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MUTRA GAVEENIKA SHOTHA — URINARY TRACT INFECTION (UTI)

Mutra Gaveenika Shotha is the NCISM/Kayachikitsa academic nomenclature covering inflammation of the urinary bladder (Gaveenika = bladder; Shotha = inflammation/infection), broadly correlating to cystitis and lower UTI in modern medicine, while the wider spectrum includes urethritis (Mutranalika Shotha) and pyelonephritis (Vrikka Shotha).

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I. DEFINITION

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II. ETIOPATHOGENESIS (CHART)

A. Etiology — Causative Organisms

CAUSATIVE ORGANISMS IN UTI
│
├── Gram-Negative Bacteria (most common)
│   ├── Escherichia coli ——————— >70% of all UTIs
│   ├── Klebsiella spp.
│   ├── Proteus mirabilis (especially in calculi, DM)
│   ├── Pseudomonas aeruginosa (nosocomial)
│   ├── Enterobacter spp.
│   └── Morganella / Citrobacter spp.
│
├── Gram-Positive Bacteria
│   ├── Staphylococcus saprophyticus (young women, community)
│   ├── Enterococcus spp.
│   └── Staphylococcus aureus (haematogenous route)
│
├── Sexually Transmitted Organisms
│   ├── Neisseria gonorrhoeae
│   └── Chlamydia trachomatis
│
└── Fungi / Viruses
    ├── Candida spp. (immunocompromised, catheterised)
    └── BK virus, Adenovirus, CMV (transplant recipients)

B. Route of Infection

PRIMARY ROUTE: ASCENDING (most common)
Perineal / periurethral bacteria
        ↓
Colonisation of urethra
        ↓
Ascent to bladder (Cystitis)
        ↓  [if untreated / host factors]
Ascent via ureters → Renal pelvis → Parenchyma (Pyelonephritis)

SECONDARY ROUTES:
• Haematogenous (Staphylococcus aureus → renal carbuncle)
• Lymphatic spread (rare)
• Direct extension (pelvic abscess)

C. Pathogenesis — Virulence vs Host Defence

PATHOGENESIS OF UTI

BACTERIAL VIRULENCE FACTORS           HOST DEFENCE FACTORS (if impaired → UTI)
• Type 1 & P-fimbriae (pili) —        • Normal urine flow (washout mechanism)
  adhesion to uroepithelium           • Urine pH, osmolality, Tamm-Horsfall protein
• Siderophores (iron acquisition)     • Intact urothelial barrier
• Toxins (haemolysin, cytotoxic       • Urinary IgA, phagocytic cells
  necrotising factor)                 • Normal bladder emptying
• Lipopolysaccharide (endotoxin)      • Mucin glycoprotein coating
        ↓                                       ↓
     Bacterial invasion of uroepithelial cells
        ↓
     Intracellular bacterial communities (IBCs) → Biofilm formation
        ↓
  Inflammatory cascade: IL-6, IL-8, TNF-α, PMN influx
        ↓
  Epithelial damage, mucosal oedema, haemorrhage → SYMPTOMS

D. Risk Factors

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III. DIAGNOSIS

A. Clinical Features

• Dysuria (burning micturition — Sadaha Mutra Pravritti)
• Frequency and urgency of micturition
• Suprapubic pain or heaviness
• Haematuria (frank or microscopic)
• Turbid, foul-smelling urine
• Absence of fever / systemic features

• Fever (>38°C), rigors
• Loin / flank pain (costovertebral angle tenderness)
• Nausea, vomiting, malaise
• Features of lower UTI may co-exist

