SlDDHA PAGE

Healing
Siddha Medicine
S. Justus Antony and Sathya Rajeswaran

Kidney diseases can Le cured effectively by using Siddka medicines. Tkese medicines given
for kidney proklems not only stimulate tke kidneys kut also improve nutritional deficiencies
and rejuvenate tke entire cells of tke kody!!

he main functions of the kidneys are the removal

of metabolic waste matter, of any toxic material and
excess of water, minerals, and bio-chemicals in order to
keep their blood levels within on optimal range. This is
done by filtering the blood and concentrating the waste
in the form of urine. In addition, the kidneys produce
hormones, which affect the salt balance and red blood
cell production.
A common kidney disorder is the formation of kidney
stones. These are mostly composed of calcium salts and
to a lesser degree of uric acid. Stones can partly block the
flow of urine and this may result in infections as well as
accumulation of waste matter in the blood. The passing
of large stones through the urethra can be extremely
painful and is called kidney colic.
Stone formation as well as bacterial infections or
accumulation of toxic material may lead to acute
or chronic inflammation of the kidneys, also called
nephritis. Symptoms are a rise in blood pressure, back
pain, fatigue, being listless and loss of appetite. Later
oedema may develop; one may feel dizzy and nauseated.
Albumin, a protein compound, will be passed in
increasing quantities with the urine.
If the condition continues to deteriorate, uraemia or
renal failure develops. High concentrations of waste
matter accumulate in the blood and all of the mentioned
symptoms become more severe. If nothing is done
about it, death will eventually occur. The conventional

medical treatment is the removal of these waste materials

by filtering the blood through an external membrane,
a dialysis machine or artificial kidney. When the
condition deteriorates still further, a kidney transplant
is attempted.

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Diaketic
Me dic ine

in

Siddk, a

Diabetes mellitus is a major cause of renal morbidity and

mortality leading to end stage kidney disease and death.
As many as 40% of both Type I and Type II diabetics
are prone to develop renal involvement. In Siddha
literatures such as Yoogi Vaidya Chinthamani Perunool,
800 diseases characterized by polyuria are mentioned
under 'Mega Neer Noihal'. The complications of
diabetes are mentioned under various disease entities and
nephropathic complications come under 'Vishabagam'.
Vishabagam is one of the disease entities which
encompasses metabolic, infective inflammatory, toxic,
immunological and renal causes of edema. Among the
8 types of Vishabagam, Slethma Vishabagam is due to
Mega Neer. The clinical features include:

Generalized itching
Cough with breathlessness
Anemia
Fever with chill
Edema
Secondary infection and sores in edematous areas

Heritage AmruthjAugust 12011j41

 Burning sensation all over the body and

Glycosuria.
According to Siddha, it is a curable (manageable)
condition if properly treated.

Diabetic N epliropatliy
Diabetic Nephropathy is a clinical syndrome
characterized by
Persistent albuminuria
Progressive decline in glomerular filtration Rate (gfr)
Elevated arterial Blood pressure.
It is one of the most significant long term complications
in terms of morbidity and mortality of patients with
Diabetes mellitus. Diabetic nephropathy is a progressive
kidney disease caused by micro angiopathy of capillaries
in the glomeruli.
Each kidney is made up of thousands of filtering units
called nephrons. Each nephron has a cluster of tiny blood
vessels called glomerulus. Together, these structures
help to remove the wastes of the body. Too much of
blood sugar can damage these structures causing them
to thicken and become scarred.
Slowly over time, more and more blood vessels are
destroyed and kidney structures begin to leak and proteins
begin to pass in urine. Uncontrolled high blood sugar
leads to the development of kidney damage especially
when high blood pressure is associated. In some cases
genetic polymorphism of genes encoding proteins of
Renin-Angiotensin system in families also play a role in
the development of the disease. Diabetic nephropathy
develops in patients only with chronic Diabetes mellitus
or only after 10 years of onset and causes death or
ESRD in 4 to 5 years if it is uncontrolled. Though it is
said that male and females are equally affected, there is a
slight dominance of males here. It develops around the
age of 60-70 in Type 2 diabetic patients.

Risk O roups fo r c levelopinent

Diabetic N epliropatliy

of

People with both Type I DM and Type II DM are at

risk.
The risk is higher if blood glucose level is poorly
controlled.
Also once nephropathy develops greatest rate of
progression is seen in patients with poor control of
BP.
Also people with high cholesterol level in their blood
have more risk than others. This is due to relative
deficiency of Insulin which normally inhibits lipase
from synthesizing excessive lipids from tissue stores.

