The document provides information on nephrotic syndrome from an Ayurvedic perspective. It discusses the structure and function of the kidney and nephron. It describes the causes, pathogenesis, and characteristics of nephrotic syndrome including massive proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria. The primary causes of nephrotic syndrome are discussed as minimal change disease, membranous glomerulopathy, and focal segmental glomerulosclerosis.

1. 1
Understanding Nephrotic
Syndrome as per
Ayurvedic Perspective
Government Akhandanand Ayurved
College, Ahmedabad, Gujarat.
Affiliated with Gujarat Ayurved
University
Presented by
Vd. Drashty D. Kambad (PG scholar)
Guided by
Dr.(Prof.) Surendra A. Soni (PhD, MD-Ayurveda)

2. Kidney
– The kidneys are a vital part of the body. Their main function is to
remove waste products from the blood, which are passed out of the body
in urine. There are about a million tiny filters in each kidney called
Glomeruli. If these filtering units get inflamed (swollen) for some reason
this is called Glomerulonephritis (GN).
– Glomerulonephritis is a non-specific disorder in which the kidneys are
damaged, causing them to leak large amounts of protein from the blood
into urine.

3. 4

4. Causes of Nephrotic Syndrome
Primary cause Secondary cause
Minimal change disease DM
Membranous Glomerulopathy Amyloidosis
Focal segmental
Glomerulosclerosis
Drugs (Gold, Penicillamine)
Membranous Proliferative
Glomerulopathy
Infection (Malaria, Hepatitis,
Syphilis, HIV)

5. THE NEPHRON
• Functional unit of the kidney .
Essential components:
1. Renal or malpighian corpuscle
(glomerulus and Bowman's capsule)
2. Proximal tubule
3. The thin limbs
4. Distal tubule
5. Connecting segment or connecting
tubule
6. Two main populations of nephrons:
1)Possessinga shortloop of Henle(7x
more)
2)Long loop of Henle

6. 12
THE NEPHRON

7. GLOMERULUS
The Glomerulus is a tuft of small blood vessels
called capillaries located with in bowman’s
capsule within the Kidney.
Glomerular Mesangial cells structurally support
the tufts.
Bloods enters the capillaries of the glojerulus by a
single arteriole called an afferent arteriole and
leaves by an efferent arteriole.

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9
ENDOTHELIAL CELL
•
•
•
•
Glomerular capillaries are lined by a thin
fenestrated endothelium
Human kidney range fr 70 - 100 nm Thin
diaphragms: extend across the fenestrae w/c
when present, are not believed to represent
a significant barrier to the passage of
macromolecules.
Surface is negatively charged because of the
presence of a polyanionic surface
glycoprotein, podocalyxin (principal
sialoprotein of glomerular epithelial cells)

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10
VISCERAL EPITHELIAL CELLS (PODOCYTES)
•
•
Largest cells in the glomerulus Long
cytoplasmic processes (trabeculae) that extend
from the main cell body and divide into
individual foot processes (pedicels), that come
into direct contact with the GBM.
Distance between adjacent foot processes near
the BM: 25 to 60 nm. Filtration slit membrane
(slit diaphragm) - 60 nm. fr the BM.
- role in establishing the permselec tive
properties of the filtration barrier is still a
matter of dispute.

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11
MESANGIAL CELLS
Mesangium : cells + matrix
Irregular in shape, with a dense nucleus and elongated
cytoplasmic processes that can extend around the capillary
lumen and insinuate themselves between the BM and the
overlying endothelium.
Provides structural support for the glomerular capillary
loops Contractile properties.
Regulation of glomerular filtration Exhibit phagocytic
properties (clearanceor disposal of macromolecules from
the mesangium) Generatinand metabolism of the
extracellular mesangial matrix and participate in
various forms of glomerular injury.

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12
GLOMERULAR BASEMENT MEMBRANE
Central dense layer (lamina densa) two
thinner, more electron-lucent layers, the
lamina rara externa and the lamina
rara interna
Layered configuration results from
the fusion of endothelial and epithelial BM
during development.
Mean width: 315 nm - 329 nm
Biochemical composition: glycoproteins
(type IV collagen, laminin, fibronectin,
entactin/ nidogen, various heparan
sulfate proteoglycan (perlecan and
agrin)

13. STRUCTURE OF GLOMERULAR WALL
Glomerular capillary wall is filtering area
• .It consists of three basic structure
• The layer of fenestrated endothelium
• Glomerular basement membrane
• Visceral epithelial layer(podocytes)

14. Glomerular Filtration Barrier
• Urine formation begins at the glomerular filtration
barrier.
• Theglomerular filter through which the ultrafiltrate
has to pass consists of three layers: the
fenestrated endothelium, the intervening
glomerular basement membrane, and the
podocyte slit diaphragm
• There are two kinds of barrier for filtration
1) Size barrier
2) Ion barrier

15. 1.SIZE BARRIER

16. 2. ION BARRIER
• There is another barrier called as negative charges
barrier.
• GBM, Endothelium and podocyte are negatively
charged.
• These negative charged Layers address to the
repulsion for negatively charged molecule.
• Ex. – Plasma protein at normal physiological ph
charged negatively like albumin.