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B. Investigations

INVESTIGATION LADDER FOR UTI
│
├── URINE DIPSTICK (first-line, rapid)
│   ├── Leukocyte esterase → pyuria proxy (sensitivity 70–90%)
│   ├── Nitrites → Gram-negative bacteria (Enterobacteriaceae reduce nitrates)
│   └── Blood (haematuria)
│
├── URINE MICROSCOPY
│   ├── Pyuria: >5–10 WBC/HPF
│   ├── Bacteriuria
│   ├── WBC casts → pyelonephritis (pathognomonic)
│   └── RBCs
│
├── URINE CULTURE & SENSITIVITY (Gold Standard)
│   ├── Mid-stream clean-catch urine
│   ├── Significant: >10⁵ CFU/mL (ASB / upper UTI)
│   ├── Significant: >10² CFU/mL (symptomatic lower UTI)
│   ├── Mandatory in: complicated UTI, pyelonephritis, pregnancy,
│   │   recurrent UTI, treatment failure
│   └── Not required: uncomplicated, first-episode cystitis
│
├── BLOOD INVESTIGATIONS (severe / complicated UTI)
│   ├── CBC — leukocytosis with neutrophilia
│   ├── ESR, CRP elevated
│   ├── Blood cultures (systemic sepsis, urosepsis)
│   └── Renal function (BUN, Creatinine)
│
└── IMAGING (selected cases)
    ├── Ultrasound KUB — structural abnormalities, hydronephrosis, calculi
    ├── X-ray KUB — radiopaque calculi, gas-forming infections
    ├── CT urogram — preferred for complicated UTI, recurrent cases, 
    │   suspected abscess or emphysematous pyelonephritis
    └── VCUG / MCU — vesico-ureteral reflux evaluation (children)

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IV. PRINCIPLES OF MANAGEMENT

A. Non-Pharmacological Management

1. Hydration — Increased oral fluid intake (>2–3 L/day) to promote urinary washout of pathogens
2. Personal hygiene — Wiping front-to-back; pre-/post-coital voiding
3. Urinary alkalinisation — Sodium bicarbonate/cranberry juice to reduce dysuria symptoms (adjunct)
4. Avoid irritants — Caffeine, alcohol, spicy foods during active infection
5. Bladder training — Scheduled voiding to reduce residual urine
6. Cranberry products — Proanthocyanidins inhibit bacterial adhesion (evidence: moderate benefit in recurrent UTI in women)
7. Probiotics — Lactobacillus spp. restoration of vaginal flora to prevent recurrence
8. Remove predisposing factors — Catheter removal, correction of obstruction, glycaemic control in DM
9. Voiding after intercourse — Key preventive measure in post-coital UTIs

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B. Pharmacological Management

1. Uncomplicated Cystitis (Acute Lower UTI)

Note: Fluoroquinolones are not recommended as first-line for uncomplicated UTI (risk of resistance, adverse effects). TMP-SMX should be used when local resistance < 20%. Nitrofurantoin and fosfomycin are preferred first-line per IDSA guidelines.

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2. Complicated UTI / Acute Pyelonephritis

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3. Recurrent UTI — Prophylaxis

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4. Special Situations

• Pregnancy: Cephalexin 500 mg BD × 3–7 days; Nitrofurantoin (avoid in 3rd trimester); TMP-SMX (avoid near term). Treat even ASB to prevent pyelonephritis (30% progression if untreated).
• Catheter-associated UTI: Treat only symptomatic cases; remove/change catheter where possible.
• Candidal UTI: Fluconazole 200 mg OD × 7–14 days.

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5. Symptomatic Relief

• Phenazopyridine (urinary analgesic) — 200 mg TDS × 2 days (turns urine orange; not antibacterial)
• NSAIDs — Evidence supports ibuprofen for symptom relief in uncomplicated UTI, though antibiotics remain superior (Cochrane 2024, PMID: 39698942)
• Anticholinergics/antimuscarinics — For bladder spasm (Oxybutynin) in selected cases

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V. AYURVEDIC PERSPECTIVE

A. Ayurvedic Nomenclature & Correlation

Mutrakrichchra = "Mutra" (urine) + "Krichra" (difficulty/pain) → painful, burning, difficult urination. UTI in Ayurveda is classified under Mutravaha Srotas Vikara.

