Vivaldis Seveclear Tablets for Dogs & Cats | Intestinal Phosphate Binder & Uremic Toxin Adsorbent | Chronic Kidney Disease (CKD) Supportive Therapy | Pack of 10 Tablets

FOR ANIMAL USE ONLY — Administer as directed by a veterinarian. Vivaldis Seveclear is a veterinary nutraceutical supplement — not a veterinary medicine and not a replacement for prescribed CKD therapy (including phosphate-restricted renal diets, ACE inhibitors/ARBs, amlodipine for hypertension, erythropoiesis-stimulating agents for non-regenerative anaemia, or anti-emetics for uraemic nausea). Seveclear is indicated as a supportive adjunct to reduce intestinal phosphate absorption and uremic toxin load in dogs and cats with diagnosed chronic kidney disease (CKD) under active veterinary management. Pets with signs of acute uraemic crisis (profuse vomiting, severe lethargy, anorexia, oral ulceration, uraemic breath, seizures, or profound weakness) require emergency veterinary assessment — Seveclear is not appropriate as sole management for acute uraemia. Keep out of reach of children. Store in a cool, dry place below 25°C away from direct sunlight.

Vivaldis Seveclear Tablets for Dogs & Cats | Intestinal Phosphate Binder & Uremic Toxin Adsorbent | Chronic Kidney Disease (CKD) Supportive Therapy | Pack of 10 Tablets

Vivaldis Seveclear is a veterinary nutraceutical tablet formulated by Vivaldis Animal Health (India) to provide supportive management of chronic kidney disease (CKD) in dogs and cats through dual intestinal action: (1) intestinal phosphate binding — reducing dietary phosphate absorption from the GI tract, thereby attenuating the hyperphosphataemia that is the primary driver of renal secondary hyperparathyroidism, renal osteodystrophy, and accelerated CKD progression; and (2) uremic toxin adsorption — reducing the intestinal absorption of uremic solutes (including protein-bound uremic toxins such as indoxyl sulphate and p-cresyl sulphate) that accumulate in CKD and contribute to uraemic syndrome, systemic inflammation, and further nephron loss. Seveclear tablets are used as a supportive adjunct alongside a phosphate-restricted renal diet and other prescribed CKD medications under veterinary supervision. Pack of 10 tablets.

Chronic Kidney Disease in Dogs & Cats — Pathophysiology and the Rationale for Intestinal Phosphate Binding & Uremic Toxin Reduction

