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- A New Day for Kidney Tubules: there’s a way to test for them
By Robin Rose MD 11/11/25 My recent deep dive in exploring RENOLOGY and kidney success has been an amazing journey into the world of kidney tubules. These delicate little structures are amazing DISCERNMENT organs. While we know that the glomerulus is the FILTER:: all of the blood traverses this kidney filter 24/7 - but it is the tubules that determine what to keep and what to excrete! This is one of the most precious processes of our bodies - downstream effects of deranged tubule function can be devastating and the cause of undesirable suffering. Let’s fix that! The tubule conversation is a big one - I encourage everyone to return to basic science and learn the kidney basics. It’s complex. All of the toxic influences that we talk about - things that harm kidney - are at play as the kidney tubules are declining. And of utmost interest - tubule decline almost always PRECEDES glomerulus decline. Things like infections, trauma, hypoxia, toxin exposures, malignancy, autoimmune and inflammatory diseases all wreak havoc on tubules. And their ability - to discern what to do with toxins that need to be excreted and nutrients and minerals that need to be reclaimed - will ultimately evolve into systemic vulnerability and illness. Unless we do something as soon as we can. One big aha has been understanding TUBULAR PROTEINURIA. We know about and monitor for protein that leaks through the glomerular filter - proteinuria and micro albuminuria is seen on the urinalysis ( a test rdered routinely). These are larger proteins that breach the filter and leak into the urine. It is an important and dangerous condition. BUT! In the tubules it’s the low molecular weight proteins that can slip through the tubule cells and navigate to the urine - also not a good thing. And we can monitor for this - and in my early bird primary care mind set, I see that it’s an important add for recognizing kidney decline and for being proactive to achieve success. So this blog is to introduce you to some early bird testing for kidney tubules - particularly the proximal convoluted tubules - the first segment after the glomerulus - loaded with mitochondria and many essential jobs. Knowing when there is decline offers Renology-thinking folks ALOT of opportunities to repair and recover. There are many tubule conversations. I’m pretty much jumping to the end of the conversation - to discuss what labs can be readily ordered. This is the first step to learning what to do. So - urinary β₂-microglobulin (β₂M) and urinary retinol-binding protein (RBP) are clinically available through major diagnostic laboratories in the U.S. and internationally. They have been validated as tubular injury markers and are very appropriate for early CKD detection, especially! before creatinine or eGFR change. Subtle. ☀️ Urinary β₂-Microglobulin (β₂M)☀️ 💫Clinical significance 🔆This is a marker of proximal tubular reabsorptive dysfunction. That means that the tubules discern what to keep - to resorb - back into the systemic circulation. Know that the blood vessels surrounding the tubules have to stay healthy for this to work. 🔆β₂M (a low-molecular-weight 11.8 kDa protein) is freely filtered at the glomerulus and then almost completely reabsorbed by healthy proximal tubules. 🔆 It elevates early in toxic, ischemic, autoimmune, or even peptide-related tubular injury (excessive dosing is a danger for vulnerable tubules ). And this happens well before albuminuria or GFR decline. A subtle sense of unwellness can accompany this first stride into kidney decline and disease. 🔆Useful test in this “Renal Vulnerability Syndrome” — early tubular stress from toxins, trauma, malignancy, autoimmunity, or infection and inflammation. 