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B. SAMPRAPTI (Pathogenesis / Etiopathogenesis) — Ayurvedic View

Nidana (Causative Factors)

• Aaharaj (Dietary): Katu (pungent), Tikshna (sharp), Ushna (hot), Ruksha (dry) foods; excess fish, marshy animal meat; alcohol; incompatible foods
• Viharaj (Behavioural): Excessive exercise, horse-riding/cycling, suppression of urinary urge (Vega-dharana), sexual excess
• Manasaj (Mental): Stress, anxiety (Vata aggravation)

• Excess exercise beyond capacity
• Habitual intake of alcohol
• Intake of food before previous meal is digested (Ama formation)
• Intake of sharp and dry substances

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Samprapti Vighatana (Pathogenesis Chart)

NIDANA (Causative factors)
        ↓
DOSHA PRAKOPA (Aggravation of Doshas)
• Vata (esp. Apana Vayu) — controls urinary elimination
• Pitta (esp. Pachaka/Ranjaka) — generates heat, daha
• Kapha — produces mucus, obstruction (Sanga)
        ↓
DUSHYA (Tissues/Elements affected)
• Mutra (urine) — primary dushya
• Mamsa (musculofibrous layer of urinary tract)
• Rakta (blood — in haematuria variant)
        ↓
SROTAS DUSHTI (Channel affliction)
• Mutravaha Srotas (urinary channels) — PRIMARY
• Raktavaha Srotas (blood channels)
• Ambu/Udakavaha Srotas (water metabolism channels)
        ↓
SROTO DUSHTI PRAKARA
• Sanga (obstruction — reduced urine flow, retention)
• Atipravritti (excessive flow/frequency — irritable bladder)
• Vimarga Gamana (altered path — pus/blood in urine)
        ↓
ADHISTHANA: Basti (Urinary Bladder) / Mutravaha Srotas
        ↓
RUPA (Signs & Symptoms)
• Sadaha Mutra Pravritti (burning micturition)
• Muhur Muhur Mutra Pravritti (frequency)
• Peetamutrata (yellowish urine)
• Basti / Mutrendriya Gurutwa (heaviness of bladder)
• Shweta, Snigdha, Picchila Mutra (turbid, mucoid urine)
• Raktamutrata (haematuria)
• Jwara (fever — in upper UTI)
• Shoola (pain — suprapubic / loin)

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C. SAMPRAPTI — Dosha-wise Analysis

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D. SHODHANA CHIKITSA (Purification/Detoxification Therapy)

1. Purvakarma (Pre-procedures)

• Snehana (Oleation): Oral medicated ghee (e.g., Panchatikta Ghrita, Gokshura Ghrita) — transports bioactives to urinary tract tissues, achieves neurological tone of bladder
• Swedana (Sudation): Steam therapy to flush toxins, restore cell metabolism

2. Pradhana Karma (Main Panchakarma Procedures)

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E. SHAMANA CHIKITSA YOGA (Palliative/Pacification Therapy with Drug Names)

1. Classical Formulations (Single Drug / Compound)

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2. Naimittika Rasayana (Rejuvenation specific to this disease)

• Shilajit with Triphala Kwatha
• Amalaki Rasayana
• Gokshuradi preparations — urinary tonic and immunomodulator

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3. Pathya-Apathya (Diet and Lifestyle)

• Takra (buttermilk), Yava (barley water), Mustakaadi Hima (cold infusions)
• Shali rice, Mudga dal (green gram), light meals
• Coconut water, sugarcane juice, tender coconut
• Adequate water intake
• Rest, avoidance of sexual activity during acute phase

• Spicy, oily, fried foods; alcohol; meat
• Suppression of natural urges (Vegadharana)
• Excessive exercise, horse-riding
• Cold, stale, and incompatible food combinations

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4. Yoga & Pranayama

• Asanas: Padangusthasana, Bhujangasana, Dhanurasana, Setu Bandha Sarvangasana, Marjariasana (target pelvic and abdominal region)
• Pranayama: Anulom-Vilom, Sheetali (cooling pranayama for Pitta)
• Meditation: Swadhisthana Chakra activation (governs urinary/reproductive system)

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VI. RECENT EVIDENCE NOTE

• A 2024 Cochrane systematic review (PMID 39698942) found that NSAIDs alone can provide symptom relief in uncomplicated UTI in women but are inferior to antibiotics in cure rates — antibiotics remain standard of care.
• A 2025 meta-analysis (PMID 40228579) confirms shorter antibiotic courses are as effective as longer courses for pyelonephritis/complicated UTI, reducing the risk of antimicrobial resistance.