• Chronic kidney disease (CKD) — overview and staging: CKD is defined as structural or functional abnormalities of one or both kidneys that have been present for more than 3 months; CKD in dogs and cats is staged using the IRIS (International Renal Interest Society) CKD staging system based on fasting plasma creatinine concentration (a surrogate for GFR, glomerular filtration rate): IRIS Stage 1 (creatinine <140 µmol/L in dogs, <140 µmol/L in cats — non-azotaemic CKD, diagnosed on the basis of other renal biomarkers: SDMA [symmetric dimethylarginine — a sensitive early GFR marker that increases when GFR declines by ∼25%; SDMA is less affected by muscle mass than creatinine, making it a more reliable early CKD biomarker in cats, which are prone to muscle wasting], urine specific gravity <1.030 [dogs]/<1.035 [cats], renal proteinuria, or renal imaging abnormalities); IRIS Stage 2 (creatinine 140–249 µmol/L dogs / 140–249 µmol/L cats — mild azotaemia); IRIS Stage 3 (creatinine 250–439 µmol/L dogs / 250–439 µmol/L cats — moderate azotaemia); IRIS Stage 4 (creatinine >440 µmol/L — severe azotaemia / uraemia); CKD is further substaged by: (a) proteinuria — urine protein:creatinine ratio (UPC): non-proteinuric UPC <0.2 (dogs) / <0.2 (cats); borderline proteinuric UPC 0.2–0.5 (dogs) / 0.2–0.4 (cats); proteinuric UPC >0.5 (dogs) / >0.4 (cats); proteinuria in CKD indicates glomerular injury (loss of glomerular barrier charge and size selectivity → albumin filtration → proteinuria → tubular albumin endocytosis → tubular inflammation → tubulointerstitial nephritis progression → further nephron loss — a vicious cycle); (b) blood pressure — CKD-associated hypertension (systolic BP >160 mmHg [ACVIM/IRIS hypertension staging II]; hypertension causes glomerular hypertension [increased transcapillary pressure → glomerular mechanical stress → podocyte foot process effacement → proteinuria → tubulointerstitial nephritis]; renal, cardiac [left ventricular hypertrophy], ocular [hypertensive retinopathy → retinal haemorrhage → blindness — particularly in cats, in whom hypertensive blindness from acute retinal detachment is the most common presenting sign of feline CKD hypertension], and CNS complications of sustained hypertension); the pathophysiology of CKD progression: nephron loss (from any cause: glomerulonephritis [immune complex deposition — particularly in dogs with protein-losing nephropathy, Lyme nephritis, post-infectious GN]; chronic tubulointerstitial nephritis [the most common histological CKD pattern in cats — characterised by lymphoplasmacytic infiltration and interstitial fibrosis; aetiology often idiopathic but associated with feline morbillivirus, feline infectious peritonitis virus, and calicivirus in some studies]; polycystic kidney disease [PKD — autosomal dominant PKD1 mutation in Persians and Persian-crossed cats; OFD1 mutation in Bull Terriers for renal cystadenocarcinoma and nodular dermatofibrosis]; amyloid deposition [AA amyloidosis in Abyssinian cats — reactive systemic amyloidosis from chronic inflammatory conditions; amyloid deposits in the renal medullary interstitium → papillary necrosis]; obstructive nephropathy [urolithiasis, feline idiopathic cystitis, neoplasia]) → reduced functional renal mass → compensatory glomerular hyperfiltration in remaining nephrons (the single-nephron GFR of surviving nephrons increases as a compensation for lost nephrons — mediated by afferent arteriolar dilatation [prostaglandin E2, nitric oxide] and angiotensin II-driven efferent arteriolar constriction; glomerular hyperfiltration initially maintains total GFR but creates intraglomerular hypertension → progressive glomerulosclerosis → further nephron loss — the Brenner hypothesis of CKD self-perpetuation); the retained-solute hypothesis of uraemic toxicity: as GFR falls, nitrogenous metabolites and other solutes that are normally filtered and excreted by the kidney accumulate in plasma and body fluids → the uraemic syndrome: the clinical constellation of anorexia, nausea/vomiting (uraemic toxins inhibit the chemoreceptor trigger zone [CRTZ] in the area postrema), uraemic encephalopathy, peripheral neuropathy, impaired immune function, platelet dysfunction (uraemic inhibition of platelet aggregation via elevated guanidinosuccinic acid and methylguanidine → platelet GPIb and GPIIb-IIIa downregulation → bleeding diathesis — the mechanism of uraemic epistaxis and GI haemorrhage), and progressive wasting (protein-energy malnutrition from anorexia, uraemic inhibition of protein synthesis, and hypercatabolic state)
• Hyperphosphataemia in CKD — the central driver of renal secondary hyperparathyroidism and CKD progression: the healthy kidney filters ∼6–8g of phosphate per day and reabsorbs ∼85–90% in the proximal tubule (via NaPi-IIa/NaPi-IIc sodium-phosphate cotransporters on the apical brush border membrane of the proximal tubular cell; NaPi-IIa/IIc expression is downregulated by PTH [parathyroid hormone] and FGF23 [fibroblast growth factor 23] → increased fractional excretion of phosphate [FePO4] as phosphate load rises; FGF23 is produced by osteocytes in response to rising plasma phosphate → acts on the proximal tubule via FGFR1/Klotho receptor complex → increased NaPi-IIa/IIc internalisation → phosphaturia; FGF23 also inhibits renal CYP27B1 [1α-hydroxylase] → reduced calcitriol synthesis → reduced intestinal calcium and phosphate absorption); in CKD: reduced functional nephron mass → reduced total phosphate excretion capacity → initial phosphate retention → FGF23 rises (adaptive) → FGF23 drives phosphaturia in remaining nephrons and inhibits calcitriol synthesis → calcitriol deficiency → reduced intestinal calcium absorption → hypocalcaemia → PTH secretion by the parathyroid glands (renal secondary hyperparathyroidism — RSHP); the consequences of sustained RSHP: (a) renal osteodystrophy — PTH-driven osteoclastic bone resorption → fibrous osteodystrophy (osteitis fibrosa cystica) — particularly the facial bones ('rubber jaw' — submandibular/maxillary bone softening seen in young dogs with severe RSHP); (b) soft tissue mineralisation — elevated plasma Ca × PO4 product (when the calcium-phosphate product exceeds ∼55 mg2/dl2) promotes dystrophic and metastatic mineralisation in soft tissues (renal medullary mineralisation — nephrocalcinosis — directly injures tubular epithelial cells → tubulointerstitial nephritis; cardiovascular mineralisation — particularly the cardiac valves and coronary arteries in cats; pulmonary mineralisation); (c) direct nephrotoxicity — high plasma phosphate concentrations directly injure renal tubular epithelial cells (tubular mineralisation, mitochondrial dysfunction, and inflammatory cytokine activation — the direct phosphotoxicity of hyperphosphataemia independent of the calcium-phosphate product); (d) accelerated GFR decline — IRIS studies confirm that controlling phosphate in CKD cats (maintaining plasma phosphate within IRIS phosphate target ranges: Stage 1/2: <1.5 mmol/L; Stage 3: <1.6 mmol/L; Stage 4: <1.9 mmol/L) slows GFR decline and prolongs survival; the intestinal phosphate binding strategy: when dietary phosphate restriction alone (via a renal diet) is insufficient to achieve IRIS phosphate targets, intestinal phosphate binders (calcium carbonate, calcium acetate, aluminium hydroxide, lanthanum carbonate, sevelamer hydrochloride/carbonate) are added to meals to bind dietary phosphate in the GI lumen before absorption: phosphate binder + intestinal phosphate → insoluble calcium/aluminium/lanthanum phosphate complex → excreted in faeces → reduced net phosphate absorption → reduced plasma phosphate → reduced FGF23 → restored calcitriol → reduced PTH → attenuated RSHP
• Uremic toxins — classification, intestinal origin, and the rationale for intestinal adsorption: uremic toxins are broadly classified by molecular size and protein binding: (a) small water-soluble solutes (MW <500 Da; freely filtered; examples: urea, creatinine, guanidines [methylguanidine, guanidinosuccinic acid], oxalic acid, hippuric acid) — removable by dialysis but not the primary target of oral sorbents (these are renally cleared if GFR is adequate; as GFR falls, accumulate proportionally); (b) middle molecules (MW 500–60,000 Da; poorly dialysed; examples: beta-2-microglobulin [β2M], PTH [MW 9.4 kDa], FGF23, asymmetric dimethylarginine [ADMA — an endogenous NOS inhibitor that reduces NO production → endothelial dysfunction → cardiovascular disease in CKD], cystatin C); (c) protein-bound uremic toxins (PBUTs — the most clinically relevant targets for intestinal sorbents): the two most extensively studied PBUTs are indoxyl sulphate (IS) and p-cresyl sulphate (pCS): indoxyl sulphate (IS; 3-(sulphooxy)-1H-indole-3-yl acetic acid; MW 251.3 Da; plasma protein binding ∼90–95% — primarily bound to albumin at the indole binding site [Sudlow Site II] → only ∼5–10% is free IS in plasma → IS is poorly dialysed [protein binding limits dialysis clearance] despite its small molecular weight; the intestinal origin of IS: dietary tryptophan → colonic bacterial fermentation by Clostridium spp., Peptostreptococcus spp., and Bacteroides spp. via tryptophanase [TnaA: L-Trp → indole + pyruvate + NH3] → indole is absorbed from the colon → hepatic CYP2E1 and CYP2A6 oxidise indole → indoxyl → SULT1A1 sulphotransferase → indoxyl sulphate [IS] → IS enters circulation; IS nephrotoxicity: (i) tubular IS cytotoxicity — free IS enters proximal tubular cells via OAT1/OAT3 organic anion transporters on the basolateral membrane → intracellular IS activates AhR [aryl hydrocarbon receptor] → CYP1A1 induction → ROS [reactive oxygen species] generation via CYP1A1-mediated redox cycling → oxidative stress → tubular cell apoptosis and necrosis; (ii) tubulointerstitial fibrosis — IS-activated AhR → TGF-β1 and TGF-β2 upregulation → Smad2/3 phosphorylation → collagen I and fibronectin synthesis by myofibroblasts → interstitial fibrosis; (iii) glomerular injury — IS promotes podocyte apoptosis and foot process effacement via AhR → claudin-1 upregulation in podocytes → podocyte-parietal epithelial cell (PEC) adhesion → glomerulosclerosis); p-cresyl sulphate (pCS; 4-(sulphooxy)phenyl acetic acid; MW 188.2 Da; protein binding ∼90%; also produced intestinally: dietary tyrosine and phenylalanine → colonic fermentation by Clostridium difficile, C. scatologenes, and Bacteroides spp. via 4-hydroxyphenylacetate decarboxylase [HpdBC: 4-hydroxyphenylacetate → p-cresol + CO2] → p-cresol absorption → hepatic SULT1A1 → pCS; pCS nephrotoxicity similar to IS via OAT1/OAT3-mediated tubular uptake → AhR → ROS → TGF-β1 → fibrosis); the intestinal sorbent strategy for PBUTs: oral intestinal sorbents (activated charcoal, oxidised cellulose/AST-120, kaolin, zeolites) administered orally adsorb the PBUT precursors (indole from tryptophan, p-cresol from tyrosine/phenylalanine) in the colonic lumen before they can be absorbed and hepatically sulphated into IS and pCS → reduced plasma IS and pCS → reduced tubular PBUT delivery → reduced AhR activation → reduced ROS and TGF-β1 → slowed tubulointerstitial fibrosis; AST-120 (Kremezin — spherical activated carbon; approved in Japan and Korea for CKD; the oral intestinal adsorbent with the best clinical evidence in CKD: randomised trials in cats demonstrate AST-120 reduces plasma IS by ∼30–40% and attenuates GFR decline) is the best-studied intestinal PBUT sorbent in veterinary medicine

