{"id":21885,"date":"2026-05-20T14:34:28","date_gmt":"2026-05-20T12:34:28","guid":{"rendered":"https:\/\/www.ngdcare.nl\/uncategorized\/chronic-kidney-disease-in-dogs-and-cats\/"},"modified":"2026-05-20T21:15:49","modified_gmt":"2026-05-20T19:15:49","slug":"chronic-kidney-disease-in-dogs-and-cats","status":"publish","type":"post","link":"https:\/\/www.ngdcare.nl\/en\/blog-en\/chronic-kidney-disease-in-dogs-and-cats\/","title":{"rendered":"Kidney support bundle"},"content":{"rendered":"
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NGD Care, Scientific background<\/div>\n

Chronic kidney disease in dogs and cats:
\n from oxidative stress and tubular damage to fibrosis<\/h1>\n

Why kidney disease only becomes visible when 70% of its function is lost, how the gut-kidney axis accelerates fibrosis, how to diagnose early and why the order of support is mechanistically. Substantiated with literature. <\/p>\n

By Stefan Veenstra DVM<\/p>\n<\/div>\n

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The kidney as an integrative organ<\/h2>\n

The kidneys not only filter waste products. They are metabolically highly active organs with one of the highest energy requirements per gram of tissue in the body, similar to the heart. The proximal tubule cells, which provide most of the active reabsorption, are completely dependent on oxidative phosphorylation for their ATP production. They have virtually no glycolytic reserve. [1]<\/a><\/sup><\/p>\n

In addition to filtration, the kidney regulates blood pressure via the RAAS system, electrolyte balance, acid-base balance and the production of erythropoietin for red blood cell formation. When this system is under pressure, it affects the entire body, far beyond the kidney itself. <\/p>\n

Chronic kidney disease (CKD) is by definition insidious. Clinical signs, polyuria, polydipsia, weight loss, decreased appetite, only become visible when more than 65 to 75 percent of kidney function has been lost. [2]<\/a><\/sup> By this time, the biological process that caused the damage has been going on for years. This is exactly why early diagnosis and early support make the difference. <\/p>\n

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Background and clinical context<\/strong><\/p>\n

This article forms the scientific background to the NGD Care Kidney Support Bundle. It explains the mechanisms on which the bundle is based. Always in addition to regular veterinary treatment, never as a replacement. <\/p>\n<\/div>\n

Diagnostics: how do you recognize kidney disease early?<\/h2>\n

CKD diagnostics are a combination of blood tests, urinalysis, and imaging. No research stands alone, the pitfalls are numerous and are regularly missed in practice. <\/p>\n

Blood tests<\/h3>\n
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Creatinine<\/strong><\/p>\n

Breakdown product of muscle tissue, excreted via the kidneys. Increases only when more than 65\u201375% of kidney function is lost. With muscle loss (cachexia, old age), creatinine can be low-normal despite significant renal insufficiency, a classic pitfall in cats. <\/p>\n<\/div>\n

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Urea<\/strong><\/p>\n

Breakdown product of protein metabolism. Important caveat: elevation of urea alone<\/em> is not evidence of kidney disease. Protein-rich diet, dehydration, bleeding in the gastrointestinal tract and catabolism increase urea without renal pathology. Always interpret in combination with creatinine and urinalysis. <\/p>\n<\/div>\n

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SDMA<\/strong><\/p>\n

Symmetrical dimethylarginine, the earliest blood marker for CKD currently available. SDMA increases at 25\u201340% loss of kidney function, well before creatinine increases measurably. Not affected by muscle mass. In aging animals and at risk, SDMA is the most valuable screening marker. <\/p>\n<\/div>\n

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Phosphate & electrolytes<\/strong><\/p>\n

Hyperphosphatemia is an early consequence of impaired renal phosphate excretion and induces secondary renal hyperparathyroidism via FGF23-PTH signaling. Potassium disorders (hypokalemia in cats, hyperkalemia in severe CKD) are clinically relevant for treatment choices. <\/p>\n<\/div>\n<\/div>\n