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SUMMARY TABLE

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VRIKKA KOSHIKA SHOTHA — NEPHRITIS (GLOMERULONEPHRITIS)

Vrikka = Kidney | Koshika = Cellular/Glomerular (microscopic unit) | Shotha = Inflammation This NCISM/Kayachikitsa term corresponds to Glomerulonephritis (GN) / Nephritis in modern medicine — inflammation of the renal glomeruli (microscopic filtering units of the kidney).

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I. DEFINITION

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II. CLASSIFICATION OF NEPHRITIS

NEPHRITIS
│
├── PRIMARY (Intrinsic Renal Disease)
│   ├── IgA Nephropathy (Berger's Disease) — most common worldwide
│   ├── Post-infectious GN (PSGN) — esp. post-streptococcal
│   ├── Membranoproliferative GN (MPGN / C3 GN)
│   ├── Anti-GBM Disease (Goodpasture Syndrome)
│   ├── ANCA-associated Vasculitis GN (Pauci-immune)
│   │   ├── Granulomatosis with Polyangiitis (GPA / Wegener's)
│   │   ├── Microscopic Polyangiitis (MPA)
│   │   └── Eosinophilic GPA (Churg-Strauss)
│   └── Tubulointerstitial Nephritis (drug-induced, idiopathic)
│
└── SECONDARY (Systemic Disease)
    ├── Lupus Nephritis (SLE)
    ├── Diabetic Nephropathy
    ├── HSP / IgA Vasculitis
    ├── Infective Endocarditis-associated GN
    └── Cryoglobulinaemia, Amyloidosis

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III. ETIOPATHOGENESIS (CHART)

A. Etiological Factors (Nidana in Modern Context)

CAUSES / TRIGGERS OF NEPHRITIS
│
├── IMMUNE COMPLEX–MEDIATED (Type III Hypersensitivity)
│   ├── Post-streptococcal (beta-haemolytic Group A Streptococcus)
│   │   — 10–21 days after pharyngitis / impetigo
│   ├── SLE — anti-dsDNA + anti-C1q antibodies → immune deposits
│   ├── IgAN — galactose-deficient IgA1 + anti-gliadin IgA → mesangial deposits
│   ├── Infective endocarditis, abscess, shunt infections
│   └── Hepatitis B, C; HIV; malaria; schistosomiasis
│
├── ANTI-GBM ANTIBODY–MEDIATED (Type II Hypersensitivity)
│   └── Goodpasture's Syndrome — Anti-α3 chain of Type IV collagen
│       → Linear IgG deposits on GBM
│
├── PAUCI-IMMUNE (ANCA-associated)
│   └── p-ANCA (anti-MPO), c-ANCA (anti-PR3)
│       → Neutrophil activation → vessel wall destruction
│
├── COMPLEMENT-MEDIATED (C3 Glomerulopathy)
│   └── Dysregulation of alternative complement pathway
│
└── NON-IMMUNE (Drugs, Toxins, Metabolic)
    ├── NSAIDs, PPIs, antibiotics → Tubulointerstitial Nephritis
    ├── Lithium, gold, penicillamine → Membranous nephropathy
    └── Diabetes, hypertension → Glomerulosclerosis

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B. Pathogenesis — Mechanism of Glomerular Injury

