Search PubMedSearch

Biomedical subjects

C J Hodson

Publications and source records attributed to C J Hodson.

At least 19 recordsLinked to original sources

Large cloisons.

Large masses of normal glomerular (cortical) tissue situated deeply within the kidney and properly called cloisons, can often be mistaken for tumors. The radiographic characteristics of 20 cases are described, including location at or above the middle one-third of the kidney (93%) and bilaterality (60%). Three unusual, but associated papillary-calicine features include the "teat and udder" sign, which derives from the relation of the cloison and its small papillae which resemble a cow's udder and teats, calicine stem displacement, and absence of calicine cup stretching. Further investigation of the cloison by nephrotomography or technetium-labeled glucoheptonate may be necessary in doubtful cases to confirm this benign condition.

Adult

Tubulointerstitial nephritis and immunologic responses to Tamm-Horsfall protein in rabbits challenged with homologous urine or Tamm-Horsfall protein.

Tubulointerstitial nephritis was produced in 19 of 23 New Zealand White rabbits challenged i.v. with adjuvant-free homologous urine for greater than or equal to 16 wk and 11 of 14 challenged with adjuvant-free rabbit Tamm-Horsfall protein for 2 to 24 wk. Lesions were identical in the two groups of rabbits and were characterized by focal mononuclear infiltrates and microscopic scarring localized to distal nephron segments identified as the thick ascending limb of the loop of Henle. Concomitant immunoglobulin deposition was not detected despite antecedent elevations in serum IgG antibody directed against Tamm-Horsfall protein in 17 of 19 and 10 of 11 affected rabbits, respectively. Peripheral lymphocytes from affected rabbits were found to be cytotoxic and underwent blast transformation in the presence of homologous urine or Tamm-Horsfall protein in vitro. These lymphocytes were shown to produce a soluble cytotoxic product upon exposure to Tamm-Horsfall protein. Neither tubulointerstitial nephritis nor this pattern of cellular and humoral immune response to Tamm-Horsfall protein was found in two age-matched control groups: one unchallenged, and the other challenged i.v. with urine that had been selectively depleted of Tamm-Horsfall protein by 95%. It is concluded that the tubulointerstitial nephritis produced in rabbits by injection of urine or Tamm-Horsfall protein is the result of a predominately cellular immune response directed against Tamm-Horsfall protein.

Animals

Renal localization of Tamm-horsfall protein in unilateral obstructive uropathy in rats.

The distribution of Tamm-horsfall protein (THP) within nephrons and in the renal interstitium of the kidney was examined in rats after unilateral ureteral ligation. Urinary casts containing THP were detected not only distal to the site of THP synthesis in cells of the ascending limbs of the loop of Henle, but also in more proximal portions of the nephron, suggesting retrograde intratubular movement of urine. THP-positive casts within Bowman's space of glomeruli were found by 6 hours and were maximal at 2 weeks after obstruction. At this time, THP was present in 25 per cent of all glomeruli, predominantly in central zones of the outer cortex. No morphologic evidence suggesting passage of THP across Bowman's capsule of these glomeruli was found. By contrast, interstitial THP aggregates resulting from urinary extravasation from tubules were detected throughout the study. These occurred earlier and were more numerous, albeit smaller, in the cortex where they were concentrated in periarterial and periglomerular sites. Multiple pathways for escape of urinary THP from tubules were demonstrated and included tubular ruptures and necrosis, forniceal tears, and venous polyps. Although occasional masses of THP in the interstitium were surrounded by inflammatory cells, the overall time course and distribution of interstitial THP deposits did not correlate closely with the development of widespread interstitial hypercellularity and scarring after obstruction. Although not directly linked to the pathogenesis of tissue injury in obstructive uropathy, THP provides an excellent marker of urinary extravasation and of the pathways of urine flow within the kidney under pathologic conditions.

Animals

Diagnostic considerations in urinary bladder wall calcification.

Though a relatively uncommon finding in general radiologic practice, urinary bladder wall calcification has relatively few etiologies. A series of 19 patients with radiographically visible bladder wall calcification encompassing most of the known causes is presented and other reported causes are discussed. Eight patients had schistosomiasis, six had primary carcinoma of the bladder, two had encrustation cystitis, and one each had amyloidosis, cyclophosphamide-induced cystitis, and tuberculosis. While a correct diagnosis is often not possible solely on the basis of the appearance of the calcification, such a diagnosis can usually be obtained expediently from a combination of history, clinical examination, appropriate laboratory studies, and radiographic evaluation of the bladder calcification and remaining urinary tract. Cystoscopy with biopsy of involved tissues is almost necessary, however, for confirmation and to rule out bladder neoplasia.

Calcinosis

Neuhauser lecture. Reflux nephropathy: a personal historical review.