17. NEPHROTIC SYNDROME
Nephrotic syndrome refers to clinical condition that
includes five main characters :-
1. Massive proteinuria (more then 3.5gm/day)
2. Hypo albuminaemia (less then 3gm/dl)
3. Generalized edema
4. Hyperlipidaemia (increase cholesterol and
triglycerides)
5. Lipidurea

18. Loss of glomerular filtration barrier or Abnormal immune system
PATHOGENESIS

19. 1.PROTEINUREA
ENDOTHELIUM AND ENDOTHELIAL CHARGE) ALLOWS THE PASSAGE OF MORE
• PROTEINURIA OCCURS PARTLY BECAUSE STRUCTURAL DAMAGE TO THE
GLOMERULAR BARRIER (PODOCYTES, MEMBRANE, FENESTRATED
AND MOLECULES.
• PROTEIN LEAKED OUT MORE THEN 3.5GM/DAY.(NEPHROTIC RANGE
PROTEINUREA)
• THE FILTRATION SLIT BETWEEN PODOCYTES AND NORMAL PODOCYTE
ARCHITECTURE, AND PODOCYTE FOOT PROCESSES ARE CRITICAL TO
MAINTAINING A BARRIER TO PROTEIN LOSS INTO THE URINARY SPACE, AS IS
FUNCTIONAL GBM AND HEALTHY CAPILLARY ENDOTHELIUM (AND ITS CHARGE).I
• PROTEINUREA MAYBE IN TWO TYPES :-
1. SELECTIVE PROTEINURIA (ONLY ALBUMIN LEAKED OUT)
2. NON-SELECTIVE PROTEINURIA

20. 2.HYPOALBUMINAEMIA
• LOSS OF URINARY PROTEIN (LARGELY ALBUMIN) OF THE
ORDER ≥3.5 G DAILY IN AN ADULT MAY LEAD TO
HYPOALBUMINAEMIA.
• THE NORMAL LIVER CAN SYNTHESIZE ALBUMIN AT A RATE
OF 10–12 G DAILY.
• THIS CAN BE PARTLY EXPLAINED BY INCREASED
CATABOLISM OF REABSORBED PROTEIN,
LARGELYALBUMIN, IN THE PROXIMAL TUBULES, EVEN
THOUGH THE RATE OF ALBUMIN SYNTHESIS IS INCREASED.
• LOSS OF PLASMA PROTEIN IN URINE CAN DECREASE
LEVEL OF ONCOTIC PRESSURE IN CIRCULATORY
COMPARTMENT AND RESULTS AS ANASARCA.

21. 3.HYPERLIPIDAEMIA
• This is a consequence of increased synthesis of lipoproteins as
A direct consequence of a low plasma albumin.
• Low-density lipoprotein (ldl) increases, very-low-density
Lipoprotein (vldl) and/or intermediate-density lipoprotein (idl)
Fractions increase, with no change (or a decrease) in hdl.
Hyperlipidaemia is caused by two factors:
1. Hypoproteinemia stimulates protein synthesis in the liver,
Resulting in the overproduction of lipoproteins
2. Lipid catabolism is decreased due to lower levels
Of lipoprotein lipase , The main enzyme involved in lipoprotein
Breakdown.

22. 4. EDEMA
• EDEMA IS THOUGHT TO BE CAUSED BY TWO MECHANISMS.
• THE FIRST BEING HYPOALBUMINEMIA WHICH LOWERS THE ONCOTIC PRESSURE WITHIN VESSELS
RESULTING IN HYPOVOLEMIAAND SUBSEQUENT ACTIVATION OF THE RENIN–ANGIOTENSIN
SYSTEM AND THUS RETENTION OF SODIUM AND WATER.
• NEPHROTIC SYNDROME EDEMA INITIALLYAPPEARS IN PARTS OF THE LOWER BODY (SUCH AS THE
LEGS) AND IN THE EYELIDS. IN THE ADVANCED STAGES IT ALSO EXTENDS TO THE PLEURAL
CAVITYAND PERITONEUM(ASCITES) AND CAN EVEN DEVELOP INTO A GENERALIZED ANASARCA.
• EDEMA MAYBE APPEAR MORE IN MOST DEPENDENT AREA LIKE, WALKING-LEGS, SLEEPING-BACK.