PATHOGENESIS OF GLOMERULONEPHRITIS

TRIGGER (Infection / Autoantigen / Drug)
        ↓
IMMUNE ACTIVATION
Antibody formation (IgG, IgA, IgM) / T-cell activation
        ↓
IMMUNE COMPLEX FORMATION & DEPOSITION
• Subendothelial (PSGN, lupus → nephritic)
• Mesangial (IgAN → mild haematuria)
• Subepithelial (Membranous → nephrotic)
        ↓
COMPLEMENT ACTIVATION (C3 consumption → hypocomplementaemia)
↓ C3, ↓ C4 (lupus), ↓ C3 only (PSGN, MPGN)
        ↓
INFLAMMATORY MEDIATORS
• PMN & macrophage influx → proteases, ROS
• Cytokines: IL-1β, TNF-α, IL-6
• Platelet activation → TGF-β, PDGF
        ↓
GLOMERULAR INJURY
┌─────────────────────────────────────────────────────┐
│ Podocyte injury → loss of charge barrier → PROTEINURIA │
│ Endothelial injury → GBM disruption → HAEMATURIA     │
│ Mesangial cell proliferation → ↓ GFR → OLIGURIA     │
│ Na+ and water retention → OEDEMA + HYPERTENSION     │
└─────────────────────────────────────────────────────┘
        ↓
HISTOLOGICAL PATTERNS
• Diffuse proliferative GN (PSGN)
• Focal segmental GN (early IgAN, vasculitis)
• Crescentic GN (RPGN — Bowman's space proliferation)
• Membranoproliferative GN (C3, immune complex)
• Tubulointerstitial nephritis (drug/infection)
        ↓
OUTCOMES
Acute: Resolution (children, PSGN) OR
Subacute: RPGN → renal failure weeks-months OR
Chronic: Fibrosis → CKD → ESKD

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IV. DIAGNOSIS

A. Clinical Features

Nephritic Syndrome (Acute GN / Vrikka Koshika Shotha)

Nephrotic Syndrome Features (if overlap)

• Massive proteinuria (>3.5 g/day), hypoalbuminaemia, generalised pitting oedema, hyperlipidaemia, lipiduria (Maltese cross bodies)

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B. Investigations

INVESTIGATION LADDER FOR NEPHRITIS
│
├── URINE ANALYSIS (Mandatory)
│   ├── Dipstick: Blood +++, Protein ++/+++
│   ├── Microscopy: Dysmorphic RBCs, RBC casts (pathognomonic of GN)
│   │              WBC casts (TIN), granular casts
│   ├── Urine protein:creatinine ratio (spot sample)
│   └── 24-hour urine protein quantification
│
├── BLOOD INVESTIGATIONS
│   ├── CBC — anaemia, leucocytosis
│   ├── RFT — ↑ serum creatinine, ↑ BUN, ↑ uric acid
│   ├── Electrolytes — hyperkalaemia, metabolic acidosis
│   ├── Albumin, total protein — low in nephrotic overlap
│   ├── Lipid profile — hyperlipidaemia
│   └── ESR, CRP — elevated (active inflammation)
│
├── SEROLOGICAL TESTS (Etiology-specific)
│   ├── ASO titre, Anti-DNAse B, Streptozyme — PSGN
│   ├── C3, C4 complement — ↓C3 (PSGN, MPGN, lupus); ↓C3+C4 (lupus, cryo)
│   ├── ANA, anti-dsDNA — Lupus nephritis
│   ├── ANCA (c-ANCA/p-ANCA) — vasculitis GN
│   ├── Anti-GBM antibody — Goodpasture's Syndrome
│   ├── Serum IgA — ↑ in IgA nephropathy
│   ├── Serum cryoglobulins — cryoglobulinaemia
│   ├── HBsAg, HCV Ab — viral nephritis
│   └── Blood cultures — endocarditis-associated GN
│
├── IMAGING
│   ├── Ultrasound KUB — kidney size, echogenicity, cortical thickness
│   │   (Enlarged in acute GN; Small scarred kidneys = chronic GN)
│   ├── Chest X-ray — pulmonary oedema, pulmonary haemorrhage (ANCA/anti-GBM)
│   └── CT scan — if obstruction or abscess suspected
│
└── RENAL BIOPSY (Gold Standard for Definitive Diagnosis)
    ├── Indications: Nephritic syndrome with unknown aetiology;
    │   RPGN; lupus nephritis; persistent GN; before immunosuppression
    ├── Light Microscopy — cellular proliferation, crescents, necrosis
    ├── Immunofluorescence (IF) — IgA, IgG, IgM, C3 deposits; pattern
    │   (Linear = anti-GBM; Granular = immune complex; Pauci-immune = ANCA)
    └── Electron Microscopy — subendothelial, mesangial,
        subepithelial electron dense deposits; GBM changes