HeritageAmruthj August 12011j41

Signs and Symptoms

In early course, Diabetic nephropathy does not show
any symptoms. They develop in later stages and may be
a result of excretion of high amounts of protein in urine
due to leaky glomeruli. The symptoms include:
Edema (this occurs due to reduced plasma oncotic
pressure).
Foamy appearance or excessive frothy urine due to
massive proteinuria.
Unintentional weight gain due to fluid accumulation
Anorexia
Nausea and vomiting
Malaise and fatigue
Headache
Frequent hiccups
Generalized itching may be present.
Once Diabetic nephropathy develops, it leads to End
Stage Renal Disease (ESRD) within 3 to 5 years if blood
sugar and BP is uncontrolled. It is detected in early stages
itself by microalbuminuria. Other tests like proteinuria,
serum creatinine, Blood Urea, Blood Urea Nitrogen and
kidney Biopsy may also be useful besides concentration
and dilution tests.
Line of treatment
The prime aim of the treatment should be to bring back
the deranged Akkini and kabam and stabilise the 7 udal
Thathus (Siddha medicine parlance).

The drug of choice should have the following activities:

1. Hypoglycemic (drugs which increases the insulin
secretion thereby preventing AGE's)
2. Anti Hypertensives (ACE inhibitors and Angiotensin
Receptor blockers and drugs which reduce glomerular
hypertension.)
3. Hypolipidemic drugs.
4. Nephro protectives and drugs which reduce blood
urea and serum creatinine levels.

increasing the secretion of insulin by the Beta cells. So this

can be used to prevent the AGE s formation in diabetes.
Allium

sativum

and Allium

cepa (Vengayam and

Siddka Drugfs

Vellai poondu, garlic and onion)

Both garlic and onion have hypo glycemic and
hypolipidemic action. Allicin, a sulphur containing
compound in garlic has significant hypoglycemic activity
by enhancing the production of insulin. SAC's (S'Allyl
Cystine Sulphoxide) the precursor of Allicin and garlic
oil prevents lipid peroxidation.

Enicostemma littorale (Vellarugu, Chota Chirayta)

It increases the secretion and sensitivity of Insulin.
Further it has hypoglycemic, hypolipidemic, hypotensive
and nephroprotective activities. It reduces serum
creatinine and blood urea levels. When it is given, the
patients tolerate this drug very well and remarkable
clinical improvement is seen in biochemical markers.

Stereospermum suaveolens (Pathiri, yellow snake tree)

It is a hypoglycemic drug with an added advantage
of correcting AGE formation. This prevents microangiopathy, the basic defect of nephropathy.
All these single drugs can be judiciously given alone or
in combination in doses of 2 to 3 grams twice a day per
single drug.

Nymphaea stellata (Alii, Blue lotus)

It increases the secretion of insulin by the B cells. So
it prevents the uncontrolled action of lipase thereby
producing hypoglycemic and hypolipidemic action.
Siddhar's Agathiar and Theraiyar specified the use of this
drug for improving the vision. Diabetic nephropathy is
often associated with retinopathy also.

O t k er fo rmula t io ns
ACE inhibitors like Swasa kudori Mathirai (Calotropis,
has ACE inhibiting property) should be given. Thiripala
Dravagam or Thiripala Chooranam or Iruveli
kyalam (Coleus forskholii) should be given judicially to
have a blood pressure at or below 120/80 mm Hg.
Precautions: Periodical Neerkuri, Neikuri, Envagai
Thervu should be carried out to assess the patient's
condition. Estimation of
Blood sugar, Blood urea,
Blood Urea Nitrogen, Serum Creatinine and Serum
Elelectrolytes and Microalbuminuria should be carried
out periodically.
Diet: Diet should be of low potassium, low proteins,
low sugar and cholesterol. Greens should be washed in
water for 20 minutes and then only be used.