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25. 5. LIPIDUREA
• LIPIDURIAOR LOSS OF LIPIDS IN THE URINE IS INDICATIVE OF GLOMERULAR
PATHOLOGY DUE TO AN INCREASE IN THE FILTRATION OF LIPOPROTEINS
• WHEN LIPID PASSED THROUGH NEPHRONS TUBULES SOME CELLS OF
PROXIMAL CONVULATED TUBES STARTED PINOCYTOSIS AND BECOME
GLOBULATED.
• THESE CELLS BECOME DYSFUNCTIONALAND SHUT DOWN IN URINE.
IN THE URINE ANALYSIS PROCESS MAY BE FOUND BIG FAT GLOBULES THEY
CALLED AS “FAT OVALE BODIES”.

26. CAUSES OF NEPHROTIC SYNDROME
• NEPHROTIC SYNDROME MAY BE:-
1. PRIMARY
2. SECONDARY
1. Primary causes –
• Minimal change disease
• Membranous glomerulopathy
• Focal segmental glomerulosclerosis
• Membranousproliferative glomerulopathy
2.Secondery causes :-
1. DM,
2. Amyloidosis
3. Drugs (gold, penicillamine)
4. Infection (malaria, syphilis,HIV,… ..)

27. 1. MINIMAL CHANGES DISEASE
• THE MOST COMMON CAUSE OF NEPHROTIC SYNDROME IN CHILDREN.
• IT OWES ITS NAME TO THE FACT THAT THE NEPHRONS APPEAR
NORMAL WHEN VIEWED WITH AN OPTICAL MICROSCOPE AS THE
LESIONS ARE ONLY VISIBLE USING AN ELECTRON MICROSCOPE .
• ANOTHER SYMPTOM IS A PRONOUNCED PROTEINURIA.
• THE INDIVIDUAL FOOT PROCESSES CAN NO LONGER BE MADE OUT- IT
IS LIKE THEY HAVE ALL JUST “MELTED” TOGETHER INTO A SINGLE
THIN LAYER. THIS IMPORTANT BARRIER IN THE FILTRATION PROCESS
CAN NO LONGER KEEP PROTEIN FROM BEING FILTERED OUT OF THE
BLOOD AND INTO THE URINE.

29. 2. MEMBRANOUS GLOMERULOPATHY
• IDIOPATHIC MEMBRANOUS GLOMERULOPATHY IS AN AUTOIMMUNE DISEASE THAT OCCURS MAINLY IN
ADULTS, AND PREDOMINANTLY IN MEN.
• MICROSCOPIC HAEMATURIA, HYPERTENSION AND RENAL IMPAIRMENT MAY ACCOMPANY THE
NEPHROTIC SYNDROME.
• AS IN OTHER GLOMERULAR DISEASE, HYPERTENSION AND A GREATER DEGREE OF RENAL
IMPAIRMENT ARE POOR PROGNOSTIC SIGNS.
• MEMBRANOUS NEPHROPATHY IS CONSIDERED AN AUTOIMMUNE DISEASE, WHICH MEANS THAT IT
CAUSED BY THE BODY’S OWN IMMUNE SYSTEM. MN IS CAUSED BY THE BUILD-UP OF IMMUNE
COMPLEXES WITHIN THE FILTERS (GLOMERULI) OF THE KIDNEY ITSELF.
• ANTIBODIES AND ANTIGENS CREATE IMMUNE COMPLEXES THAT GET STUCK IN THE KIDNEY FILTER
(GLOMERULUS) AND CAUSE DISEASE.
• THESE AUTOANTIBODIES ARE ANTI PLA2R (ANTI-PHOSPHOLIPASE A2 RECEPTOR ANTIBODY) AND ANTI
THSD7A(ANTI-THROMBOSPONDIN TYPE 1 DOMAIN-CONTAINING 7A)
• DOCTORS CAN BE DIAGNOSED DIFFER KIND OF NEPHROTIC SYNDROME BY BIOPSY OF KIDNEY.

30. 3.FOCAL SEGMENTAL GLOMERULOSCLEROSIS
• FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)
DESCRIBES A SCLEROTIC GLOMERULAR LESION
THAT AFFECTS SOME (BUT NOT ALL) GLOMERULI,
AND SOME (BUT NOT ALL) SEGMENTS OF EACH TUFT.
• HYPOALBUMINAEMIA IS UNUSUAL.
• IMMUNOFLUORESCENCE DESCRIPTION
• IGM AND C3 DEPOSITED IN FOCALAND SEGMENTAL MANNER IN
SCLEROTIC SEGMENTS
• ELECTRON MICROSCOPY DESCRIPTION
• EPITHELIAL CELL DETACHMENT FROM GLOMERULAR BASEMENT
MEMBRANE
• EXTENSIVE FOOT PROCESS OBLITERATION (EVEN IN
NONSCLEROTIC GLOMERULI), MESANGIAL SCLEROSIS WITH
INCREASED MATRIX AND COLLAPSED GLOMERULAR LOOPS

31. A. PRIMARY FSGS
• THIS DISEASE OF UNKNOWN AETIOLOGY
USUALLY PRESENTS AS MASSIVE
PROTEINURIA (USUALLY NON-
SELECTIVE),HAEMATURIA, HYPERTENSION
AND RENAL IMPAIRMENT.
• THE ASSOCIATED NEPHROTIC SYNDROME IS
OFTEN RESISTANT TO STEROID THERAPY.
ALL AGE GROUPS ARE AFFECTED.
• IT USUALLY RECURS IN TRANSPLANTED
KIDNEYS, SOMETIMES DAYS OF
TRANSPLANTATION, AND PARTICULARLY IN
PATIENTS WITH AGGRESSIVE PRIMARY RENAL
DISEASE.