Composition

• Calcium Carbonate — intestinal phosphate binder (binds dietary phosphate in the GI lumen → insoluble calcium phosphate → faecal excretion → reduced phosphate absorption → reduced plasma phosphate → attenuated renal secondary hyperparathyroidism)
• Intestinal uremic toxin adsorbent (activated charcoal / oxidised cellulose / spherical carbon — adsorbs indole, p-cresol, and other uremic toxin precursors in the colonic lumen → reduced indoxyl sulphate [IS] and p-cresyl sulphate [pCS] generation and absorption)
• Refer to the Vivaldis Seveclear product label / veterinary datasheet for the current complete composition, excipients, and per-tablet quantities
• Pack: 10 tablets

Indications

• Supportive management of chronic kidney disease (CKD) in dogs and cats — all IRIS stages under veterinary supervision
• Reduction of hyperphosphataemia — as an intestinal phosphate binder adjunct to a phosphate-restricted renal diet when dietary restriction alone is insufficient to achieve IRIS phosphate targets
• Reduction of plasma uremic toxin (indoxyl sulphate, p-cresyl sulphate) burden in CKD dogs and cats to slow tubulointerstitial fibrosis progression
• Supportive adjunct to prescribed renal diets, ACE inhibitors, and other CKD-specific veterinary medications

Directions for Use

• Administer as directed by a veterinarian; dose and frequency are determined by body weight, IRIS CKD stage, plasma phosphate concentration, and clinical response
• Tablets may be administered directly (whole or crushed) or mixed with food; administering with or immediately after meals maximises phosphate binding efficacy (the phosphate binder must be present in the GI lumen simultaneously with the dietary phosphate load)
• Regular monitoring (plasma creatinine, SDMA, phosphate, calcium, UPC, blood pressure) is essential during CKD management — follow the veterinarian's monitoring schedule

Safety Information

• For animal use only — keep out of reach of children
• Not a replacement for a phosphate-restricted renal diet or prescribed CKD medications — Seveclear is a supportive adjunct, not a standalone CKD treatment
• Calcium carbonate-based phosphate binders can cause hypercalcaemia with excessive doses — monitor plasma calcium as directed by the veterinarian
• Pets with acute uraemic crisis (severe vomiting, anorexia, lethargy, oral ulcers, or uraemic seizures) require immediate veterinary assessment
• Store below 25°C in a cool, dry place away from direct sunlight