Nephrotic syndrome- An Ayurveda perspective.

understanding Nephrotic Syndrome as per the principles of Ayurveda.

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.

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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: Renal or malpighian corpuscle (glomerulus and Bowman's capsule) Proximal tubule The thin limbs Distal tubule Connecting segment or connecting tubule Two main populations of nephrons: 1)Po ss e ss in g a short lo o p of Henl e (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 M esangial 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.

8. 22 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)

9. 24 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.

10. 26 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 E x hib i t p h a g o c y t i c p r o p e r ti e s ( c l ea r an c e o r di s p o sa l of m a c r o m o l ec u l e s from the mesangium ) Ge n e r a t i nand m e t a b o li s m o f th e e x tr a ce ll u l a r m es ang i a l m a tr i x and participate in various forms of glomerular injury.

11. 27 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)

12. 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 )

13. 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

14. 1.SIZE BARRIER

15. 2 . ION BARRIER There is another barrier called as negative charges barrier. GBM, E ndothelium 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.

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

17. Los s o f glomer u lar fi l t r a tion barr i er o r Abnor m al immune system PATHOGENESIS

18. 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

19. 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, LARGELY ALBUMIN, 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.

20. 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.

21. 4. EDEMA • EDEMA IS THOUGHT TO BE CAUSED BY TWO MECHANISMS. • THE FIRST BEING HYPOALBUMINEMIA WHICH LOWERS THE ONCOTIC PRESSURE WITHIN VESSELS RESULTING IN HYPOVOLEMIA AND SUBSEQUENT ACTIVATION OF THE RENIN–ANGIOTENSIN SYSTEM AND THUS RETENTION OF SODIUM AND WATER. • NEPHROTIC SYNDROME EDEMA INITIALLY APPEARS IN PARTS OF THE LOWER BODY (SUCH AS THE LEGS) AND IN THE EYELIDS. IN THE ADVANCED STAGES IT ALSO EXTENDS TO THE PLEURAL CAVITY AND 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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23. 5. LIPIDUREA • LIPIDURIA OR 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 DYSFUNCTIONAL AND SHUT DOWN IN URINE. IN THE URINE ANALYSIS PROCESS MAY BE FOUND BIG FAT GLOBULES THEY CALLED AS “FAT OVALE BODIES”.

24. 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,… ..)

25. 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.

26. 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.

27. 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 FOCAL AND 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

28. 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.

29. 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

30. 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

31. 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.

32. CONGENITAL NEPHROTIC SYNDROME Presents in first 3 months of life Etiology: heterogenous Finnish form –NPHS1 Mu tation,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.

33. 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 .

34. 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

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36. COMPLICATIONS •

37. 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.

38. 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 INTERMITTENT AND 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.

39. 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 .

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41. Ayurvedic Approch of Nephrotic Syndrome

42. (5 ) Ayurvedic Approach To Nephrotic Syndrome Mutranirman prakriya(as per sushruta) Anatomical aspect of mutranirman. नाभिपृष्ठकटीमुष्कगुदवङ्क्षणशे फसाम् । एकद्वारस्तनुत्वक्को मध्ये बस्तिरधोमुखः ।।१८।। अलाब्वा इव रूपेण सिरास्नायुपरिग्रहः । बस्तिर्बस्तिशिरश्चैव पौरुषं वृषणौ गुदः ।।।१९।। एकसम्बन्धिनो ह्येते गुदास्थिविवराश्रिताः / मूत्राशयो मलाधारः प्राणायतनमुत्तमम् ।।२०।। 47

43. 48 Ayurvedic Approach To Nephrotic Syndrome Mutranirman prakriya(as per sushruta) Physiological aspect of mutranirman. पक्वाशयगतास्तत्र नाड्यो मूत्रवहास्तु याः । तर्पयन्ति सदा मूत्रं सरितः सागरं यथा ।।२१।। सूक्ष्मत्वान्नोपलभ्यन्ते मुखान्यासां सहस्रशः । नाडीभिरुपनीतस्य मूत्रस्यामाशयान्तरात् ।।२२।। जाग्रतः स्वपतश्चैव स निःस्यन्देन पूर्यते । आमुखात्सलिले न्यस्तः पार्श्वेभ्यः पूर्यते नवः ।।२३।। घटो यथा तथा विद्धि बस्तिर्मूत्रेण पूर्यते ।

44. 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 .