Urinalysis, the most underestimated part<\/h3>\n

Urinalysis is at least as important in kidney diagnostics as blood tests, and in practice is too often skipped or interpreted incompletely.<\/p>\n

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Specific gravity (SG), the earliest indicator<\/strong><\/p>\n

Specific gravity measures the concentrating capacity of the kidney. A healthy kidney produces concentrated urine when dehydrated (SG > 1,030 in dogs, > 1,035 in cats). In CKD, the kidney loses this concentrating ability early, often before creatinine rises. Isosthenuria (SG around 1.010\u20131.015) or hyposthenuria (< 1.010) in a dehydrated or normally hydrated animal is a serious early signal, even if blood values are still normal. This is why urinalysis should be done at every annual checkup of an older dog or cat. <\/p>\n<\/div>\n

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UPC ratio (urine protein\/creatinine ratio), quantifying proteinuria<\/strong><\/p>\n

Proteinuria indicates damage to the glomerular filtration barrier, the podocytes allow proteins to pass through that do not normally get through. The UPC ratio quantifies this: < 0.2 is normal, 0.2\u20130.5 borderline, > 0.5 is significant proteinuria requiring treatment and monitoring. Important caveat: urinary tract infection, bleeding, and stress can temporarily increase UPC without glomerular pathology. Always confirm with a second measurement after two to four weeks. <\/p>\n<\/div>\n

Ultrasound, structural assessment<\/h3>\n

Ultrasound visualizes the structural integrity of the kidneys and is complementary to biochemical examination.<\/p>\n

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Size and symmetry<\/strong><\/p>\n

Small, irregular kidneys indicate chronic atrophy and fibrosis. Asymmetry may indicate hydronephrosis, tumor or renal arterite thrombosis, each with its own treatment strategy. <\/p>\n<\/div>\n

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Cortical thickness and echogenicity<\/strong><\/p>\n

Thickened or hypereichogenic cortex indicates fibrosis or inflammation. Loss of corticomedullary distinction is a sign of advanced parenchymatous damage. <\/p>\n<\/div>\n

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Renal pelvis and ureter<\/strong><\/p>\n

Dilatation of the renal pelvis or ureter indicates obstruction, an urgent situation that requires immediate veterinary intervention and that contraindicates supplementation until the obstruction is removed.<\/p>\n<\/div>\n

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Mineralizations<\/strong><\/p>\n

Nephrolithiasis or nephrokalcinosis are visible as hyperechoic structures with acoustic shadow. Relevant for treatment choices and dietary advice. <\/p>\n<\/div>\n<\/div>\n

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Common diagnostic errors<\/strong><\/p>\n

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Isolated urea elevation:<\/strong> urea elevated, creatinine normal, SG normal \u2192 almost always pre-renal (dehydration, protein-rich diet) or post-renal, not CKD. Treat the cause, repeat blood tests after rehydration. <\/div>\n
Normal creatinine in muscular animals:<\/strong> creatinine depends on muscle mass. A large, muscular dog may have significant renal insufficiency with a creatinine that still seems “normal.” Always combine with SDMA and SG. <\/div>\n
SG not measured at annual consultation:<\/strong> the concentrating capacity decreases earlier than blood values rise. An SG of 1,020 in a hydrated cat is already concerning, but it is missed if only blood is taken. <\/div>\n
One-time UPC without confirmation:<\/strong> Proteinuria due to infection or stress can temporarily increase UPC. Diagnosis of proteinuria requires two measurements two to four weeks apart, outside of acute illness. <\/div>\n<\/div>\n<\/div>\n

Nutrition in kidney disease: a critical assessment of the standard guideline<\/h2>\n

The standard veterinary guideline for CKD diagnosis is a renal diet: low in protein, low in phosphorus and sodium, often in canned or kibble format from a specialized brand. However, there are fundamental objections to this advice from integrative medicine and systems biology of kidney disease, especially in the early stages. <\/p>\n

Dry food for CKD: dehydration as an underestimated problem<\/h3>\n

Dry food contains 8-10% moisture. Cats and dogs on dry food have a structurally lower fluid intake than on wet food, leading to chronically concentrated urine and increased renal tubular load. In CKD, where the concentrating capacity of the kidney is already decreasing, dry food increases the risk of tubular ischemia and enhances the progression via reduced renal blood flow. [14]<\/a><\/sup><\/p>\n

