Rosamond Janis

Cellular Origin of Hyaluronateprotein in the Human Synovial Membrane

Bright fluorescent staining, which indicates the presence of hyaluronateprotein, was observed in the lining cells of the synovial membrane following application of rabbit antiserum to hyaluronateprotein and a fluorescein-labeled antiserum to rabbit γ-globulin. Staining was shown to be specific and due to antigenic determinants on or closely associated with the protein moiety of hyaluronateprotein.

Resolution of Nephrotic Syndrome and Lack of Progression of Heroin-Associated Renal Amyloidosis

The case of a patient with nephrotic syndrome and renal insufficiency due to renal amyloidosis secondary to chronic subcutaneous heroin abuse who discontinued her drug habit is reported. During the 6 years following the initial renal biopsy, the patients nephrotic syndrome remitted: urinary protein decreased from 6.8 g/d to 170 mg/d, serum albumin increased from 2.5 g/dL to 3.9 g/dL, and she was no longer edematous. Serum creatinine remained stable at 1.8 mg/dL and creatinine clearance was also unchanged at 34 mL/min. Repeat renal biopsy showed AA amyloidosis involving the glomeruli, with minimal interstitial inflammation. This appears to be the first case of clinical improvement in heroin-associated renal amyloidosis after cessation of drug injections. As in other cases of AA amyloidosis that have improved, the clinical picture does not correlate with the findings on renal biopsy.

Synovial cell synthesis of a substance immunologically like cartilage proteinpolysaccharide.

Fluids from joints contain a substance that reacts immunologically like one of two known antigenic components of articular cartilage proteinpolysaccharide. This newly recognized substance occurs in the lining cells of synovial membranes as shown by indirect immunofluorescence. The localization of this substance in tissue culture cells derived from synovial membranes and its identification in the culture medium supports the suggestion that it is synthesized by lining cells. Rheumatoid synovial cells contain less of this substance.

Salicylate nephropathy in the Gunn rat: Potential role of prostaglandins

We examined the potential role of prostaglandins in the development of analgesic nephropathy in the Gunn strain of rat. The homozygous Gunn rats have unconjugated hyperbilirubinemia due to the absence of glucuronyl transferase, leading to marked bilirubin deposition in renal medulla and papilla. These rats are also highly susceptible to develop papillary necrosis with analgesic administration. We used homozygous (jj) and phenotypically normal heterozygous (jJ) animals. Four groups of rats (n = 7) were studied: jj and jJ rats treated either with aspirin 300 mg/kg every other day or sham-treated. After one week, slices of cortex, outer and inner medulla from one kidney were incubated in buffer and prostaglandin synthesis was determined by radioimmunoassay. The other kidney was examined histologically. A marked corticomedullary gradient of prostaglandin synthesis was observed in all groups. PGE2 synthesis was significantly higher in outer medulla, but not cortex or inner medulla, of jj (38 +/- 6 ng/mg prot) than jJ rats (15 +/- 3) (p less than 0.01). Aspirin treatment reduced PGE2 synthesis in all regions, but outer medullary PGE2 remained higher in jj (18 +/- 3) than jJ rats (9 +/- 2) (p less than 0.05). PGF2 alpha was also significantly higher in the outer medulla of jj rats with and without aspirin administration (p less than 0.05). The changes in renal prostaglandin synthesis were accompanied by evidence of renal damage in aspirin-treated jj but not jJ rats as evidenced by: increased incidence and severity of hematuria (p less than 0.01); increased serum creatinine (p less than 0.05); and increase in outer medullary histopathologic lesions (p less than 0.005 compared to either sham-treated jj or aspirin-treated jJ). These results suggest that enhanced prostaglandin synthesis contributes to maintenance of renal function and morphological integrity, and that inhibition of prostaglandin synthesis may lead to pathological renal medullary lesions and deterioration of renal function.