45. Approach to urinary Disorder according to ayurveda Lakshana Of Ajirna (Grahani chikitsa Charaksamhita) तस्य लिङ्गमजीर्णस्य विष्टम्भः सदनं तथा । शिरसो रुक् च मूर्च्छा च भ्रमः पृष्ठकटिग्रहः ॥४५॥ जृम्भाऽङ्गमर्दस्तृष्णा च ज्वरश्छर्दिः प्रवाहणम् । अरोचकोऽविपाकश्च, घोरमन्नविषं च तत् ॥४६॥ संसृज्यमानं१ पित्तेन दाहं तृष्णां मुखामयान् । जनयत्यम्लपित्तं च पित्तजांश्चापरान् गदान् ॥४७॥ यक्ष्मपीनसमेहादीन् कफजान् कफसङ्गतम् । करोति वातसंसृष्टं वातजांश्च२ गदान् बहून् ॥४८॥ मूत्ररोगांश्च मूत्रस्थं कुक्षिरोगान् शकृद्गतम् । रसादिभिश्च संसृष्टं कुर्याद्रोगान् रसादिजान् ॥४९॥

46. 51 Ayurvedic Corelation Acharya explained Shotha in following way Nidana of Sotha by Charak : शुद्ध्यामयाभक्तकृशाबलानां क्षाराम्लतीक्ष्णोष्णगुरूपसेवा । दध्याममृच्छाकविरोधिदुष्टगरोपसृष्टान्ननिषेवणं च ॥५॥ अर्शांस्यचेष्टा न च देहशुद्धि र्मर्मोपघातो विषमा प्रसूतिः । मिथ्योपचारः प्रतिकर्मणां च निजस्य हेतुः श्वयथोः प्रदिष्टः ॥६॥ Nidana of Sotha by Sushruta : तत्रापतर्पितस्याध्वगमनादतिमात् रमभ्यवहरतो वा पिष्टान्नहरितकशाकलवणानि क्षीणस्यवाऽतिमात्रमम्लमुपसेवमानस्यवाऽतिमात्रमम्लमुपसेवमानस्य मृत्पक्वलोष्टकटशर्करानूपौदकमांससेवनाद जीर्णि नोवा हस्त्यश्वोष्ट्ररथपदातिसङ्क्षोभणादयो सितस्य दोषा धातून् प्रदूष्य श्वयथुमापादयन्त्यखिले शरीरे ।।४।।

47. 52 Types of sotha (sushruta) तत्र वातश्वयथुररुणः कृष्णो वा मृदुरनवस्थितास्तोदादयश्चात्र वेदनाविशेषाः ; पित्तश्वयथुः पीतः सरक्तो वा मृदुः शीघ्रानुसार्यूषादयश्चात्र वेदनाविशेषाः ; श्लेष्मश्वयथुः पाण्डुः शुक्लो वा स्निग्धः कठिनः शीतो मन्दानुसारी , कण्ड्वादयश्चात्र वेदनाविशेषाः ; सन्निपातश्वयथुः सर्ववर्णवेदनः ; विषनिमित्तस्तु गरोपयोगाद्दुष्टतोयसेवनात् प्रकुथितोदकावगाहनात् सविषसत्त्वदिग्धचूर्णेनावचूर्णनाद्वा Samprapti of sotha Charaka : बाह्याः सिराः प्राप्य यदा कफासृक्पित्तानि सन्दूषयतीह वायुः । तैर्बद्धमार्गः स तदा विसर्पन्नुत्सेधलिङ्गं श्वयथुं करोति ॥८॥ Samprapti of sotha Sushruta : दोषाः श्वयथुमूर्ध्वं हि कुर्वन्त्यामाशयस्थिताः । पक्वाशयस्था मध्ये च वर्चःस्थानगतास्त्वधः ।।६।। कृत्स्नं देहमनुप्राप्ताः कुर्युः सर्वसरं तथा ।