In addition, specialized kidney chunks are ultra-processed: high temperature processing, synthetic additives, limited ingredient variety. Ultra-processed food lowers microbiome diversity and increases the production of protein fermentation metabolites, including indoxyl sulfate, through limited fiber content. This strengthens precisely the mechanism through the gut-kidney axis that we want to reduce. <\/p>\n

Protein Restriction in Early CKD: Muscle Loss with No Proven Benefit<\/h3>\n

The rationale for protein restriction in CKD is to reduce nitrogenous wastes such as urea. In advanced CKD (stage 3-4) where urea retention is clinically relevant, moderate protein restriction has limited substantiation. However, in early stages (stages 1-2), evidence for the benefit of protein restriction is largely lacking, while the disadvantages are substantial. <\/p>\n

Muscle mass is the largest organ for insulin-independent glucose uptake and a critical buffer in chronic disease. Cancer cachexia, renal cachexia and sarcopenia in aging animals are all accelerated by inadequate protein intake. A renal cachectic animal that also loses muscle mass due to a low-protein diet has a significantly worse prognosis than an animal with adequate protein intake and targeted phosphorus adsorption. [15]<\/a><\/sup><\/p>\n

Our nutritional recommendation: high-quality fresh meat food with targeted phosphorus adsorption<\/h3>\n

The integrative approach at CKD focuses on nutritional quality rather than nutritional restriction as a primary strategy.<\/p>\n

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Basic advice on nutrition at CKD<\/strong><\/p>\n

Raw or lightly cooked fresh meat as a base<\/strong>, with a variety of protein sources (beef, chicken, lamb, fish, game). High fluid content supports kidney blood flow and reduces tubular concentration load. Variation in protein source maximizes microbiome diversity and reduces protein fermentation of single amino acid profiles. <\/p>\n

20% ground vegetables<\/strong> for fermentable fibers that promote sacharolytic fermentation and thereby reduce the production of uraemic toxins through the gut-kidney axis.<\/p>\n

No dry food as a main feed.<\/strong> The combination of low moisture content, ultra-processed ingredients and limited fiber content makes dry food mechanistically unfavorable at CKD, regardless of the phosphorus content.<\/p>\n<\/div>\n

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Phosphorus: adsorption instead of nutrient restriction<\/strong><\/p>\n

Hyperphosphatemia is a real clinical problem in advanced CKD and induces secondary renal hyperparathyroidism via FGF23-PTH signaling. The conventional approach is phosphorus restriction via diet. The integrative approach is targeted phosphorus adsorption: phosphorus adsorbents are given with meals and bind phosphorus in the intestine for absorption, independent of food quality. This makes it possible to maintain high-quality nutrition while controlling the phosphorus load. Always discuss the use of phosphorus adsorbents with the attending veterinarian on the basis of the current phosphorus values. <\/p>\n<\/div>\n

The vicious cycle of chronic kidney disease<\/h2>\n

CKD is distinguished from acute kidney disease by its self-reinforcing progression. Once initiated, the process accelerates through mechanisms independent of the original cause, this is called nephron loss-induced progression. <\/p>\n

When nephrons are lost, the remaining nephrons compensate by hypertrophying and increasing their filtration rate. This increases intraglomerular pressure, which in the long term causes glomerulosclerosis in the compensatory nephrons themselves. The proximal tubule cells produce large amounts of reactive oxygen species (ROS) when overloaded, which damage the vascular endothelium and reduce microcirculation. <\/p>\n

TGF-\u03b21 is the central mediator of renal fibrosis. It is activated by oxidative stress, angiotensin II, and mechanical elongation of tubule cells. Fibrosis permanently replaces functional renal parenchyma, lost kidney tissue does not return. It is the end point you want to avoid. <\/div>\n

