Diagnosis Of The Decade The Seventies

Running head: DIAGNOSIS 1

Diagnosis of the Decade: The Seventies

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DIAGNOSIS 2

Diagnosis of the Decade: The Seventies

Wilson and Dixon (1974) seek in this study to diagnose the clinical features and

pathologies of kidney disease by establishing the specific pathway and mechanism of immune

responses that cause renal immunopathology, that is, renal inflammation. Their aim is to

establish specific treatment of renal disease through the identification and close study of immune

complexes (anti-GBM antibodies or circulating nonglomerular antigens) and mediator systems

that cause glomerular injury and possibly tubular and interstitial lesions. At issue is diagnosis,

how to make more specific identification and treatment. The problem is that even if the damage

potential of these antibodies and antigens has been established, there may be found similar

mediating agents that cause harm and different types of glomerular diseases even from a single

immunological cause.

As a tool of detection for deposition of immunoglobulins (Ig) and similar formations

within renal tissue, the authors recommend fluorescent methods of investigation. Now,

flourescence as a tool employs a starting light with an appropriate wavelength that will out of

itself emit a longer wavelength in a secondary light. Immunofluorescence looks for fluorochrome

antibodies in renal biopsy specimens to detect Ig and associated protein formations. Evidence of

immune complexes deposit that can cause renal inflammation may be found in the uneven,

interrupted, grainy nature of the deposits in comparison to the evenly distributed pattern of anti-

GBM antibodies reacting with antigens throughout the glomerular basement membrane (GBM)

of a healthy person. A filter without a reflecting surface focuses a very powerful light on the

tissue under investigation. Much depends on the quality of fluorescein interference filters and

exciter systems for accuracy and meaningful interpretation of findings

DIAGNOSIS 3

We are looking for the sake of accurate diagnosis of kidney diseaser the anti-GBM

antibodies and glomerular deposition of circulating immune complexes as the mechanisms of

glomerular and tubular injury. These may be diagnosed through immunofluorescence research.

The problem is that the quality of the diagnosis depends on the quality of the reagent employed

(fluoresceinated anti-light chain sera) and the quality of the renal tissue which should be frozen

while fresh. Care in studying tissues is especially underlined. It is recommended that the

investigator examine the quantity and the pattern, not the intensity, of the florescence that is in

turn ultimately derived from the reagent, not the tissue under study.

At this point in the diagnosis, distinctions need to be made. Specifically, though

gbomeruli attracts the most attention, other types of deposits may be tubular in some patients,

interstitial in others, while vascular deposits are found in still other patients. Serun proteins are

easy to confuse with the deposits that are sought. As well, it may happen that deposits of calcium

poses a barrier to the quality of the florescence. There need also be sufficient samples employed

to produce meaningful results.

The researchers then turn to nephrites due to anti-glomerular basement membrane (GBM)

antibodies as possible symptoms of renal inflammation.. Now, anti-GBM antibodies have a

linear feature until meeting a threat and signs of damage when the straight line of the Ig deposits

becomes uneven and fragmented. Only, the flourescence method of investigation needs to be

corroborated by other means. A procedure called radioimmunoessay is mentioned as available,

though not much elaborated upon, demonstrating a level of uncertainty about the accuracy of the

corroborating methods for the screening of the nephritic population. Although there are in place

various ways of measuring cellular sensitivity, at this point when the study was made there was

very little evidence of sensitized cells as the direct and proven cause of glomerular injury.

DIAGNOSIS 4

Similarly, while it is firmly established that GBM antibodies are responsible for at least some of the

renal injuries in the samples tested ( 5%) and the most important IgG is easily identified, tests tend to

miss IgA and IgM , while the actual role of the subclasses of IgG have not yet been firmly determined.

Yet again, although fibrinogen-related antigens have been found in the rapidly progressing forms of the

disease , their actual purpose remains unclear.

There are at this stage of the investigation many paths proposed that may be fruitful in the

future . As an example, in the case of Goodpasture's syndrome (anti-GBM antibody-induced

glomerulonephritis and pulmonary hemorrhage), the alveolar basement membrane contains Ig

deposits. At the same time, antibodies related to GBM has been found in the lungs of these

patients as well as in the lungs of experimental animals. The previously mentioned mediation

mechanism is suspected, though further research in this area is needed yet again to confirm the

relevance of this phenomenon, most especially to determine whether renal abnormalities, lung

abnormalities or a combination of both bring about the syndrome. To make matters still more

confusing, nephritis may strike without the associated pulmonary disease and patients may be

suffering from glomerulonephritis without the evident deposits within the glomerli. That leads in

the end to what the investigators think as the most hopeful of approaches through the antiviral

antibody responses in animals with attempts made to identify, isolate and work with the viral

agents from renal biopsy. In the end, the particles that seemed to work like virus in kidney

diseases have been found in other conditions, from which we may conclude that the particles are

a byproduct of, not the cause, of kidney disease. Yet again, what seemed at first a hopeful

direction becomes a dead end after a while, which in turn raises still other scientific path and new

hopes of establishing the much needed and sought after accurate diagnosis of kidney illness. That

is, after all, how science progresses.

DIAGNOSIS 5

References

Wilson, C. B., & Dixon, F. J. (1974). Diagnosis of immunopathologic renal disease. Kidney International,

5(6), 389-401.

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