cyclosporin-A-treated renal allograft recipients.

Intrarenal vasoconstriction is a characteristic feature of CsA nephrotoxicity. The influence of nifedipine, a dihydropyridine calcium channel blocker and potent renal vasodilator, on renal haemodynamics was investigated in 11 cyclosporin A (CsA)- and 9 azathioprine (Aza)-treated normotensive long-term renal allograft recipients. Baseline Cr51-EDTA clearance and effective renal plasma flow (ERPF) were similar in both groups. Nifedipine 20 mg twice daily for 28 days significantly increased Cr51-EDTA clearance (+14.8%) in the CsA group; however, ERPF, renal vascular resistance (RVR), and filtration fraction did not change. Nifedipine did not influence renal haemodynamics in the azathioprine group. The increase in Cr51-EDTA clearance in the CsA group did not correlate with baseline renal function, CsA dose or whole blood levels, donor age, duration of graft, or renal functional reserve capacity. This study suggests that nifedipine confers a beneficial effect on renal haemodynamics in long-term CsA-treated renal allograft recipients and appears to improve renal function by a non-haemodynamic mechanism.

Adult↗
PubMed1990

Acute renal failure associated with a labetalol overdose.

A case of acute renal failure in association with a deliberate labetalol overdose is described. The possible pathogenetic mechanisms behind the deterioration in renal function are discussed. Treatment of beta-blockade overdose, with special emphasis on the place of glucagon in such poisoning, is reviewed.

Acute Kidney Injury↗
PubMed1990

Systemic vasculitis in the 1980s--is there an increasing incidence of Wegener's granulomatosis and microscopic polyarteritis?

Thirty-six cases of Wegener's granulomatosis (WG) and microscopic polyarteritis (MPA) presenting to the nephrology service in Leicester between 1980 and 1989 were reviewed. Apart from the diagnostic respiratory tract lesions seen in WG, cases of MPA and WG could not be distinguished by age and sex, range and severity of organ involvement, response to treatment (oral prednisolone and cyclophosphamide), mortality or renal outcome. The combined incidence of WG and MPA in 1980-86 was 1.5/million/year. Following the introduction in January 1987 of an assay for anti-neutrophil cytoplasmic antibody (ANCA), the incidence of WG and MPA increased in 1987-89 to 6.1/million/year (p less than 0.0001). Cases seen during these two periods did not differ by any clinical parameter except that later cases had less severe renal disease at referral and improved renal outcome. Median serum creatinine was significantly lower at presentation in 1987-89 (p less than 0.02). Of those surviving 3 months from presentation only 1/20 in 1987-89 had end stage renal failure compared with 4/10 in 1980-86 (p less than 0.02). These findings may reflect increasing diagnostic awareness of WG and MPA among physicians since the introduction of ANCA.

Adult↗
PubMed1990

Adrenal dysfunction in patients with renal amyloid.

Amyloidosis is a multi-system disease. Renal involvement often leads to end-stage renal failure, which carries a poor prognosis. This paper reports the adrenal status of 22 patients with renal amyloid who were considered for or who had been commenced on renal replacement therapy. Twelve patients were considered or found to have AA amyloid and the remaining 10 had AL amyloid. Of 16 patients tested, seven demonstrated an abnormal response to a synacthen test. Four patients died at Addisonian crisis and hypo-adrenalism probably contributed to the deaths of a further two patients. Amyloid deposition was found in the adrenal glands in seven patients who died of systemic amyloidosis and renal failure. It is recommended that all patients with renal amyloid should have an assessment of adrenal function performed and if abnormal replacement steroid therapy should be commenced.

Adrenal Gland Diseases↗
PubMed1989

Does increasing haemoglobin concentration and haematocrit have a pressor effect in dialysis patients?

The haemodynamic consequences of differing rates of rise of haemoglobin and haematocrit in haemodialysis and CAPD patients were examined. Pre-dialysis mean arterial pressure, weight and haematological indices were recorded in 100 established haemodialysis patients prior to a 2-unit blood transfusion and repeated, pre-dialysis, within 1 week. Haemoglobin rose from 6.7 +/- 0.2 to 9.3 +/- 0.1 g/dl, weight was unchanged, and there was a small fall in mean arterial pressure. Similar indices were recorded, including the mid-arm circumference (MAC) in 100 CAPD patients 1 month after starting CAPD and at the time of maximum haemoglobin within the first year. Haemoglobin rose from 8.5 +/- 0.1 to 10.7 +/- 0.1 g/dl, weight increased slightly, but there was no change in MAC: weight ratio and there was a small fall in mean arterial pressure. In neither group was there a change in antihypertensive medication. In conclusion, increasing the haemoglobin concentration and haematocrit of dialysis patients within the range described in this study did not promote elevated blood pressure.

Adult↗
PubMed1988

Dietary protein manipulation in experimental nephrotic syndrome.

Evidence that glomerulosclerosis may be accelerated by high-protein diet and ameliorated by low-protein diet has led to debate concerning appropriate dietary recommendations in nephrotic syndrome. In this study, dietary protein was manipulated in a chronic, non-uraemic experimental model of nephrotic syndrome. Groups of 12 AS rats received 12, 24 or 48% protein diet after nephrotic syndrome was induced by adriamycin. Animals were sacrificed 8 weeks after change of diet when all were normotensive and none were uraemic. Animals on 24 and 48% maintained initial body weight and had persistent nephrosis. There was renal hypertrophy and histology showed tubular casts, focal tubulo-interstitial injury and glomerulosclerosis. Animals on 48% diet had more renal hypertrophy and worse histological damage but no differences in other parameters compared to 24% diet. On a 12% protein diet animals lost 15 +/- 3% of initial body weight (from 221 +/- 6 to 188 +/- 6 g; p less than 0.001). There was less proteinuria (p less than 0.0001), and lower serum cholesterol (p less than 0.0001) and triglyceride (p less than 0.01). Serum albumin was not different but total protein was lower than on 24 and 48% diet (p less than 0.01). Renal histological damage, although less severe than on 48% diet, did not differ from 24% diet. There was fatty infiltration of the liver. In view of the effects of low-protein diet in this model of nephrotic syndrome, dietary protein restriction should be applied with caution in human nephrotic syndrome.

Animals↗