💫Availability ✨✨Commercially available in the U.S. Labcorp: Test 141503 – Beta-2 Microglobulin, Urine. Method: Immunoassay. Specimen: Random or 24-hour urine. CPT: 82232. Notes: Indicates tubular damage; it is orderable along with serum β₂M which reflects glomerular decline - together they indicate tubular vs filtration differential. Labcorp link Quest Diagnostics: Test Code 372 – Beta-2 Microglobulin, Urine. Similar methodology and interpretation. Quest link ARUP Laboratories and Mayo Clinic Labs also offer it (Mayo: Test ID B2MU). 💫Interpretive pearls 🔆Reference range: typically <0.3 mg/L random urine (method-dependent). 🔆Degrades rapidly in acidic urine; best to alkalinize (pH > 6) and refrigerate or freeze promptly. uRBP more accurate in acidic urine. 🔆Persistent elevation → proximal tubular dysfunction (Fanconi-type pattern, toxin, heavy metals, FGF-23/Klotho stress, etc.). ☀️ Urinary Retinol-Binding Protein☀️ 💫Clinical significance of RBP 🔆Another low-molecular-weight protein (21 kDa) RBP is reabsorbed by megalin/cubilin complex; increases with proximal tubule dysfunction. 🔆Often more stable in urine than β₂M and less pH-sensitive. 🔆Excellent for subclinical tubular proteinuria (diabetic, autoimmune, toxic nephropathy, excessive peptide protocols). 💫Availability ✨✨ Commercially available Labcorp: Test 084640 – Retinol-Binding Protein, Urine. Method: Immunonephelometry. CPT: 82373. Labcorp link Mayo Clinic Laboratories: RBPUR – Retinol Binding Protein, Urine. Mayo link ARUP Laboratories: Test 0092161 – Retinol-Binding Protein, Urine. 💫Interpretive pearls 🔆Normal: <0.5 mg/L random urine. 🔆Elevated levels track closely with β₂M (and α₁-microglobulin) as part of the “tubular proteinuria” panel. 🔆Recommended when creatinine and ACR are normal - and yet - you use your educated intuition and knowledge base to suspect early nephron injury from chronic issues like autoimmunity, excessively used peptide therapies, heavy metals, ortoxicants. ☀️☀️REFRAMING HOW TO THINK : Renology Clinical teaching points ☀️☀️ 👉🏿Albuminuria = glomerular stress. 👉🏿β₂M / RBP = tubular stress Both together → mixed injury or declining nephron synchrony. These tests can document “Stage 1–2 CKD” long before eGFR shifts—::> supporting early intervention, detoxification, or appropriate peptide use and modulation. Remember eGFR> 60 is not normal- many pathological processes are already taking hold in Stage 2- and we have strategies to deal with these. ☀️☀️Practical takeaway for Clinicians☀️☀️ 🔆Both β₂M and RBP urine tests are readily orderable through Labcorp, Quest, Mayo, or ARUP with standard CPT codes, covered by most insurance when justified (CKD risk, toxin exposure, autoimmune monitoring, etc.). ☀️These tests can definitely be added to a “Functional CKD Panel” or “Renology Tubular Biomarker Panel” to differentiate glomerular vs tubular processes in early disease. 🔆Both are FDA-cleared clinical assays💜 🪷 TUBULES ARE BEAUTIFUL 🪷 Join me in learning to include kidney tubules in our thinking and in our regenerative intentions. In the RENOLOGY PEPTIDES mindset, the kidney bioregulator Pielotax has a beautiful supportive role in tubule repair. Each person deserves a personalized array of bioregulators to achieve regenerative benefits. And we also bring protective therapeutics to mitochondria, to the endothelium and the gut microbiota. Does all this start with low hanging fruit? Absolutely! The basics first. Diet is queen. Alkalinize! Organic only! PLADO and fiber, pre and probiotics. Elaborate intentions called for here. Exercise. Sleep. Hydration. Toxin eradication. Including toxic people. Stress reduction. Oral health. A self loving kidney lifestyle. I will continue to share some strategies and untangle the tubule wisdom in future blogs. Start envisioning the tubules and be grateful for them. Forgive yourself for any harm you’ve incurred and dance into the future in kidney success. Please consider buying my book RENOLOGY PEPTIDES - the definitive text - (available on this site) to learn the basic tenets of the art and clinical science of kidney success!