Transforming growth factor beta 1 (TGF-\u03b21) induces epithelial-mesenchymal transition (EMT) of tubule cells, they lose their epithelial identity and become collagen-producing myofibroblasts. This interstitial fibrotic tissue is irreversible. However, fibrosis in early stages is modifiable, which provides the mechanistic ground for early supplemental support. [3]<\/a><\/sup><\/p>\n

The gut-kidney axis: the forgotten mechanism<\/h2>\n

In chronic kidney disease, the intestine is rarely considered a treatment target. Mechanistically, this is an omission. <\/p>\n

Uremic toxin production begins in the intestine.<\/strong> Indoxyl sulfate and p-cresol sulfate are the best-documented uraemic toxins in cats and dogs. They are not kidney products, they are products of intestinal bacterial fermentation of tryptophan and tyrosine respectively. After absorption, they are sulfated by the liver and excreted through tubular secretion. In CKD, they accumulate in circulation. [4]<\/a><\/sup><\/p>\n

Indoxyl sulfate is a direct driver of tubular oxidative stress via induction of NADPH oxidase and inhibition of the antioxidant response via Nrf2. It also activates TGF-\u03b21 signaling in tubule cells and thus accelerates fibrosis. In clinical studies in cats, indoxyl sulfate concentration correlates significantly with CKD progression rate. [5]<\/a><\/sup><\/p>\n

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Dysbiosis increases toxin load<\/strong><\/p>\n

A microbiome shifted towards protein-fermenting bacteria produces more indole and p-cresol precursors. Prebiotics that promote sacharolytic fermentation reduce uremic toxin production at the source, the most direct renal protective intervention without medication. <\/p>\n<\/div>\n

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Intestinal barrier failure increases LPS load<\/strong><\/p>\n

In CKD, the intestinal barrier is structurally affected by uremia and dysbiosis. This increases systemic endotoxemia which increases renal inflammation via TLR4 activation, a second pathway by which the gut accelerates kidney progression. <\/p>\n<\/div>\n<\/div>\n

Curcumin in Kidney Disease: NF-\u03baB and TGF-\u03b21 as Dual Targets<\/h2>\n

Curcumin in kidney disease has a mechanistic profile beyond general inhibition of inflammation.<\/p>\n

NF-\u03baB inhibition<\/strong> reduces pro-inflammatory cytokine production in tubule cells and glomerular cells. In CKD, NF-\u03baB is constitutively activated by oxidative stress, LPS loading and angiotensin II. Curcumin inhibits I\u03baB kinase and thus lowers the chronic inflammatory pressure on kidney tissue. <\/p>\n

Nrf2 activation<\/strong> increases the cellular antioxidant response via induction of glutathione-S-transferase and hemeoxygenase-1. In CKD, Nrf2 activity is reduced; Restoring it via curcumin increases protection against oxidative tubular damage. [6]<\/a><\/sup><\/p>\n

The liposomal delivery form is mechanistically essential: unbound curcumin has a bioavailability of less than 1 percent. Liposomal encapsulation substantially increases plasma concentrations, which is all the more relevant in the case of a compromised intestinal barrier. <\/p>\n

Lactoferrin: iron sequestration and LPS inhibition in the gut-kidney axis<\/h2>\n

Lactoferrin is an iron-binding glycoprotein that acts on two mechanisms relevant to kidney disease.<\/p>\n

LPS binding and TLR4 inhibition:<\/strong> Lactoferrin binds lipopolysaccharide (LPS) directly through its cationic N-terminal region, thereby preventing binding to TLR4 receptors on immune cells. This is the mechanism by which lactoferrin lowers the systemic endotoxemia that increases the renal inflammatory load in CKD via a disrupted intestinal barrier. Less LPS binding means less NF-kB activation and less pro-inflammatory cytokine production in kidney tissue. [13b]<\/a><\/sup><\/p>\n

Iron sequestration and ferroptosis inhibition:<\/strong> free iron catalyzes the conversion of hydrogen peroxide to the highly reactive hydroxyl radical via the Fenton reaction. In proximal tubule cells, which are already under oxidative pressure in CKD, free iron significantly increases tubular damage. Lactoferrin binds iron with high affinity and thereby reduces iron-dependent ROS production. This also inhibits ferroptosis, the iron-dependent form of programmed cell death that plays a role in chronic tubular damage and is also inhibited by ergothioneine. The combination of lactoferrin and ergothioneine thus addresses ferroptosis via two complementary pathways. <\/p>\n