High pressure reflux may be a major cause of chronic renal failure both with and without associated urinary tract infection. The concept of reflux nephropathy includes not only the entity previously known as "chronic atrophic pyelonephritis," but other forms of renal disease such as the Ask-Upmark kidney, renal segmental hypoplasia, and the generalized changes that resemble those of obstructive nephropathy but which are secondary to reflux. Lobar and papillary anatomic variations play an important role in predisposing certain kidneys or parts of a kidney to damage from high pressure reflux, with or without infection. Prolonged high pressure sterile reflux can not only cause focal scarring in papillae susceptible to intrarenal reflux, but can cause the conversion of nonsusceptible papillae, so that scarring may then become generalized. The mechanisms of scar production induced by intrarenal reflux remain unclear, but mechanical immunologic, bacterial, and vascular factors are current subjects of investigation. There is mounting evidence that it is in infancy that a train of events starts which culminates in this renal damage and that much of this may be well under way quite early in childhood and remain clinically undetected until later in life, when the end results (i.e., hypertension and/or renal failure) become manifest.

Adolescent

Home screening for the detection of urinary tract infection in infancy.

One hundred sixty-five infants of both sexes, 2 weeks to 2 years of age, were screened by their parents at home for bacteriuria. Parents were instructed during a single brief period during the initial office visit to collect and to culture their infants' urine at home. Urine was collected by specimen bag and cultured promptly at cribside using a newly developed culture kit and inoculating swab. The same specimen was cultured by the office laboratory staff by kit and swab and, as a reference standard, by the loop-MacConkey method. Infants were screened at home after three consecutive office visits. Then, 870 specimens were processed. Urinary tract infection (UTI) was diagnosed in 3.6% of the study population. Results show that home screening of infants for UTI by the parent compares favorably with screening by the office laboratory.

Bacteriological Techniques

Antibody to Tamm-Horsfall protein in patients with urinary tract obstruction and vesicoureteral reflux.

Urinary tract obstruction and vesicoureteral reflux, which are often associated with urinary tract infections, may lead to progressive renal damage. Relatively little is known about the pathophysiology of this process, and a need exists for noninvasive methods of its detection in its early stages. Because urine is refluxed into the venous and lymphatic drainage of the kidney in severe vesicoureteral reflux and urinary tract obstruction, an immune response to urinary tract components might play a role in the pathophysiology of progressive renal damage and serve as a serologic marker for its presence. A solid-phase radioimmunoassay for a protein found only in the urine (Tamm-Horsfall protein [THP]) was developed and used to measure antibody to THP in the serum of 60 subjects. Significant elevations of antibody to THP were observed in five of 15 patients with obstruction and infection of the urinary tract and in one of 10 patients with infection alone, when these patients were compared with 12 healthy control subjects. Similar elevations of antibody to THP were not seen in uninfected patients with urinary tract obstruction or in patients with low-grade vesicoureteral reflux or sepsis of nonrenal origin. These results suggest that the measurement of antibody to THP might be useful in the identification of patients with obstruction and infection of the urinary tract.

Adolescent

Renal parenchymal radiographic measurement in infants and children.

An analysis of the urograms of 433 pairs of normal human kidneys performed on patients ranging from birth to 80 years was carried out with the object of relating the mass of the renal parenchyma to the overall size of the kidney at different ages. Statistical analysis of the results showed that there was a highly significant difference in the ratio of mass to overall size in the age periods of 0-5 and 5-10 years, with a significant difference in the third quinquenium. Adult proportions are not reached until the latter half of the second decade of life. Recognition of this aspect of the process of maturation of normal kidneys is essential if radiographic measurement is to be used as a means of estimating kidney damage in the very young.

Adolescent

The pathogenesis of reflux nephropathy (chronic atrophic pyelonephritis).

The relationship between vesico-ureteric reflux and coarse renal scarring (atrophic pyelonephritis) has been studied in swine. Scars were observed to develop where reflux took place into the kidney substance via the renal papillae (intrarenal reflux). They were confined to these regions and were similar in size, distribution and other features peculiar to those found in the human from early childhood onwards. Intrarenal reflux was found to be related to the pressure within the urinary tract as well as to vesico-ureteric reflux. Infection was not an essential factor in scar-formation, but it appeared to intensify the scarring process. The histological findings were a progressive focal interstitial fibrosis confined to the zones of intrarenal reflux, extending from the capsule to the papillary tip, and varying in severity with pressure, time and the extent of intrarenal reflux. Nephron and tubular damage accompanied all grades of fibrosis, with the possible exception of the earliest. In many respects the histological changes closely resemble those due to obstruction, except they are focal in distribution. Added features are the early peripheral lymphocytic aggregations and interstitial fibrosis which appear to suggest that some "irritant"--possibly urine--reaches the interstitium and drains away via the lymphatic system. Many of the phenomena observed were strikingly similar to those present in children with the more severe grades of vesico-ureteric reflux. In some cases a mixture of generalized obstructive nephropathy and focal scarring developed; in others focal scarring took place with normal papillae elsewhere. The results are readily reproducible. The basic questions as to whether it is bladder pressure, or infection, or a mixture of the two which is responsible for scar-formation are discussed.

Adult