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Adhesions of 211 strains of uropathogenic Escherichia coli and 19 strains of normal fecal E. coli were characterized by patterns of agglutination with human erythrocytes, Saccharomyces cerevisiae, and horse erythrocytes coated with the P blood-group receptor (P). Mannose-resistant (MR) hemagglutination was significantly associated with P agglutination (P less than .001). E. coli expressing MR and/or P (MR/P) agglutinins concurrently with mannose-sensitive (MS) agglutinins predominated in all clinical categories. The highest percentage of E. coli demonstrating MR/P agglutinins, in the absence of MS agglutinins, was recovered from patients with acute pyelonephritis (35%) compared with percentages of patients with chronic pyelonephritis (13%), asymptomatic bacteriuria (16%), cystitis (11%), and normal fecal control E. coli (11%). Sixty-nine percent of E. coli isolates causing acute pyelonephritis agglutinated P-coated horse erythrocytes compared with only 11% of the fecal isolates. Strains expressing MR/P agglutinins (in the absence of MS agglutinins) isolated from patients with acute pyelonephritis, chronic pyelonephritis, and asymptomatic bacteriuria were significantly associated with the presence of antibody-coated bacteria in patients' urine sediments (P less than .010), an observation indicative of an immune response associated with bacterial invasion of host tissues.

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Urine specimens from 65 adult patients with symptomatic urinary tract infections that involved 91 episodes of well-defined acute pyelonephritis or cystitis were tested for antibody-coated bacteria (ACB) by a fluorescent antibody assay, unbound bacteria-specific antibody by radioimmunoassay (RIA), and levels of total protein and IgG. Acute pyelonephritis was associated with positive tests for ACB (22 [69%] of 32), elevated levels of unbound antibody (28 [88%] of 32), and a mean RIA binding ratio of 9.4. Cystitis was associated with negative tests for ACB (56 [95%] of 59), low levels of antibody in urine (38 [64%] of 59), and a mean RIA binding ratio of 3.2. The results showed that a negative test for ACB may occur with elevated levels of unbound antibody in the urine because, although elevated, levels were still too low to result in detectable antibody coating of the bacteria. There was often, but not always, a correlation between RIA binding ratios and levels of urinary protein and IgG.

Forty-five women with diabetes mellitus and urinary tract infections have been followed an average of 34 mo on treatment protocols based on localization of infection as determined by the presence or absence of antibody-coated bacteria (ACB). Treatment was usually, but not exclusively, trimethoprim-sulfamethoxazole. Two weeks of oral therapy was equally efficacious to 6 wk of treatment in asymptomatic women with antibody-coated bacteria (ACB)-positive infection in eradicating bacteriuria. Recurrences in all groups were predominantly reinfections with differing serotypes or species of microorganisms. The sustained remission rate (fractional extraction) after initial treatment was similar to other reported groups, but possibly less efficacious with recurrences. Suppressive therapy with trimethoprim-sulfamethoxazole for repeated recurrences effectively prevented infection but provided no posttreatment benefit. A high prevalence of underlying structural genitourinary tract abnormalities, usually detectable on pelvic examination, and which were not direct consequences of diabetes mellitus, were possible contributing factors to recurrent infection in this patient group. Progressive elevation in serum creatinine in seven patients with initial ACB-positive infections appeared to relate more closely to diabetic nephropathy rather than chronic pyelonephritis. ACB-positivity correlated well with elevated serum antibody titers and the presence of underlying anatomic abnormalities, but ACB categorization did not lead to improved therapeutic strategy or outcome and hence was of limited clinical usefulness.

The separation of patients with idiopathic nephrotic syndrome into those with lipoid nephrosis and membranous nephropathy on the basis of ultrastructural study of renal biopsy material is supported by contrasts in the natural history and response to therapy of the groups. Nineteen patients with the latter lesion have been followed for periods of up to eleven years. Nine are known to have expired with a mean duration of clinical illness of six years. Nine survivors are known with a mean duration of clinical illness of 5.3 years. Corticosteroid therapy rarely appears to provide sustained clinical improvement. However, remissions with loss of clinical features of the illness have been observed in five patients. Serial renal biopsies indicate the morphologic lesion is usually unchanged or progressive, despite subsidence of proteinuria and clinical remission. In one patient a renal biopsy in her third year of remission showed striking regression of a previously marked membranous change. Morphologic differentiation from renal involvement with systemic lupus erythematosus may be difficult and diagnosis depends on evidence of multisystem disease and additional laboratory studies. Review of reported immunofluorescent studies of biopsy material and comparison with experimental lesions suggest the glomerular membranous lesion is immunologically determined.