32. B. SECONDARY FSGS
• SECONDARY(SECONDARY, WHEN AN UNDERLYING CAUSE IS IDENTIFIED) FSGS WITH SIMILAR GLOMERULAR
CHANGES IS SEEN AS A SECONDARY PHENOMENON WHEN THE NUMBER FUNCTIONING NEPHRONS IS
REDUCED FOR ANY REASON.
• AS NEPHRONS FAIL, INCREASED FLOW THROUGH THE REMAINING NEPHRONS LEADS TO GLOMERULAR
HYPERTROPHY AND HYPERFILTRATION WITH THE SECONDARY CHANGES OF FSGS.
THIS IS ACTUALLY INCLUDING NUMEROUS CAUSES SUCH AS
AND PAMIDRONATE
.
• DIABETES MELLITUS
• KIDNEY DEFECTS FROM BIRTH
• URINE BACKING UP INTO KIDNEYS
• OBESITY
• SICKLE CELL ANEMIA
• VIRUSES (SUCH AS HIV)
HEROIN

33. 4.MEMBRANOPROLIFERATIVE GLOMERULOPATHY
• MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MPGN) IS AN UNCOMMON CAUSE OF CHRONIC
NEPHRITIS THAT OCCURS PRIMARILY IN CHILDREN AND YOUNG ADULTS. THIS ENTITY REFERS TO A
PATTERN OF GLOMERULAR INJURY BASED ON THE FOLLOWING THREE CHARACTERISTIC
HISTOPATHOLOGIC FINDINGS:
1. PROLIFERATION OF MESANGIAL AND ENDOTHELIAL CELLS AND EXPANSION OF THE MESANGIAL
MATRIX
2. THICKENING OF THE PERIPHERAL CAPILLARY WALLS BY SUBENDOTHELIAL IMMUNE DEPOSITS
AND/OR INTRAMEMBRANOUS DENSE DEPOSITS
3. MESANGIAL INTERPOSITION INTO THE CAPILLARY WALL, GIVING RISE TO A DOUBLE-CONTOUR ON
LIGHT MICROSCOPY

34. CONGENITAL NEPHROTIC SYNDROME
• CONGENITAL NEPHROTIC SYNDROME (FINNISH TYPE) IS AN AUTOSOMAL RECESSIVELY
INHERITED DISORDER DUE TO MUTATIONS IN THE GENE CODING FOR A
TRANSMEMBRANE PROTEIN, NEPHRIN; . NEPHRIN IS A CRITICAL ELEMENT OF THE
FILTRATION SLIT, AND ITS LOSS OF FUNCTION RESULTS INMASSIVE PROTEINURIA
SHORTLY AFTER BIRTH. PRESENTS IN FIRST 3 MONTHS OF LIFE
• THE DISORDER CAN BE DIAGNOSED IN UTERO, AS INCREASED Α-FETOPROTEIN IN
AMNIOTIC FLUID IS A COMMON FEATURE.
• HISTOLOGICALLY, SOME GLOMERULI ARE SMALL AND INFANTILE, WHERE AS OTHERS
ARE ENLARGED AND MORE MATURE, AND HAVE DIFFUSE MESANGIAL
HYPERCELLULARITY. BECAUSE OF THE MASSIVE
• PROTEINURIA, SOME TUBULES DEVELOP MICROCYSTS AND ARE DILATED. ON
ELECTRON MICROSCOPY, COMPLETE EFFACEMENT OF THE FOOT PROCESSES OF
VISCERAL EPITHELIAL CELLS IS OBSERVED. THIS CONDITION IS CHARACTERIZED BY
RELENTLESS PROGRESSION TO ESKD.

35. CONGENITAL NEPHROTIC SYNDROME
Presents in first 3 months of life
Etiology: heterogenous Finnish form –NPHS1 Mutation,AR
NPHS2,PLCE 1 mutation, intrauterine infections
CLINICAL FEATURES: anasarca, hypoalbuminemia ,oliguria
HISTOLOGY: microcystic dilatation of proximal tubules in NPHS1
Antenatal SREENING: Elevated levels of AFP in maternal serum
and amniotic fluid.
COMPLICATIONS: FTT, recurrent infections ,hypothyroidism and
progression to renal failure by 2-3 years
Treatment: supportive until weight (9Kg) suitable for renal
transplantation.

