Kidney Cyst - Wilms - Nephroblastoma
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The Mechanism of Origin of Nephroblastoma
The beginning of the genesis of nephroblastoma lies in water or fluid conflict. A so-called “biological conflict,” in which we find necrosis (cell loss) in the renal parenchyma (kidney tissue) at the organic level and hypertension (high blood pressure) to compensate for this parenchymal necrosis.
This occurs in the conflict-active phase, i.e., as long as the conflict remains active, so does renal parenchymal necrosis and hypertension.
On CCT, we see a shooting target configuration in the cerebrum’s cerebral medulla immediately above the midbrain during this phase.
Conflictolysis (conflict resolution): once there is a resolution of the water or fluid conflict, amazing things happen in renal parenchymal necrosis:
The renal parenchymal necrosis now gets “internal edema pressure.” The biological purpose is to replenish the parenchymal defect and create additional renal tissue to prevent later water or fluid conflict through increased possible urine excretion.
The cerebrally controlled edema in the necrosis or the edema pressure now presses up the renal capsule precisely, especially if the necrosis was peripheral. It expands and becomes highly elastic with cell proliferation. We call this process a renal cyst.
The stronger the biological conflict had been and the longer it had lasted, i.e., the greater the conflict mass (= conflict intensity + duration), the larger the renal cyst that now develops, namely in the form of a bubble, starting from the isthmus above the renal necrosis.
We can distinguish four stages in renal cyst:
(a) Protrusion of the renal capsule to form a renal cyst:
Renal necrosis pushes a liquid protrusion outward from the renal parenchyma by local distension of the renal capsule at the site above, or peripheral to, the renal necrosis.
b) The enlargement of the renal cyst:
Under amplification (cell proliferation) while maintaining the cyst wall’s elasticity, the cyst begins to enlarge, i.e., to “run” due to the increased internal pressure. That is, it works its way, flat as a flounder, in the direction of least resistance retroperitoneally and enlarges. The size depends, as said, on the conflict mass.
Such a (liquid) renal cyst may occasionally burst if abdominal pressure is suddenly increased by shock or percussion.
c) Attachment of the cyst capsule to the surrounding area for emergency blood supply.
To create an emergency blood supply for the nephroblastoma to be built later, the cyst wall grows all over the surrounding area. We misinterpreted this as “malignant infiltrative tumor growth” and inferred special “malignancy” from it. This adherence is only temporary, as we shall see because by growing to the surrounding area, the flounder-like cyst also acquires certain stability so that tearing off at the isthmus becomes less likely.
d) Filling of the renal cyst with mesodermal cells,
which shall later take over renal cell function and construction of an own vascular system (artery and vein) through the isthmus, starting from the former renal parenchymal necrosis: This passive phase of (semi-liquid) cell filling up to complete induration (solidification) we used to call “Wilms” in our ignorance.
The “biological sense” of this passive “Wilms’ formation” is, of course, in the final formation, namely in the indurated state of the nephroblastoma, which becomes an additional part of the kidney and takes over urine excretion.
From the beginning of the healing phase to the nephroblastomatous final formation, the whole time is nine months, as much as a pregnancy.
With a shorter life span (and shorter pregnancy), the times are correspondingly shorter in the animals.
During this “Wilms phase,” the renal cyst loses all liquidity, likewise, with increasing induration, its blood supply through the isthmus forms better and better, and the adhesion, which we had mistakenly regarded as “infiltration” of a tumor event, now spontaneously regresses!
At the end of the Wilms passage, the structure which we now call nephroblastoma, surrounded by a rough capsule, has grown nowhere; the blood pressure at the latest then returns to normal.
The mature (after nine months) nephroblastoma is completely indurated, has a coarse capsule, has a vital artery and vein through the isthmus, and is involved in urine production. It is like a solidified sac sprouted from the site of the original renal parenchymal necrosis. The nephroblastoma is then a part of the kidney.
We ignorant doctors had always operated on the Wilms at an early stage when they were still attached. However, I had already published ten years ago that renal cysts, Wilms, and nephroblastomas were the same, only in different maturation stages, just as an infant, a man, and an old man same person at different ages.
The oncologists had smelled an opportunity and issued the motto that Wilms had to be treated with chemo for a few months, then he would collapse and could be operated on.
The only correct approach was to wait, which they had copied from Hamer.
The Wilms encapsulates in such a way, namely always, if one only waits. Therefore, it is best to wait!
Premature intervention is only necessary if the patient has liver tuberculosis (healing phase of liver cancer) with liver swelling. We get abdominal space problems with portal vein compression.