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J P SANFORD

Publications and source records attributed to J P SANFORD.

At least 19 recordsLinked to original sources
PubMed1976

Acute diffuse interstitial nephritis related to chemotherapy of tuberculosis.

Acute renal insufficiency developed in three patients receiving chemotherapy for tuberculosis. It is proposed that acute diffuse interstitial nephritis related to the drugs was responsible for the renal injury. Recovery of renal function was slow and incomplete. Physicians administering chemotherapy to patients with tuberculosis must be aware of the potential nephrotoxicity of the common treatment regimens.

Antitubercular Agents↗
PubMed1964

THE ROLE OF IMMUNITY IN THE PATHOGENESIS OF EXPERIMENTAL RETROGRADE PYELONEPHRITIS.

Retrograde pyelonephritis was produced in rats by the intravesical injection of Proteus mirabilis. When animals were preimmunized against Proteus mirabilis by (a) prior infection, (b) administration of antigen, or (c) passively transferred antiserum, they were resistant to infection by proteus when challenged by the retrograde route. The protective effect of specific preimmunization in retrograde pyelonephritis indicates that a major site of action is retardation of bacterial growth within the parenchyma of the kidney.

Animals↗
PubMed1962

Localization and fate of Escherichia coli in hematogenous pyelonephritis.

1. Hematogenous E. coli pyelonephritis was produced in rats. The localization of the organisms and the persistence of bacterial antigens was followed by fluorescent antibody techniques as well as by standard histological and bacteriological methods. 2. Salient sequential features were as follows: Single organisms passed through vessel walls into the renal interstitium and began multiplication and subsequently evoked a leucocytic response. Bacterial multiplication did not occur in glomeruli or renal tubular cells. Bacteria did not appear within renal tubular lumina until microabscesses were well developed in the renal interstitium. Bacteriuria appeared late and represented secondary invasion rather than filtration of organisms. The infection healed spontaneously but, while sterile, the parenchymal scars contained large amounts of residual bacterial antigen. The persistence of bacterial antigen did not result in continuing inflammatory changes or progressive scarring. 3. The persistence of bacterial antigens is postulated to constitute a major antigenic stimulus responsible for active immunity in experimental hematogenous pyelonephritis.

Animals↗
PubMed1962

Viral orchitis.

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Humans↗
PubMed1962

The role of immunity in the pathogenesis of experimental hematogenous pyelonephritis.

Hematogenous pyelonephritis was produced in rats utilizing multiple strains of Escherichia coli, a strain of Klebsiella pneumoniae, and a strain of Proteus mirabilis. Three patterns of hematogenous pyelonephritis occurred which represent an interrelationship between an immune response to the infecting bacteria and the development of obstructive uropathy as a consequence of infection. First, the course of pyelonephritis due to strains of Escherichia coli was acute, self-limited, and associated with the development of circulating agglutinins. Following healing, this pattern of infection was associated with acquired resistance to reinfection with the same bacterial strain. Second, the course of pyelonephritis due to a strain of Klebsiella pneumoniae type C was chronic. This infection was not associated with the production of circulating agglutinins against encapsulated strains. Acquired resistance to reinfection by the homotypic strain could not be demonstrated following eradication of infection but was produced by the passive transfer of concentrated antiserum. Third, pyelonephritis due to Proteus mirabilis was associated with circulating agglutinins and resistance to reinfection with the same organism following eradication of infection, yet the course was chronic. The chronicity appeared to be the consequence of obstructive uropathy resulting from calculi which developed during the course of the infection. Resistance to reinfection was demonstrated in infections with strains of E. coli and P. mirabilis. The resistance is associated with specific immunity as demonstrated by the observation that: (a) it is type-specific, (b) it is of at least 3 months' duration, and (c) it can be passively transferred by means of rabbit antiserum. Since K. pneumoniae failed to evoke capsular antibodies in the rat, resistance to infection with K. pneumoniae was produced only by means of passively transferred concentrated rabbit antiserum and not by prior infection. Immunity can be demonstrated to have a significant role in the pathogenesis of experimental hematogenous pyelonephritis only in the absence of obstructive uropathy.

Animals↗