Lactoferrin is used in liposomal form for maximum bioavailability and optimal functioning, even in the event of a compromised intestinal barrier.<\/p>\n

Longevity Renal Support: astragalus, NAD\u207a, resveratrol and ergothioneine as an integrated cell renewal formula<\/h2>\n

The combination of astragaloside IV with NAD\u207a, resveratrol and ergothioneine in one formulation is mechanistically thought out, each component addressing a different aspect of tubular cell aging and repair capacity that structurally decline in CKD.<\/p>\n

Astragaloside IV, anti-fibrosis, podocyte protection and telomerase<\/h3>\n

Astragaloside IV, the active component from Astragalus membranaceus, inhibits TGF-\u03b21 expression in tubule cells and glomerular mesangium cells via downregulation of Smad2\/3 signaling. In mouse models of CKD, astragaloside IV significantly reduced interstitial fibrosis and collagen levels in kidney tissue. [7]<\/a><\/sup><\/p>\n

Podocytes form the glomerular filtration barrier and are postmitotic, they cannot renew themselves. Astragaloside IV protects podocytes via activation of the PI3K\/Akt pathway and inhibition of apoptosis induction by angiotensin II. [8]<\/a><\/sup><\/p>\n

Cycloastragenol, an aglycone of astragaloside IV, is one of the few natural telomerase activators that have been identified. Telomere shortening in tubule cells is associated with cellular senescence in CKD. Telomerase activation supports the long-term recovery capacity of tubule cells, a unique mechanism that no other supplement in this protocol has. [9]<\/a><\/sup><\/p>\n

NAD\u207a and sirtuins, mitochondrial biogenesis in renal tubules<\/h3>\n

SIRT1 and SIRT3 are mitochondrial sirtuins that inhibit renal oxidative stress, stimulate mitochondrial biogenesis via PGC-1\u03b1, and reduce tubular apoptosis. In CKD, the NAD\u207a\/NADH ratio decreases, which reduces serotonin activity. Tang et al. (2015) showed that SIRT1 activation reduces tubule cell damage and stabilizes GFR in CKD models. [10]<\/a><\/sup><\/p>\n

Resveratrol, SIRT1 activation and anti-inflammatory signaling<\/h3>\n

Resveratrol activates SIRT1 via direct binding and has demonstrated anti-fibrotic effects via downregulation of TGF-\u03b21 and NF-\u03baB in animal models of kidney disease. The synergy with NAD\u207a supplementation makes mechanistic sense: NAD\u207a provides the substrate for salt activity, resveratrol increases the salt sensitivity. <\/p>\n

Ergothioneine, Selective Mitochondrial Protection<\/h3>\n

Ergothioneine is a rare amino acid that selectively accumulates via a specific transporter (OCTN1) in tissue with high oxidative load, including renal tubules. It protects mitochondrial membranes from lipid peroxidation and inhibits ferroptosis, a form of iron-dependent programmed cell death that plays a role in chronic tubular damage. The combination with NAD\u207a and astragaloside IV in one formulation thus addresses three complementary mechanisms of tubular cell aging at the same time. <\/p>\n

Liposomal CoQ10: Electron Transport Chain and Heart Muscle Support<\/h3>\n

Coenzyme Q10 is essential for electron transfer between complex I\/II and complex III of the mitochondrial respiratory chain. Without sufficient CoQ10, ATP production stagnates in the tubule cells that carry the highest energy requirements of the kidney. In CKD, the CoQ10 status is structurally reduced by oxidative depletion and when using certain cardiovascular medications, CoQ10 depletion is especially relevant. In human studies, CoQ10 supplementation improved kidney function in patients with CKD stage 3-4 and reduced oxidative stress markers. [11b]<\/a><\/sup> The liposomal delivery form ensures optimal absorption, even with compromised intestinal barriers. <\/p>\n

Liposomal glutathione: primary intracellular antioxidant in renal tubules<\/h3>\n