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V. PRINCIPLES OF MANAGEMENT

A. Non-Pharmacological Management

1. Rest — Bed rest during acute phase to reduce metabolic demand on kidneys
2. Dietary restriction:
   • Sodium restriction (<2 g/day) — to manage hypertension and oedema
   • Protein restriction — moderate (0.8 g/kg/day) in renal impairment; avoid excessive restriction
   • Potassium restriction — if hyperkalaemia present
   • Fluid restriction — only if oliguric
3. Weight monitoring — daily to track fluid retention
4. Blood pressure control (lifestyle) — DASH diet, exercise when appropriate, cessation of smoking
5. Treat underlying infections — streptococcal pharyngitis/impetigo (penicillin) in PSGN
6. Avoid nephrotoxins — NSAIDs, aminoglycosides, contrast media, PPIs (in TIN)
7. Glycaemic control — in diabetic nephropathy
8. Avoid triggers — in IgAN: treat tonsillitis, URI promptly; fish oil supplementation shown to slow progression

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B. Pharmacological Management

1. Oedema and Fluid Overload

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2. Hypertension and Proteinuria Reduction (Renoprotection)

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3. Immunosuppressive Therapy (Disease-Specific)

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4. Additional Drugs

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VI. AYURVEDIC PERSPECTIVE

A. Ayurvedic Nomenclature and Correlation

In Ayurveda, the kidney (Vrikka) is the root of Medovaha Srotas and the seat of Apana Vayu. Nephritis is understood as a complex vitiation of Tridosha (predominantly Pitta-Kapha with Vata) affecting the Vrikka, Mutravaha Srotas, and Medovaha Srotas.

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B. SAMPRAPTI VIGHATANA (Pathogenesis Chart — Ayurvedic)

Nidana (Causative Factors)

• Viruddha Ahara (incompatible food combinations)
• Lavana (excessive salt), Amla (sour), Katu (pungent), Ushna (hot) foods
• Abhishyandi (mucus-producing) foods: curd, fish, heavy food
• Kshira-viruddha (milk incompatibilities), Paryushita Ahara (stale food)
• Excess alcohol (Madyasevana)

• Vegadharana (suppression of natural urges)
• Ati vyayama (excessive exertion)
• Diwaswapna (day sleep — Kapha aggravation)
• Exposure to cold, damp environments
• Mithuna ati (sexual excess — Ojakshaya)

• Shoka (grief), Bhaya (fear), Chinta (anxiety) — Vata-Pitta aggravation

• Jwara-anubandhaja Vikara (post-febrile kidney damage — parallels post-streptococcal GN)
• Ama formation secondary to Mandagni

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Samprapti Ghataka (Components of Pathogenesis)

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Samprapti Vighatana — Pathogenesis Flow Chart

