=Definition.=—A chronic inflammation of the kidney, involving the
epithelium, glomeruli and interstitial tissue, characterized by dropsy,
increasing anemia, albuminous urine and acute uremia.
=Osteopathic Etiology and Pathology.=—It may be the result of acute
nephritis. It follows the same diseases as already mentioned in acute
nephritis. More often it follows the same diseases as already mentioned
in the acute form, syphilis, tuberculosis, purulent conditions,
focal infections (streptococcus), alcohol, scarlatina and pregnancy
contributing the greater number. It is more common in the male sex and
in early adult life. Habitual exposure to cold and dampness; chronic
lesions of the spine, chiefly in the lower dorsal region, are causative
factors.
=Pathologically=, the =large white or a yellowish white kidney= is the
most common kidney lesion. In this form the kidney is enlarged, often
to twice its normal size, is smooth, and the capsule very thin. The
tubes, on microscopic examination, are found to be choked with broken
down granulated epithelium and fibrinous casts. The capillaries show
hyaline changes. The interstitial tissue is increased everywhere, but
not to an extreme degree. Catarrhal swelling and hyperemia (to a slight
degree) are found in the pelvis of the kidney.
In the =second stage=—that of the =small white kidney=—there is a
reduction in the size of the organ, due to the destruction of the renal
epithelium and the contraction of the overgrown connective tissue.
Some hold that this may be a primary, independent form and not always
preceded by the large white kidney. The organ is pale in color, rough
and granular, the capsule being thickened and somewhat adherent. There
is an accumulation of fatty epithelium in the convoluted tubules,
constituting marked areas of fatty degeneration and giving the organ
a white or whitish yellow appearance. It is this which gives the name
of small granular fatty kidney to this form. There are extensive
interstitial changes, degeneration of tubules and destruction of great
numbers of the glomeruli.
=Chronic hemorrhagic nephritis= is a variety associated with this
stage. The organ is enlarged, and scattered throughout the cortex are
found brown hemorrhagic foci due to hemorrhages into and about the
tubes. Otherwise the changes are similar with those found in the first
form.
=Symptoms.=—It usually begins as a chronic affection and the symptoms
slowly become apparent. Failing health and loss of strength,
dyspepsia and anemia, waxy appearance with puffiness of the face,
dropsy and increased arterial tension with hypertrophy of the left
ventricle, gradually make their appearance. Uremic symptoms are
common, while dropsy is marked and persistent. Vomiting and sometimes
profuse diarrhea occur; in fatal cases there is sometimes found to
be ulceration of the colon. The urine, as a rule, is diminished in
quantity, is often very scanty, although it is frequently normal
in color and appearance. There is an abundance of albumin, heavy
sediment, hyaline and granular tube casts, epithelium from the kidneys
and pelvis, leukocytes and often red blood-corpuscles. If fatty
degeneration takes place, there will be fatty casts and oil globules.
In the later stages the urine is abundant, low specific gravity,
considerable albumin, and many casts.
=Diagnosis.=—In the inflammatory stage, where there is enlargement of
the kidney, extreme pallor, scanty urine, albumin, and tube casts,
history of infections, pregnancy, or exposure to cold and wet, and
lesions in the lower dorsal region, the diagnosis is clear.
=Prognosis.=—Always give a guarded prognosis; relapses are frequent,
but cases have been cured. There is always a tendency for the
subchronic forms to become chronic.
=Treatment.=—The treatment requires persistent work, especially over
the renal splanchnics, and strict attention on the part of the patient
to hygienic principles. The lower dorsal lesions are very apt to be
refractory owing to extensive fibrotic changes of the deep muscles and
capsular ligaments. But repeated effort will usually secure results.
Care should be taken as to exposure to cold and overexertion. The
quality of the blood should be improved, as it is anemic and contains
various toxic products. Strict attention should be paid to the diet.
Iron is largely used for anemic conditions, but this principle we hold
to be wrong. It is not more iron that is wanted, but an ability of the
system to assimilate the iron which it has. Relative to diuretics von
Noorden says: “It would be the greatest paradox to economize the renal
work to the utmost in one direction (diet, sweating, etc.) and on the
other hand excite them to increased activity by means of the strongest
stimulants we possess, (drugs). I regard such prescribing as radically
wrong.” The diet should be carefully selected and of minimum amount.
The pure milk diet is undoubtedly the best. The use of meat seems to
favor uremic convulsions.
The digestive organs should be kept in as good condition as possible,
particular attention being paid to the liver and bowels. The use
of suitable clothing is important; wool should be worn next to the
body. The skin is a powerful adjuvant to kidney elimination, and the
suppression of the action of the skin throws extra work on the kidneys.
Possibly stimulation of the lung function would aid in the elimination.
Rest, with a proper amount of fresh air and outdoor exercise, is
essential.
In conditions calling for attention to the skin and bowels the
treatment will be the same as in acute parenchymatous nephritis. There
is a ganglion on each side of the umbilicus within a radius of an inch
that sends fibers to the kidneys (Dr. Still). Just what is the function
of these ganglia is unknown. The treatment of the complications is
independent of that for the renal trouble. For direct treatment to the
kidneys see acute Bright’s disease.