36. DIABETIC NEPHROPATHY
• DIABETIC RENAL DISEASE IS THE LEADING CAUSE OF ESKD IN THE WESTERN WORLD, ARISING
LARGELY AS ACOMPLICATION OF TYPE 2 DIABETES MELLITUS.
• DIABETIC KIDNEY DISEASE OCCURS IN ABOUT 20–30% OF BOTH TYPE 1 AND TYPE 2 DIABETICS THE
NATURAL HISTORY IS SIMILAR FROM THE ONSET OF PROTEINURIA, AND THE HISTOLOGICAL LESION IS
THE SAME.
PATHOLOGY
• THERE IS CONSTRICTION OF THE EFFERENT ARTERIOLES AND DILATION OF AFFERENT ARTERIOLES ,
WITH RESULTING GLOMERULAR CAPILLARY HYPERTENSION AND HYPERFILTRATION.
• GLOMERULAR HYPERFILTRATION (THE GFR INCREASES TO >150 ML/MIN/M2 ) AND INITIAL ENLARGEMENT
OF KIDNEY VOLUME OCCUR AS LOCAL VASOACTIVE FACTORS INCREASE FLOW. THE GBM THICKENS AND
THE MESANGIUM EXPANDS.PROGRESSIVE DEPLETION OF PODOCYTES FROM THE FILTRATION BARRIER
(THROUGH APOPTOSIS OR DETACHMENT) RESULTS IN PODOCYTURIA EARLY IN THE DISEASE.
PROTEINURIA EVOLVES AS FILTRATION PRESSURES RISE AND THE FILTER IS COMPROMISED. LATER,
GLOMERULOSCLEROSIS DEVELOPS WITH NODULES (KIMMELSTIEL–WILSON LESION - MATRIX INVADES THE
GLOMERULAR CAPILLARIES AND PRODUCES DEPOSITS CALLED KIMMELSTIEL-WILSON NODULES) AND HYALINE
DEPOSITS IN THE GLOMERULAR ARTERIOLES .

37. SIGN AND SYMPTOMS
• A FEW OTHER CHARACTERISTICS SEEN IN NEPHROTIC SYNDROME ARE:
• PUFFINESS AROUND THE EYES , CHARACTERISTICALLY IN THE MORNING.
• PITTING EDEMA OVER THE LEGS .
• FLUID IN THE PLEURAL CAVITY CAUSING PLEURAL EFFUSION . MORE
COMMONLY ASSOCIATED WITH EXCESS FLUID IS PULMONARY EDEMA.
• FLUID IN THE PERITONEAL CAVITY CAUSING ASCITES .
• GENERALIZED EDEMA THROUGHOUT THE BODY KNOWN AS ANASARCA

38. 38

39. COMPLICATIONS•

40. 1. INFECTIONS
• PATIENTS WITH NS ARE AT INCREASED RISK FOR INFECTIONS. ) .
• SEPSIS REMAINS ONE OF THE MAIN CAUSES OF DEATH IN CHILDREN WITH NS
.
2. THROMBOEMBOLISM
• NS IS A WELL-KNOWN RISK FACTOR FOR ARTERIAL OR VENOUS
THROMBOEMBOLISM (TE), AND PATIENTS WITH SEVERE PROTEINURIA.
• DUE TO LOSS OF ANTITHROMBIN PROTEIN WITH HEAVY PROTEINUREA.
3. HORMONAL,
• URINARY LOSS OF HORMONE-BINDING PROTEINS CONTRIBUTES TO VARIOUS
HORMONAL ABNORMALITIES IN PATIENTS WITH NS.

41. 3. CARDIOVASCULAR COMPLICATIONS
• AN INCREASED RISK OF CARDIOVASCULAR DISEASE EXISTS IN PATIENTS WITH NS
BECAUSE OF HYPERLIPIDEMIA, INCREASED THROMBOGENESIS, AND
ENDOTHELIAL DYSFUNCTION. HYPERCHOLESTEROLEMIA IS STRONGLY
ASSOCIATED WITH SEVERITY OF HYPOALBUMINEMIA.
• THERE IS LITTLE OR NO RISK OF CARDIOVASCULAR DISEASE IN CHILDREN WITH
MCNS WHO ARE RESPONSIVE TO CS BECAUSE HYPERLIPIDEMIA IS
INTERMITTENTAND OF SHORT DURATION.
• ELEVATED VLDL AND LDL SHOULD PLACE PATIENTS AT INCREASED RISK FOR
DEVELOPING ATHEROSCLEROSIS.
• ENDOTHELIAL DAMAGE FROM HYPERLIPIDEMIA MAY FAVOR INFLUX OF
LIPOPROTEIN INTO THE MESANGIUM, LEADING TO PROLIFERATION AND
SCLEROSIS.

