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Biomedical subjects

D H Clyne

Publications and source records attributed to D H Clyne.

14 recordsLinked to original sources
PubMed1988

Alport's syndrome: risk of glomerulonephritis induced by anti-glomerular-basement-membrane antibody after renal transplantation.

Two patients with Alport's syndrome developed glomerulonephritis induced by anti-glomerular-basement-membrane (anti-GBM) antibody after renal transplantation. One patient presented at 5 months after transplantation the second patient 18 months after transplantation. Both grafts failed and the patients returned to dialysis. Our observations suggest that the patients with Alport's syndrome are at risk of developing anti-GBM antibody type glomerulonephritis in the transplanted kidney. This does not occur in the early period after transplantation, probably because of heavy immunosuppression.

Adult↗
PubMed1984

Abnormalities of fibrinolysis in essential hypertension.

A highly-standardized plate method was used to study fibrinolytic profiles in 14 patients with essential hypertension and 245 normotensive healthy control subjects. Compared with the normotensive group, the group with essential hypertension showed a defect in fibrinolysis, as evidenced by a significant increase in the mean level of inhibitor of plasminogen activation, and a subset of the hypertensive patients also showed a significant decrease in the mean level of vascular plasminogen activator. There were no significant differences between the two groups in relation to plasma fibrinogen level, total fibrinolytic activity and plasmin inhibitor. The alterations in inhibitor of plasminogen activation and vascular plasminogen activator in the patients with essential hypertension may reflect a defect in the fibrin-clearing mechanism and, perhaps, contribute to the vascular complications of hypertension.

Adult↗
PubMed1979

Nephrotoxicity of Bence Jones proteins in the rat: importance of protein isoelectric point.

Bence Jones proteins (BJP) were isolated from the urine of 12 patients with multiple myeloma and various degrees of renal dysfunction. Proteins were characterized as to type (six type lambda and five type kappa), isoelectric point (pI), and secondary structure by circular dichroism (CD). Clinical renal function was more impaired with type-lambda proteins and with proteins of pI greater than 5.7. CD studies distinguished kappa from lambda proteins in most cases but did not correlate with nephrotoxicity. Protein dimer preparations were tested for nephrotoxicity in aciduric, hydropenic, female, Sprague Dawley rats by following renal function and morphology over 6 hours after injection i.p. of 300 mg of protein. Twelve rats of urine pH less than 5.5 injected with four BJP of pI less than 5.7 showed a mean rise in SUN of 5.3 mg/dl and in creatinine of 0.06 mg/dl, compared with a mean rise of 28.0 mg/dl (SUN) and 0.75 mg/dl (creatinine) in 21 rats injected with seven BJP of pI greater than 5.7 (P less than 0.01). Seven sodium-bicarbonate-fed rats of urine pH greater than 8 injected with a BJP of pI 6.2 showed mean rise in SUN of 1.8 mg/dl and in creatinine of 0.01 mg/dl, compared with 19.3 mg/dl (SUN) and 0.55 mg/dl (creatinine) in 7 aciduric rats injected with the same BJP (P = 0.009). Morphologic and immunohistologic studies showed distal cast formation in 9 rats with acute deterioration in renal function. It is concluded that BJP of pI greater than urine pH are acutely nephrotoxic in the rat by a mechanism that may involve a charge interaction in the distal nephron.

Animals↗
PubMed1979

Nephrotoxicity of low molecular weight serum proteins: physicochemical interactions between myoglobin, hemoglobin, bence-jones proteins and tamm-horsfall mucoprotein.

Three types of low molecular weight serum proteins, myoglobin, hemoglobin and BENCE-JONES proteins, are associated clinically with acute renal failure. All have isoelectric points which render them anionic at blood pH but cationic in the distal nephron under conditions of aciduria. Experiments in which these proteins were mixed with TAMM-HORSFALL mucoprotein in vitro and the pH lowered with lN HCl showed co-precipitation of proteins at pH levels of 5.5 and below. In vivo experiments in which 11 different BENCE-JONES proteins of pl ranging from 5.2 to 6.6 were injected into aciduric, hydropenic rats showed an acute rise in serum urea nitrogen and creatinine concentrations with BENCE-JONES proteins of pl greater than 5.7 compared with little change in rats injected with BENCE-JONES proteins of pl less than 5.7. These data suggest that protein pl and urine pH are important in determining nephrotoxicity; a mechanism by which these low molecular weight serum proteins and TAMM-HORSFALL proteins interact in the distal nephron to initiate acute renal failure in postulated.

Acute Kidney Injury↗
PubMed1978

Carbenicillin nephrotoxicity.

A patient with biopsy-proven interstitial nephritis associated with nafcillin and dicloxacillin therapy developed fever, hematuria, pyuria, and renal insufficiency after the administration of carbenicilin five months later. Cephalosporin therapy was given to this patient without signs of renal toxicity. This is the first reported case of probable carbenicillin-induced interstitial nephritis and serves to emphasize the danger of giving any penicillin analogue to patients with a history of pencillin-induced interstitial nephritis.

Anemia, Aplastic↗