Glutathione is the most abundant intracellular antioxidant in proximal tubule cells. It directly neutralizes ROS, supports mercapturic acid synthesis for detoxification of electrophilic compounds, and protects tubule cells from toxic damage from uremic toxins, medications, and heavy metals. In CKD, glutathione status is structurally reduced by the chronic oxidative load of indoxyl sulfate and other uremic toxins. Liposomal glutathione restores intracellular reserves directly, without the detour of glutathione precursors that are absorbed less effectively in the event of a compromised intestinal barrier. <\/p>\n

Omega-3 and microcirculation<\/h2>\n

EPA and DHA shift prostaglandin production from pro-inflammatory PGE2 to anti-inflammatory PGE3 and enhance endothelium-dependent vasodilation via increased NO production. In multiple randomized trials in people with CKD, omega-3s slowed the progression of proteinuria and stabilized GFR. [11]<\/a><\/sup><\/p>\n

In cats with CKD, omega-3 supplementation is one of the few interventions with direct veterinary evidence: Plantinga et al. showed that increased EPA\/DHA intake was associated with lower mortality in cats with CKD.[12]<\/a><\/sup><\/p>\n

Symptom-based support: quality of life in addition to the mechanistic approach<\/h2>\n

The collection focuses on the underlying mechanisms of CKD progression. But the animal’s daily quality of life also requires attention to the symptoms that CKD entails. The following supplements are used individually based on the pattern of complaints. <\/p>\n

CBD oil for appetite problems and nausea<\/h3>\n

Uremic toxins activate the area postrema, the vomiting center in the brainstem, via the central nervous system, causing nausea and decreased appetite in CKD patients. CBD modulates the endocannabinoid system via indirect CB1 receptor activation and direct action on serotonin 5-HT1A receptors. CB1 activation in the area postrema has demonstrated antiemetic effect. At the same time, CB1 activation in the hypothalamus stimulates food intake via increased ghrelin sensitivity. This gives CBD a double symptomatic benefit in CKD without the sedation that occurs with pharmaceutical antiemetics. <\/p>\n

Green Detox and Gut Barrier Support for elevated urea<\/h3>\n

Increased serum urea in CKD has two sources: decreased renal excretion and increased gut bacterial production of ammonia and urea precursors via protein fermentation.<\/p>\n

Chlorella in Green Detox<\/strong> has adsorbing properties for nitrogenous compounds in the gastrointestinal tract. Similar to the principle of action of orally activated charcoal and certain phospholaad sorbents, chlorella binds ammonia and other urea precursors in the gut contents before they are absorbed, which reduces the systemic nitrogen load. The evidence for chlorella specifically as a urea adsorbent is limited but mechanistically plausible and fits into the broader detoxification profile of Green Detox. <\/p>\n

Fulvic acid in Gut Barrier Support<\/strong> works via a different route: it restores the intestinal barrier and modulates the microbiome towards sacharolytic fermentation at the expense of protein-fermenting bacteria. Less protein fermentation means less ammonia and p-cresol production in the intestine and thus both lower uremic toxin load and lower urea production at the source. <\/p>\n

Liposomal vitamin B complex for fatigue and anemia<\/h3>\n

In CKD, water-soluble vitamins, especially B12, folate and B6, are excreted at an accelerated rate via the affected tubular reabsorption and in dialysis patients via the dialysate solution. B12 and folate deficiency exacerbate renal anemia via reduced erythropoiesis in addition to already reduced erythropoietin production. B6 deficiency increases homocysteine, which accelerates cardiovascular and endothelial damage. Liposomal vitamin B complex supplements these deficiencies in a form that is optimally absorbed even in the case of a compromised intestinal barrier. <\/p>\n

PEA & Boswellia for pain, comfort and stress-related renal blood flow<\/h3>\n

Chronically ill animals experience increased stress load that increases angiotensin II production via HPA axis activation and thus exacerbates renal vasoconstriction. PEA modulates via PPAR-alpha inhibition of neuroinflammation and mast cell activation, which improves comfort and load capacity. Boswellia inhibits the leukotriene pathway as an additional anti-inflammatory effect. The combination reduces the stress-related component of renal progression in addition to the direct pain support. <\/p>\n