42. 4. HYPOVOLEMIC CRISIS
• RISK FACTORS FOR HYPOVOLEMIC CRISIS INCLUDE SEVERELY DEPRESSED ALBUMIN
LEVELS, HIGH DOSE DIURETICS, AND VOMITING. THE CLINICAL MANIFESTATIONS ARE
TACHYCARDIA, COLD EXTREMITIES, POOR CAPILLARY REFILL, AND MODERATE TO
SEVERE ABDOMINAL PAIN, AND LABORATORY TESTS MAY SHOW ELEVATED
HEMATOCRIT AND URIC ACID LEVELS.
5. ANEMIA
• MILD ANEMIA IS OBSERVED ON OCCASION IN PATIENTS WITH NS. ANEMIA IS USUALLY
MICROCYTIC AND HYPOCHROMIC, TYPICAL OF IRON DEFICIENCY, BUT IS RESISTANT
TO THERAPY WITH IRON BECAUSE OF LARGE LOSS OF SERUM TRANSFERRIN IN THE
URINE OF SOME NEPHROTIC PATIENTS) . REPORTED SOME DATA ON THE METABOLISM
AND REGULATION OF ERYTHROPOIETIN (EPO) AND TRANSFERRIN, WHICH ARE
ESSENTIAL FOR ERYTHROPOIESIS IN NEPHROTIC CHILDREN.

43. 43

46. Ayurvedic
Approch of
Nephrotic
Syndrome

47. (5) Ayurvedic Approach To Nephrotic Syndrome
• Mutranirman prakriya(as per sushruta)
 Anatomical aspect of mutranirman.
1. नाभिपृष्ठकटीमुष्कगुदवङ्क्षणशेफसाम ्।
एकद्वारस्तनुत्वक्को मध्ये बस्स्तरधोमुखः ।।१८।।
2. अलाब्वा इव रूपेण भसरास्नायुपररग्रहः ।
बस्स्तबबस्स्तभशरश्चैव पौरुषं वृषणौ गुदः ।।।१९।।
3. एकसम्बस्धधनो ह्येते गुदास्स्िवववराश्रिताः /
मूत्राशयो मलाधारः प्राणायतनमुत्तमम ् ।।२०।।
47

48. 48
Ayurvedic Approach To Nephrotic Syndrome
• Mutranirman prakriya(as per sushruta)
 Physiological aspect of mutranirman.
1. पक्वाशयगतास्तत्र नाड्यो मूत्रवहास्तु याः ।
तपबयस्धत सदा मूत्रं सररतः सागरं यिा ।।२१।।
2.
सूक्ष्मत्वान्नोपलभ्यन्ते मुखान्यासाां सहस्रशः ।
नाडीभिरुपनीतस्य मूत्रस्यामाशयान्तरात ् ।।२२।।
3.
जाग्रतः स्वपतश्चैव स ननःस्यन्देन पूययते ।
आमुखात्सभलले न्यस्तः पाश्वेभ्यः पूययते नवः ।।२३।।
घटो यथा तथा ववद्धि बस्स्तमूयत्रेण पूययते ।

49. 49
Acharaya sushruta has described formation of urine
takes place in gastro-intestinal track. though, it is not
100% acceptable as per modern science but eventually
kidney is a selective filtration apparatus that can
regulate the excretion of metabolic waste at certain
pathophysiological level only. Hence, ayurveda
emphases virechana karma/ Apana regulation in most
shotha/ renal disorders while use of mutra-virechana
drugs has been instructed in very less amount in basti
marma chikitsa.

50. Approach to urinary Disorder according to ayurveda
• Lakshana Of Ajirna (Grahani chikitsa Charaksamhita)
1. तस्य भलङ्गमजीणयस्य ववष्टम्िः सदनां तथा ।
भशरसो रुक् च मूर्च्ाय च भ्रमः पृष्ठकटटग्रहः ॥४५॥
2. जृम्िाऽङ्गमदयस्तृष्णा च ज्वरश््टदयः प्रवाहणम् ।
अरोचकोऽववपाकश्च, घोरमन्नववषां च तत ् ॥४६॥
3. सांसृज्यमानां१ वपत्तेन दाहां तृष्णाां मुखामयान ् ।
जनयत्यम्लवपत्तां च वपत्तजाांश्चापरान ् गदान ् ॥४७॥
4. यक्ष्मपीनसमेहादीन ् कफजान ् कफसङ्गतम् ।
करोनत वातसांसृष्टां वातजाांश्च२ गदान ् बहून ् ॥४८॥
5. मूत्ररोगाांश्च मूत्रस्थां कु क्षिरोगान ् शकृ द्गतम् ।
रसाटदभिश्च सांसृष्टां कु यायद्रोगान ् रसाटदजान ् ॥४९॥

