KIDNEYS, DISEASES, TREATMENT OF
Arsenicum in Bright's Disease.
General anasarca, oedema and puffiness ; albuminous urine ; waxy casts ; skin pale and waxy looking ; exhausting diarrhoea ; burning and thirst ; frequent vomiting.
The presence of blood boils is also an indication.
Mercurius corrosivus in kidney disease.
The urine is thick, and micturition difficult ; urine contains albumen, granular and fatty tube casts and epithelial cells ; there is more or less inflammation at the neck of the bladder ; face pale and swollen ; pulse irregular and uneven.
Digitalis in renal affections.
Dropsy ; feeble or slow pulse ; scanty, dark, turbid urine, which is albuminous ; similar to Arsenic, without its restlessness and irritability.
Apis in Bright's Disease
Urine scanty and albuminous ; anasarca with white, shining skin ; ascites, with soreness of abdominal walls.
Pressure in kidneys while sitting ; urine scanty, smoky and dark ; much albumen and bloody casts.
Bloody urine is the keynote.
The pain is burning and extends into right hip.
Aching across loins ; albuminous, high colored urine, with scalding.
Renal symptoms of Berberis
Deep and severe pains in region of the kidney, extending down back and along the uterus into the pelvis.
Pains seem to radiate in all directions from the kidneys.
Useful for renal calculi.
Phosphorus the remedy in Bright's Disease
The urine contains epithelial, fatty or waxy casts ; abuse of alcoholic stimulants, lung complications, vomiting or diarrhoea.
Urine is whitish, flocculent, iridescent.
If your father or mother has PKD there is chance you might have it as well.
Better to check yourself just to be sure that you don’t have any and if you do , it would be an early stage which means you might only have couple of cyst in your kidney so you could take precautions. This is one of the diseases with no cure at the moment.
Over time the cysts in the kidneys grow, replacing normal healthy tissue and causing the kidneys to lose their function.
So one way or the other this progresses and there is nothing, nothing one can do.
In polycistic kidney disease (PKD), fluid-filled cysts develop in the kidneys usually causing symptoms in midlife, although it may become apparent much sooner.
What is PKD?
In PKD, fluid-filled cysts develop in the kidneys, giving them a honeycomb appearance. Gradually these cysts replace the normal kidney tissue, enlarging the kidneys but making them less and less able to function normally. Eventually, the kidneys fail completely.
In addition to the kidney damage, the fluid in the cysts may become infected, which can cause pain in the back and abdomen, and trigger fever. They can also burst, causing pain, or blood in the urine.
Adults may not develop symptoms for many years. When they do arise they may also include:
Vague discomfort or aching in the abdomen and/or lower back
Attacks of sudden and severe pain in the abdomen and/or lower back
Urinary tract infections
Cysts in the liver and pancreas
Abnormal heart valves
Brain aneurysms (bulges in the walls of blood vessels)
Diverticulosis (small bulges in the wall of the colon)
High blood pressure (hypertension) may develop as a result of kidney damage. This may exacerbate the problem by damaging the kidneys further. However, progress of the disease is usually very slow and it may go undetected for years.
What causes it?
There are two types of inherited PKD:
Approximately 85-90 per cent of patients have ADPKD1 (with an abnormality on chromosome 16).
The remaining patients have ADPKD2 (abnormality on chromosome 4).
It needs only one parent to pass on the abnormal gene, giving a person a one-in-two chance of developing the disease later in life.
The childhood form, autosomal recessive PKD, (ARPKD), is much rarer. It affects about one in 10,000 babies. In at least some cases, the gene is found on chromosome 6. It needs both parents to pass on an abnormal gene - meaning a child has a one in four chance of developing the disease in childhood which progresses rapidly.
The genes responsible for causing ADPKD in most patients have been identified. This means those with a family history of the disease can receive genetic counselling to help with family planning.
Babies with ARPKD are usually identified soon after birth because the enlarged kidneys cause the abdomen to be very swollen, although this is very rare. Other organs such as the liver may be involved and, although severity varies, some babies die soon after birth.
If there's a family history of the disease, an ultrasound scan during pregnancy may detect the disease before the baby is born.
Adults with ADPKD may be discovered by chance when someone is undergoing tests for a separate problem. An ultrasound is the normal means of diagnosis. If there's a family history, it may be discovered when members of the family are routinely screened.
It's possible to screen for most ADPKD genes using DNA analysis during pregnancy.
Treatment and recovery
At present, it isn't possible to prevent the cysts forming within the kidneys. However, it's possible to slow the damage.
Keeping blood pressure at a safe level helps prevent further damage to the kidneys. If infection develops, it needs to be treated promptly and effectively.
Eventually, complete kidney failure often occurs. In 50 per cent of people with ADPKD, this happens by the age of 60. At this stage, kidney dialysis or transplant can be necessary.