NIDANA (Diet / Lifestyle / Infection / Mental stress)
        ↓
DOSHA PRAKOPA
Pitta (inflammation, haematuria, fever, burning)
Kapha (oedema, proteinuria, mucoid urine, heaviness)
Apana Vata (impaired renal elimination)
        ↓
AMA FORMATION (Jatharagni + Dhatvagni Mandya)
Ama + Doshas = Samadosha → circulates in Rasavaha / Raktavaha Srotas
        ↓
SROTAS DUSHTI
Mutravaha Srotas: Sanga + Vimarga Gamana
Medovaha Srotas: Dhatwagni Mandya of Meda → Ojakshaya
Raktavaha Srotas: Ranjaka Pitta vitiation → Raktamutrata
        ↓
VRIKKA KOSHIKA SHOTHA
(Inflammation at cellular/glomerular level of kidney)
        ↓
RUPA (Clinical Manifestations)
• Shotha — Oedema (periorbital, pedal, ascites)
• Raktamutrata — Haematuria
• Ojasavimokshana — Proteinuria (Ojas leaking into urine)
• Jwara — Fever (Pitta)
• Daurbalya — Weakness (Ojakshaya)
• Udarda / Kandu — Itch (uraemia)
• Shwas-nishwas krichra — Dyspnoea (pulmonary oedema)
• Shiroruja — Headache (hypertension)
        ↓
COMPLICATIONS (if untreated)
Vrikka Nishkriyata → Chronic Renal Failure (Ashu / Chirakaari)

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C. SHODHANA CHIKITSA (Purification Therapy)

1. Purvakarma

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2. Pradhana Karma (Main Shodhana Procedures)

Note: In acute severe nephritis with uraemia, Shodhana must be done carefully with prior nourishing therapy (Brimhana). In paediatric cases, Virechana should be substituted with Mrudu Basti.

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D. SHAMANA CHIKITSA YOGA (Palliative Drug Therapy)

1. Single Drug Herbs (Mutrala + Shothahara + Nephroprotective)

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2. Classical Compound Formulations (Shamana Chikitsa Yoga)

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3. Naimittika Rasayana (Disease-specific rejuvenation)

• Punarnava Rasayana — primary nephroprotective Rasayana
• Amalaki Rasayana — antioxidant, tissue-regenerating
• Shilajit with warm water / Triphala decoction — renal tonic
• Guduchi Sattva (Tinospora starch) — immunomodulator, Rasayana

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4. Pathya-Apathya

• Mudga (green gram) soup, Takra (buttermilk — with rock salt), Laja (puffed rice), old Shali rice
• Yava (barley) water — diuretic, anti-inflammatory
• Coconut water, tender coconut
• Bitter vegetables: Patola (Trichosanthes), Nimba leaves (in moderation)
• Adequate water intake (unless oliguria/fluid restriction)
• Light, easily digestible foods (Laghu Ahara)

• Lavana (excess salt), Amla (sour), Katu (hot-spicy) foods
• Dadhi (curd), Matsya (fish), Mamsa (meat — especially marshy animals)
• Viruddha Ahara (incompatible food combinations)
• Alcohol, carbonated drinks
• Heavy, greasy, deep-fried foods
• Excessive physical exertion
• Vegadharana (suppression of natural urges)
• NSAIDs, nephrotoxic drugs (Apathya from Viharaj perspective)

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5. Yoga and Pranayama

• Asanas: Pawanmuktasana (wind-relieving — reduces gas, improves circulation), Setu Bandha Sarvangasana, Viparita Karani (inverted — reduces oedema), Balasana, Vajrasana, Savasana
• Pranayama: Anulom-Vilom (Nadi Shodhana), Bhramari (reduces stress → cortisol → renal protection), Sheetali/Sheetkari (cooling Pranayama — Pitta pacification)
• Meditation: Manasa Shanti — reduces stress (adrenal-renal axis); Trataka
• Avoid: Kapalbhati and Bhastrika in acute nephritis (increases intra-abdominal pressure)

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VII. RECENT EVIDENCE NOTE

• 2023 Nature Reviews Immunology review (PMID 36635359) confirms immunopathogenesis of GN involves complement, T-cells and B-cells — targeted immunotherapy is the frontier of treatment.
• 2025 Nature Reviews Nephrology review (PMID 39232245) highlights complement pathway inhibitors (Iptacopan — Factor B inhibitor) and SGLT2 inhibitors as emerging treatments for IgA nephropathy — significantly changing management.
• 2023 Nature Reviews Disease Primers (PMID 38036542) on IgA nephropathy establishes that sparsentan and budesonide (targeted-release) are now first-line options.

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SUMMARY TABLE

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