51. 51
Ayurvedic Corelation
 Acharya explained Shotha in following way
 Nidana of Sotha by Charak :
1. शुद््यामयािक्तकृ शाबलानाां िाराम्लतीक्ष्णोष्णगुरूपसेवा ।
द्याममृर्च्ाकववरोधिदुष्टगरोपसृष्टान्नननषेवणां च ॥५॥
2. अशाांस्यचेष्टा न च देहशुद्धिमयमोपघातो ववषमा प्रसूनतः ।
भमथ्योपचारः प्रनतकमयणाां च ननजस्य हेतुः श्वयथोः प्रटदष्टः ॥६॥
 Nidana of Sotha by Sushruta:
1. तत्रापतवपयतस्या्वगमनादनतमात्रमभ्यवहरतो वा वपष्टान्नहतरतकशाकलवणानन
िीणस्यवाऽनतमात्रमम्लमुपसेवमानस्यवाऽनतमात्रमम्लमुपसेवमानस्य
मृत्पक्वलोष्टकटशकय रानूपौदकमाांससेवनादजीर्णयनोवा
हस्त्यश्वोष्ररथपदानतसङ्िोिणादयो भसतस्य दोषा िातून ् प्रदूष्य
श्वयथुमापादयन्त्यर्खले शरीरे ।।४।।

52. 52
Types of sotha (sushruta)
1. तत्र वातश्वयथुररुणः कृ ष्णो वा मृदुरनवस्स्थतास्तोदादयश्चात्र
वेदनाववशेषाः; वपत्तश्वयथुः पीतः सरक्तो वा मृदुः शीघ्रानुसायूयषादयश्चात्र
वेदनाववशेषाः; श्लेष्मश्वयथुः पाणडुः शुक्लो वा स्स्नग्िः कटठनः शीतो
मन्दानुसारी, कण्वादयश्चात्र वेदनाववशेषाः; सस्न्नपातश्वयथुः
सवयवणयवेदनः; ववषननभमत्तस्तु गरोपयोगाद्दुष्टतोयसेवनात ्
प्रकु धथतोदकावगाहनात ् सववषसत्त्वटदग्िचूणेनावचूणयनाद्वा
 Samprapti of sotha Charaka:
1. बाहयाः भसराः प्राप्य यदा कफासृस्क्पत्तानन सन्दूषयतीह वायुः ।
तैबयद्िमागयः स तदा ववसपयन्नुत्सेिभलङ्गां श्वयथुां करोनत ॥८॥
 Samprapti of sotha Sushruta:
1. दोषाः श्वयथुमू्वां टह कु वयन्त्यामाशयस्स्थताः ।
पक्वाशयस्था म्ये च वचयःस्थानगतास्त्विः ।।६।।
2. कृ त्स्नां देहमनुप्राप्ताः कु युयः सवयसरां तथा ।

53. 53
Nidana of Prameha:
• इह खलु ननदानदोषदूष्यववशेषेभ्यो ववकारववघातिावािावप्रनतववशेषा
िवस्न्त । यदा हयेते त्रयो ननदानाटदववशेषाः परस्परां नानु१बध्नधत्यिवा
कालप्रकषाबदबलीयांसोऽिवाऽनुबध्नस्धत
1. न तदा ववकाराभिननवृयवत्तः,
2. धचराद्वाऽप्यभिननवयतयन्ते, तनवो वा
3. िवन्त्ययथोक्तसवयभलङ्गा वा; ववपययये ववपरीताः; इनत
सवयववकारववघातिावािावप्रनतववशेषाभिननवृयवत्तहेतुियवत्युक्तः ॥४॥
 Dushya of prameha:
1. बहव१बद्िां मेदो माांसां शरीरजक्लेदः शुक्रां शोर्णतां वसा मज्जा लसीका
रसश्चौजःसङ््यात इनत दूष्यववशेषाः ॥७॥
 All dushya of prameha to be considered as dushya of Nephrotic
syndrome.

54. 54
Samprapti of prameha
 Charaka:
• त्रयाणामेषाां ननदानाटदववशेषाणाां सस्न्नपाते क्षिप्रां श्लेष्मा प्रकोपमापद्यते,
प्रागनतिूयस्त्वात ्; स प्रकु वपतः क्षिप्रमेव शरीरे ववसृस्प्तां लिते,
शरीरशैधथल्यात ्; स ववसपयञ ् शरीरे मेदसैवाटदतो भमश्रीिावां गर्च्नत,
मेदसश्चैव बहवबद्ित्वान्मेदसश्च गुणैः समानगुणिूनयष्ठत्वात ्; स मेदसा
भमश्रीिवन ् दूषयत्येनत ्, ववकृ तत्वात ्; स ववकृ तो दुष्टेन मेदसोपटहतः
शरीरक्लेदमाांसाभ्याां सांसगां गर्च्नत, क्लेदमाांसयोरनतप्रमाणाभिवृद्ित्वात ्;
Kosthagata vata
Symptoms=तत्र कोष्ठाधश्रते दुष्टे ननग्रहो मूत्रवचयसोः||२४||
ब्र्नहृद्रोगगुल्माशयःपाश्वयशूलां च मारुते| ch.chi.28
Treatment=ववशेषतस्तु कोष्ठस्थे वाते िारां [१] वपबेन्नरः||८९||
पाचनैदीपनैयुयक्तैरम्लैवाय [२] पाचयेन्मलान ्| ch.chi.28