Nelumbium speciosum (Thamarai, Pink lotus)

It has hypoglycemic and hypolipidemic activities. Also
it reduces hypertension by vasodialatation of arteries.
Renal arteriosclerosis is the main cause for glomerular
hypertension in which this drug may act.
Aegle marmelos (Vilvam, Wood apple)
Vilvam reduces blood sugar, serum cholesterol and
blood urea. Hence it can be used for nephro protection
in Nephropathy due to Diabetes mellitus.
Aloe vera (Katralai)

Aloe vera possesses hypoglycemic action through

Management of Kalladaippu (renal calculi) in Siddha

Renal calculi or kidney stone is one of the most common
hardships of the urinary tract. The etiology of stones
remains approximate. The therapies mentioned in
traditional Siddha texts provide space for palliative care
described in for the management of Urolithiasis.

Siddlia d esc ript ion

Urolithiasis, is called as Kalladaippu noi in Siddha texts,
as described in Yugi Vaithiya Chintamani. Four types
of Kalladaippu noi is described by Yugi muni based on
three Thodam (Three humors in our body). Many herbal
and herbo-mineral formulations have been described
in ancient Siddha texts which may be evaluated in the
management of Urolithiasis.

HeritageAmruthj August12011j 41

E tiology in Siddha
Kalladaippu results due to intake of turbid water, food
with stones, bones, hair and sand, intake of deteriorated
starch foods and eating while indigestion.
Male female ratio
It occurs more frequendy in men than in women. It is rare
in children. There is a definite familial predisposition.
Urinary calculus
Urinary calculus is a stone-like body composed of urinary
salts bound together by a colloid matrix of organic
materials. It consists of a nucleus around which concentric
layers of urinary salts are deposited. It is deposited
commonly in kidneys, ureter, bladder or urethra.

T ypes
Basically the renal stones can be divided into two major
groups I. Primary stones
II. Secondary stones
PRIMARY STONE
According to the grapevine they appear in healthy urinary
tract without any antecedent inflammation.
(a) Calcium oxalate
(b) Uric acid calculi
(c) Cystine calculi
(d) Xanthine calculi
(e) Indigo calculi
Calcium oxalate and calcium phosphate stones make up
75 to 85% of the total and may be admixed in the same
stone. Approximately 50% of people who form a single
calcium stone eventually form another within the next 10
years. The average rate of new stone formation in recurrent
stone formers is about one stone every 2 or 3 years.
SE CONDARY STONE
They are usually formed as a result of inflammation.
(a) Triple phosphate calculus
(b) Mixed stones
SIGNS AND SYMPTOMS
Intense, colicky pain radiates from the costal arch
obliquely to the lower abdomen, groins, and testes.
Nausea and vomiting.
Earlier episodes are often recognized from the history,
and there are cases in the family
Tendency for recurrences is 50% in 10 years
The patient has difficulty in keeping still
Tenderness of the kidneys on percussion is often
observed
Microscopic, or rarely macroscopic, haematuria in 90%

42 | Heritage Amruth| August 12011

Sing le kerbs useful in Kallac i a ippu

1. Sirupeelai (Aerva lanata)
2. Mookirattai (Boerhaavia diffusd)
3. Nerunjil (Tribulus terrestris)
4. Neermulli (Asteracantha longifolia)
5. Maavilangam (Crataeva nuruvala)
6. Elumicham thulasi (Ocimum gratissimuni)
7. Murungai (Moringa oleiferd)
8. Mullangi (Raphanus sativus)
9. Nannari (Hemidestnus indicus)
10. Santhanam (Santalum album)
Do's
Drink at least 8 - 1 0 glasses of water per day and
increase it in summer
Reduce protein-intake (meats, beans, and nuts)
Consume dairy products (Buttermilk, ghee)
Eat foods with high fibre which include vegetables,
fruits, grains, salads etc.
Go for a walk or exercise daily
Avoid intake of coffee and tea
Take orange juice daily
Take plantain pith either in the form of juice or as
a food
Don'ts
Consumption of high-salt foods which contribute
to more calcium in urine
Don't eat meat and other food with rich protein
Don't drink carbonated drinks (they contain
phosphorus) which include all sodas
Don't eat foods with high sugar content
Don't sleep after eating

po m e Siddl la fo rmula t io ns useful in

Ka lla da ippu

Neermulli Kudineer
Nerunjil kudineer
Sirupeelai Kudineer
Nandukkal Parpam
Vediyuppu chunnam
Kalludaikudori Maathirai
Amirthadhi Chooranam

Dr. S. Justus Antony is Assistant Lecturcr,

Government Siddha Medical College, Palayamkottai
and Dr.Sathya Rajeswaran is Research Officer,
Siddha Central Research Institute, Arumbakkam,
Chennai