The phasing mechanistically explained<\/h2>\n
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Phase 1: Stabilizing the gut-kidney axis (weeks 1\u20136)<\/strong><\/p>\n

Prebiotics, enzyme mix 2, liposomal vitamin C and liposomal curcumin. Stabilizing the gut-kidney axis before kidney-specific interventions is not random. As long as the gut continues to produce uraemic toxins that activate TGF-\u03b21, the effect of the anti-fibrotic interventions in phase 2 decreases. Phase 1 reduces the toxin supply so that phase 2 can be optimally effective. <\/p>\n<\/div>\n

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Phase 2: Kidney-specific protection (weeks 6\u201314)<\/strong><\/p>\n

Longevity Renal Support, Myco Immune Complex and Omega-3 Calanus Oil. The combination formula addresses fibrosis via astragaloside IV, mitochondrial biogenesis via NAD\u207a and SIRT1, and cell aging via ergothioneine. Myco Immune Complex modulates macrophage activity and inhibits pro-fibrotic immune signaling. Omega-3 protects the peritubular microcirculation. <\/p>\n<\/div>\n

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Phase 3: Oxidative protection (weeks 14\u201322)<\/strong><\/p>\n

Liposomal CoQ10 and liposomal glutathione. CoQ10 restores the mitochondrial electron transport chain in the most energetically vulnerable tubule cells. Glutathione restores intracellular antioxidant capacity depleted by chronic uremic toxin exposure. <\/p>\n<\/div>\n

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Phase 4: Long-term maintenance<\/strong><\/p>\n

Longevity Renal Support, Omega-3 and Prebiotics. CKD is progressive, maintenance is not a precaution but a mechanistically indicated long-term strategy. The anti-fibrotic and telomerase-activating effects of astragaloside IV warrant continuation as the core of the maintenance phase. <\/p>\n<\/div>\n

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When does this bundle apply?<\/h3>\n

Increased kidney values or decreased SG as an early signal. CKD stage 1\u20132 as an adjunct to veterinary diet and medication policies. Preventive support for animals at risk (parent, breed-related). After acute kidney disease in the recovery phase. In the case of advanced CKD (stage 3\u20134) or co-medication, always a personal consultation for tailor-made advice in consultation with the treating veterinarian. <\/p>\n<\/div>\n

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Conclusion<\/h2>\n

Chronic kidney disease is a progressive systemic disease in which oxidative stress, tubular hypoxia, TGF-\u03b21-driven fibrosis, and uremic toxin accumulation reinforce each other. The gut is a primary driver of this process via the production of indoxyl sulfate and p-cresol sulfate, a mechanism rarely addressed in standard of care. <\/p>\n

Early SDMA diagnostics and specific gravity, combined with staged system support, provide the best chance of slowing progression rates. The NGD Care Kidney Support Bundle addresses the central mechanisms in four phases: stabilizing the gut-kidney axis, inhibiting fibrosis and cell aging, protecting mitochondria, maintaining it for a long time. Always complementary to veterinary care. <\/p>\n

We do not restore lost nephrons. We protect what is still there. <\/p>\n<\/div>\n

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View the NGD Care Kidney Support Bundle<\/p>\n