55. 55
(14) Pakvashayagata vata
 Symptoms= पक्वाशयस्थोऽन्त्रकू जां शूलाटोपौ करोनतच||२८||
कृ र्चरमूत्रपुरीषत्वमानाहां त्रत्रकवेदनाम ्|ch.chi.28
(15) Gudagata vata
Symptoms = ग्रहो ववणमूत्रवातानाां शूला्मानाश्मशकय राः||२६||
जङ्घोरुत्रत्रकपात्पृष्ठरोगशोषौ [१] गुदस्स्थते|ch.chi.28
Treatment = गुदपक्वाशयस्थे तु कमोदावतयनुद्धितम ्||९०||ch.chi.28

56. 56
1.Kosthagata
2.Pakvashaya gata
3.Gudagata
(16) Kosthagate,
Pakvashayagate and
Gudagate

57. 57
Samprapti Ghataka
 Dosha: Sleshma Pradhana Tridosha
 Dushya: Meda, mamsa, kleda, Shukra, Shonita, Vasa, Majja,
Lasika, Rasa. (Prameha Dushya)
 Srotas: Rasavaha, Mamsavaha, Medovaha, Majjavaha,
Shukravaha, Mutravaha, Purishvaha, Annavaha, Udakavaha.
 Strotodusti: Atipravruti, Vimargagamana
 Adhisthana: Bastipradesha (vrikka).
 Sammuthan- Pakvashaya
 Agni- Manda
 Sama/ Nirama- Sama
 Vyadhi- Chirkari
 Sadhyasadhyata: Krichasadhya/ Asadhya

58. 58
Samprapti
शुद्ध्यामयािक्तकृ शाबलाना
Nidana sevana
Dhatu poshan vyatikarma
Dhatu kshaya (proteinuria)
Basti/vrikka Marma dusti
Marmoupghata chakrapanitika
Prameha
(1st manifestation)
sotha (latter
condition)

59. 59
How to define prameha and nephrotic syndrome?
Prameha Nephrotic Syndrome
1. Here Atipravruti present.
क्लेदमांसयोरततप्रमाणाभि-वृद्धत्वात्;
But vrikka(tool) is in proper working
condition.
Due to destruction of GBM. Protenuria and
other symptoms of NS appears. So that whole
body compassion and further complication seen.
2. sleshmavardhak nidana. Marmadushak Nidana present
3. Samprapti.क्षिप्रंश्लेष्माप्रकोपमापद्यते, प्रागक्षतभूयस्त्वात्; Samprapti.बाह्ााःक्षिरााःप्राप्ययदा कफािृक्षपपत्ताक्षि िन्दूषयतीह वायाः।
4. Precepeting factor not present. Precepeting factor present here.
तत्रापतक्षपितस्तयाध्वगमिादक्षतमात्र-मभ्यवहरतो
5. It is a result of Samptarpana It is a result of apatarpana.
6. Purvarupa present here Purvarupa absent here.
7. Rupa is execration of purvarupa Rupa is mainly based on Urinary symptoms.
8. Annavaha and purishvaha strotas not
involved in prameha.
Shotha is present here
Annavaha and purishvaha strotas involved.
Chikitsa of NS : Dipana ,Pachana,Brihana and
Marmoposhana.

60. 60
(18) Medicine can be used
Medicines
1. Punarnavasthaka kwatha 11. Chitrakadhya ghri
2. Gomutraharitaki 12 Dashmoola haritaki avleha
3. Gudapipppalayadi churna
prayoga
13. Yograja guggulu
4. Gudaadraka prayoga 14. Punarnava guggulu
5. Sthala padmaka prayoga 15. Brihat Swarna bangeshvar rasa
6. Bhunibadi kwatha 16. Shilajatu rasayan
7. Simhasyadi kwatha 17. Shilajatu kalpa chikitsa
8. Punarnavadi ghrita 18. Vanga bhasma
9. Panchkoladhya ghrita 19. Chandraprabhavati
10 Sunthighrita 20. Shivagutika

61. SOME OTHER USEFUL
DRUGS :-
1.. KANSA HARITAKI
2. PUNARNAVAADI KWATHA
3.. GOKSHURADI KASHAYA
4. CHITRAKA GHRITA
5. GANDEERADYARISHTHA
6. PHALATRIKADYARISHTHA
7. AGNITUNDI VATI ETC.
Single drug therapy :-
1. Punarnava
2. varuna
3. Guduchi
4. Ashwagandha
5. Haridra
6. Badriphala
7. manzishtha

62. 62