48. 53 Nidana of Prameha: इह खलु निदानदोषदूष्यविशेषेभ्यो विकारविघातभावाभावप्रतिविशेषा भवन्ति । यदा ह्येते त्रयो निदानादिविशेषाः परस्परं नानु१बध्नन्त्यथवा कालप्रकर्षादबलीयांसो ऽथवाऽ नुबध्नन्ति 1 . न तदा विकाराभिनिर्वृत्तिः , 2. चिराद्वाऽप्यभिनिर्वर्तन्ते , तनवो वा 3 . भवन्त्ययथोक्तसर्वलिङ्गा वा ; विपर्यये विपरीताः ; इति सर्वविकारविघातभावाभावप्रतिविशेषाभिनिर्वृत्तिहेतुर्भवत्युक्तः ॥४॥ Dushya of prameha: बह्व१बद्धं मेदो मांसं शरीरजक्लेदः शुक्रं शोणितं वसा मज्जा लसीका रसश्चौजःसङ्ख्यात इति दूष्यविशेषाः ॥७॥ All dushya of prameha to be considered as dushya of Nephrotic syndrome.

49. 54 Samprapti of prameha Charaka: त्रयाणामेषां निदानादिविशेषाणां सन्निपाते क्षिप्रं श्लेष्मा प्रकोप मापद्यते , प्रागतिभूयस्त्वात् ; स प्रकुपितः क्षिप्रमेव शरीरे विसृप्तिं लभते , शरीरशैथिल्यात् ; स विसर्पञ् शरीरे मेदसैवादितो मिश्रीभावं गच्छति , मेदसश्चैव बह्वबद्धत्वान्मेदसश्च गुणैः समानगुणभूयिष्ठत्वात् ; स मेदसा मिश्रीभवन् दूषयत्येनत् , विकृतत्वात् ; स विकृतो दुष्टेन मेद सोपहितः शरीरक्लेदमांसाभ्यां संसर्गं गच्छति , क्लेदमांसयोर तिप्रमाणाभिवृद्धत् वात् ; Kosthagata vata Symptoms= तत्र कोष्ठाश्रिते दुष्टे निग्रहो मूत्रवर्चसोः||२४|| ब्रध्नहृद्रोगगुल्मार्शःपार्श्वशूलं च मारुते| ch.chi.28 Treatment= विशेषतस्तु कोष्ठस्थे वाते क्षारं [१] पिबेन्नरः||८९|| पाचनैर्दीपनैर्युक्तैरम्लैर्वा [२] पाचयेन्मलान्| ch.chi.28

50. 55 (14) Pakvashayagata vata Symptoms= पक्वाशयस्थोऽन्त्रकूजं शूलाटोपौ करोतिच||२८|| कृच्छ्रमूत्रपुरीषत्वमानाहं त्रिकवेदनाम्| ch.chi.28 (15) Gudagata vata Symptoms = ग्रहो विण्मूत्रवातानां शूलाध्मानाश्मशर्कराः||२६|| जङ्घोरुत्रिकपात्पृष्ठरोगशोषौ [१] गुदस्थिते| ch.chi.28 Treatment = गुदपक्वाशयस्थे तु कर्मोदावर्तनुद्धितम्||९०|| ch.chi.28

51. 56 1.Kosthagata 2.Pakvashaya gata 3.Gudagata (16) Kosthagate , Pakvashayagate and Gudagate

52. 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

53. 58 Samprapti शुद्ध्यामयाभक्तकृशाबलाना Nidana sevana Dhatu poshan vyatikarma Dhatu kshaya (proteinuria) Basti/vrikka Marma dusti Marmoupghata chakrapanitika Prameha (1 st manifestation) sotha (latter condition)

54. 59 How to define prameha and nephrotic syndrome? Prameha Nephrotic Syndrome 1. Here Atipravruti present. क्लेदमांसयोर तिप्रमाणाभि - वृद्धत् वात् ; 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 , प्रागतिभूयस्त्वात् ; Samprapti. बाह्याःसिराःप्राप्ययदा कफासृक्पित्तानि सन्दूषयतीह वायुः। 4. Precepeting factor not present. Precepeting factor present here. तत्रापतर्पितस्याध्वगमनादतिमात् र- 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.

55. 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

56. 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

57. 62 Thank you