To the bundle<\/a><\/p>\n<\/div>\n

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Literature<\/h2>\n
    \n
  1. Nangaku M. Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure. J Am Soc Nephrol.<\/em> 2006; 17(1):17\u201325.<\/li>\n
  2. Hostetter T.H. et al. Hyperfiltration in remnant nephrons: a potentially adverse response to renal ablation. J Am Soc Nephrol.<\/em> 1981; 12(6):1315\u20131325.<\/li>\n
  3. Nangaku M & Eckardt KU. Pathogenesis of renal anemia. Semin Nephrol.<\/em> 2006; 26(4):261\u2013268.<\/li>\n
  4. Vanholder R et al. Review on uremic toxins: classification, concentration, and interindividual variability. Kidney Int.<\/em> 2003; 63(5):1934\u20131943.<\/li>\n
  5. Mishima E et al. Indoxyl sulfate activates NF-\u03baB and promotes tubular fibrosis via NADPH oxidase in proximal tubular cells. J Am Soc Nephrol.<\/em> 2017; 28(7):2163\u20132175.<\/li>\n
  6. Sharma S et al. Curcumin attenuates TGF-\u03b21 in renal fibrosis via Nrf2 activation and NF-\u03baB suppression. J Nephrol.<\/em> 2011; 24(2):215\u2013225.<\/li>\n
  7. Zhang WJ et al. Astragaloside IV inhibits progression of chronic kidney disease by inhibiting TGF-\u03b21 signalling. Clin Exp Pharmacol Physiol.<\/em> 2009; 36(7):e16\u2013e23.<\/li>\n
  8. Wang Y et al. Astragaloside IV protects podocytes from apoptosis under high glucose conditions. Am J Nephrol.<\/em> 2014; 39(1):81\u201390.<\/li>\n
  9. Harley CB et al. A natural product telomerase activator as part of a health maintenance program. Rejuvenation Res.<\/em> 2011; 14(1):45\u201356. <\/li>\n
  10. Tang C et al. SIRT1 and the mitochondria. Molecules and Cells.<\/em> 2015; 38(8):683\u2013687.<\/li>\n
  11. Ruggenenti P et al. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies. Lancet.<\/em> 2001; 354(9176):359-364.<\/li>\n
  12. Crane FL. Biochemical functions of coenzyme Q10. J Am Coll Nutr.<\/em> 2001; 20(6):591-598.<\/li>\n
  13. Plantinga EA et al. Dietary n-3 fatty acids and feline chronic renal failure. Fat Rec.<\/em> 2005; 157(7):193\u2013195.<\/li>\n
  14. Buckley CM et al. Effect of dietary water intake on urinary output, specific gravity and relative supersaturation for calcium oxalate and struvite in the cat. Br J Nutr.<\/em> 2011; 106(Suppl 1):S128-S130.<\/li>\n
  15. Goncalves MD et al. Diet and body composition in CKD: a critical review of protein restriction. J Ren Nutr.<\/em> 2016; 26(4):209-215.<\/li>\n
  16. Martinez ACM et al. Lactoferrin against bacterial pathogens: antimicrobial and immunomodulatory mechanisms. Front Cell Infect Microbiol.<\/em> 2025. doi:10.3389\/fcimb.2025.1603689. <\/li>\n<\/ol>\n<\/div>\n

    This information is educational in nature and based on available scientific literature. The studies mentioned are not always directly veterinary or specific to the formulation described here. This text does not replace a veterinary consultation and does not contain any therapeutic claims. <\/p>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

    NGD Care, Scientific background Chronic kidney disease in dogs and cats: from oxidative stress and tubular damage to fibrosis Why kidney disease only becomes visible when 70% of its function is lost, how the gut-kidney axis accelerates fibrosis, how to diagnose early and why the order of support is mechanistically. Substantiated with literature. By Stefan … Read more<\/a><\/p>\n","protected":false},"author":2,"featured_media":21895,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"wds_primary_category":0,"footnotes":""},"categories":[178,8537],"tags":[11828,11823,11637,11825,11827,11824,11822,11636,11829,11830,7747,11826,11831],"class_list":["post-21885","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-blog-en","category-integrative-veterinary-medicine","tag-astragalus","tag-ckd","tag-diagnostics","tag-fibrosis","tag-indoxyl-sulfate","tag-intestine-kidney-axis","tag-kidney-disease","tag-mitochondria","tag-sdma","tag-specific-gravity","tag-stefan-veenstra-dvm","tag-tgf-1","tag-upc-ratio","infinite-scroll-item"],"_links":{"self":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/posts\/21885","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/comments?post=21885"}],"version-history":[{"count":2,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/posts\/21885\/revisions"}],"predecessor-version":[{"id":21971,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/posts\/21885\/revisions\/21971"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/media\/21895"}],"wp:attachment":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/media?parent=21885"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/categories?post=21885"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/tags?post=21885"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}