Cell-mediated immune response in acute poststreptococcal glomerulonephritis.

To evaluate the role of cell-mediated immunity in acute poststreptococcal glomerulonephritis (APSGN), we identified the immune cell population infiltrating the glomeruli. Renal biopsies were obtained from 22 patients with APSGN, 16 with overt and 6 with asymptomatic disease, one to 30 days after onset. Samples of normal renal tissue were used as controls.

Role of a streptococcal antigen in the pathogenesis of acute poststreptococcal glomerulonephritis. Characterization of the antigen and a proposed mechanism for the disease.

We studied the significance of a streptococcal protein (preabsorbing Ag) (PA-Ag) in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN). This protein was isolated from nephritogenic streptococci. Purification of PA-Ag was achieved by chromatography, followed by Sephadex IEF.

Evidence for an HIV-related nephropathy: a clinico-pathological study.

The existence of an HIV-related nephropathy as a distinct disease entity is controversial. We observed a high incidence of renal disease in our AIDS patients. Of 182 patients, 59 patients (32.

Hyponatremia in patients with the acquired immunodeficiency syndrome.

Of 103 patients with the acquired immunodeficiency syndrome (AIDS) admitted for acute opportunistic infections, 36 had serum sodium less than or equal to 130 mEq/l (130 mmol/l). In 12 the hyponatremia was associated with volume depletion and corrected with saline replacement therapy. In 23 it was associated with the syndrome of inappropriate antidiuretic hormones secretion (SIADH).

Renal cytomembranous inclusions in idiopathic renal disease as predictive markers for the acquired immunodeficiency syndrome.

Tubuloreticular inclusions (TRI) and cylindrical confronting cisternae (CCC) are present in cells of patients with the acquired immunodeficiency syndrome (AIDS) and have also been detected in the kidneys of individuals with AIDS and heavy proteinuria. We examined renal biopsy tissue from 13 patients with proteinuria and/or renal insufficiency. At the time of biopsy, two of the patients had AIDS (group A), four had AIDS-related complex (ARC) (group B), and seven presented without any clinical signs or symptoms characteristic of AIDS or ARC.

Renal ultrastructural markers in AIDS-associated nephropathy.

Renal tissues from two groups of patients with acquired immune deficiency syndrome (AIDS) were examined: Group A had severe proteinuria and varying degrees of renal insufficiency, designated AIDS-associated nephropathy (AAN), and Group B had no renal involvement. Control Group C consisted of patients with heroin-associated nephropathy (HAN) with proteinuria comparable to patients in Group A but without AIDS or its related complex (ARC). The most frequent finding, common to both AAN and HAN, was focal glomerular sclerosis.

IgA nephropathy occurring in the context of previous acute glomerulonephritis.

A 37-year-old female presented with acute onset of glomerulonephritis 10 days following an upper respiratory infection. Serum complement components were depressed and proteinuria exceeded 3.0 g daily.

Pasteurella multocida septicemia and peritonitis in a patient with cirrhosis: case report and review of the literature.

A case of Pasteurella multocida septicemia and peritonitis in a patient with cirrhosis is reported and the literature reviewed. Patients with cirrhosis and exposure to domestic animals are at risk for this infection. Initial empiric therapy of spontaneous bacterial peritonitis in such patients should include a penicillin to which this organism is usually susceptible.

Circulating immune complexes in patients with uncomplicated group A streptococcal pharyngitis and patients with acute poststreptococcal glomerulonephritis.

To investigate the role of circulating immune complexes (CIC) in the pathogenesis of acute poststreptococcal glomerulonephritis (AGN), sera were obtained serially from 13 patients with biopsy-proven AGN, 16 patients with group A streptococcal infection, and 20 age- and sex-matched controls. Samples were analysed for Clq-binding activity (Clq-BA), levels of IgG, IgA, IgM, C3 and C4, and antibody titres to streptococcal enzymes. Significant elevation of Clq-BA was observed in 11 patients (84.

Cellular immunity in systemic lupus erythematosus as evidenced in vitro by leucocyte migration inhibition tests.

A leucocyte migration inhibition test was performed on 26 patients with systemic lupus erythematosus (SLE) and on 35 control subjects using three different antigens, fetal calf thymus DNA, baker's yeast RNA, and calf thymus extractable nuclear antigen (ENA). Leucocyte migration was inhibited by DNA in 17 out of 26 SLE patients (65-3%), and in only 2 of the 35 controls (5-7%). When RNA or ENA was added none of the patients or controls showed inhibition.

A hitherto unknown streptococcal antigen and its probable relation to acute poststreptococcal glomerulonephritis.

In the initial phase of acute poststreptococcal glomerulonephritis (AGN), antigenic sites not covered by specific antibody can be demonstrated in the glomeruli. These sites are on the endothelial side of the glomerular basement membrane and in the mesangial matrix. The antigen is contained in a water-soluble fraction of nephritogenic streptococci.

Epidemic glomerulonephritis in Maracaibo. Evidence for progression to chronicity.

In 1968 an outbreak of 348 cases of acute poststreptococcal glomerulonephritis (AGN) was observed in Maracaibo, Venezuela. During the year, the epidemic had three peaks of incidence. Districts with better sanitation showed a lower incidence of disease than those with less adequate facilities.

Demonstration of antigenic sites in glomeruli of patients with acute poststreptococcal glomerulonephritis by immunofluorescein and immunoferritin technics.

The presence and localization of antigenic sites in glomeruli of 14 patients with acute poststreptococcal glomerulonephritis (AGN) were studied by immunofluorescein and immunoferritin technics. Labeled IgG fractions from the same patients were used for the identification of antigenic sites. The staining capacity of these IgG fractions depended on the time when sera were obtained.

Relationship of nervous tissue transketolase to the neuropathy in chronic uremia.

Patients with chronic uremia develop neurologic defects which are similar to the demyelinating lesions seen in thiamine deficiency. The present study describes inhibitory effects of uremic material on nervous tissue transketolase, a thiamine-dependent enzyme of the pentose phosphate pathway which has been reported to have functional importance in the metabolism of myelinated nervous structures. Transketolase activity (TKA) of normal human brain and spinal cord was measured by the conversion of ribose-5-phosphate (R5P) to sedoheptulose-7-phosphate (S7P).

Independence of the nephritogenicity of group A streptococci from their M types.

Fluorescein labelled IgG fractions of serum from patients with acute post-streptococcal glomerulonephritis (AGN) stained the glomerular basement membrane of renal tissue from the same and other patients with AGN obtained during the early phase of the disease. Using a spectrofluorometric method it was quantitatively shown that the staining capacity of these serum fractions was reduced after they had been preabsorbed with disrupted nephritogenic group A streptococci (type 12, 49 and a non-typeable strain) or their isolated plasma membranes. No such effect was observed when group A streptococci of types 3, 4, 6, 12, 14 and 25 or their plasma membranes obtained from patients without AGN were used for preabsorption.

Partial characterization of antigenic streptococcal plasma membrane components in acute glomerulonephritis.

Fluorescein-labeled immunoglobulin G (IgG) fractions of serum from patients with acute poststreptococcal glomerulonephritis stained parts of the glomerular basement membrane and mesangium of kidney tissue obtained from the same patients during the early phase of the disease. Renal tissue obtained from normal individuals and from patients with other kidney diseases failed to stain with these IgG fractions. Preabsorption of the serum fractions with various freezethawed bacteria demonstrated that only certain group A streptococci abolished the staining capacity.

Antigenic streptococcal components in acute glomerulonephritis.

Fluorescein-labeled immunoglobulin G fractions from serums of patients with acute glomerulonephritis and from many normal serums stained the glomerular basement membrane and mesangium of renal tissue from patients with early acute glomerulonephritis; these serums did not stain the corresponding tissues from patients with any other kidney disease. Previous absorption of the serum fraction with frozen and thawed nephritogenic beta hemolytic streptococci abolished all staining. Other bacteria studied did not abolish the staining.