- Functional Foods and Chronic Kidney Decline: Nourishing the Kidneys Naturally
by Robin Rose MD ( October 28, 2025) A True Functional Medicine Perspective Functional medicine recognizes food as information — biochemical instructions that shape inflammation, detoxification, and mitochondrial efficiency. Functional foods offer health benefits beyond essential “nutrition” - they contain biologically active constituents that enhance health and reduce the risk of chronic diseases - they are truly Medicines. Food is medicine! 🍇🥑🥭🥦🫛🍉🍏 In CKD “functional foods” will offer protection for tubular cells, modulate fibrosis, and balance oxidative stress - all while supporting gut-kidney and liver-kidney crosstalk and taste good! Functional food empowers us to embrace our own healing ! This blog is a brief ( and incomplete) presentation and introduction to pique our interest in the concept that Food As Medicine truly and positively impacts the outcomes of kidney decline and disease. When we are empowered to self care and self love, innate healing becomes a reality - inducing the right biochemistry to invite kidney success. There is a lot more to this topic than this blog brings- yet once the idea takes root - choosing wisely becomes a natural tendency. The tropism to heal is a comforting gift. Everyone with renal decline is unique and personalizing diet is essential - and yet the truth is that functional food is a potent part of the Renology intention. Choose well! So: Why Organic Matters For CKd and CKD patients - minimizing the ingestion of pesticide residues, phosphate additives, and heavy metals is essential . Organic foods are also naturally lower in cadmium and synthetic nitrogen compounds — both also quite nephrotoxic. Studies show organic produce enhance antioxidant enzyme activity (SOD, GPx) and lower inflammatory cytokines (IL-6, TNF-α). Core Functional Food Categories 1. Polyphenol-Rich Fruits (Low Potassium) Blueberries, cranberries, pomegranate (small amounts): Modulate NF-κB, inhibit AGE formation, and support endothelial Klotho expression. Organic apples and pears: Support gut butyrate production; pectin binds uremic toxins. 2. Anti-Fibrotic and Detoxifying Vegetables Broccoli sprouts & arugula: Source of sulforaphane — upregulates Nrf2, reduces TGF-β1-driven fibrosis in renal tubules. Cabbage family (steamed): Indole-3-carbinol and glucosinolates balance estrogen and improve detox enzyme expression in proximal tubules. Dietary sources of carotenoids include colorful fruits and vegetables, such as carrots, tomatoes, spinach, and bell peppers. Carotenoid bioavailability is enhanced when consumed with dietary fats, and with cooking methods such as boiling or sautéing (increases bioavailability.) They reduce chronic illness risk and affect gene expression linked to inflammation and cellular repair processes - plus antioxidant qualities, - offering a true protective effect. Flavonoids are a group of polyphenolic compounds found in various plant kingdoms, known for their vibrant colors and health benefits.Flavonoids are classified into several subclasses, including flavonols, flavones, flavanones, isoflavones, flavan-3-ols (also known as catechins), and anthocyanins. These compounds are abundantly found in fruits, vegetables, tea, red wine, and various herbs, contributing not only to the color and flavor of these foods but also to their health-promoting properties. Flavonoids have a variety of forms, each with distinct biological activities and structures. Quercetin, a flavanol found in apples, berries, and onions, is a prominent anti-inflammatory with antioxidant properties. Kaempferol, a flavanol found in kale, spinach, and beans, exhibits vigorous antioxidant activity linked to cancer prevention. Catechins, a flavanol found in green tea. recognized for potent antioxidant effects and cardiovascular benefits. Anthocyanins give fruits such as blueberries and blackberries red, blue, and purple colors, possess strong antioxidant properties - linked to improved heart health. Flavonoids exhibit a diverse range of pharmacological activities that contribute to their therapeutic potent - antioxidant activity, anti-inflammatory effects, anticancer properties, cardiovascular health, neuroprotective effects, antimicrobial activity, and metabolic benefits. 3. Omega-3 and Anti-Inflammatory Seeds Organic flax, chia, and hemp seeds: Reduce MCP-1, IL-1β, and oxidative stress in CKD models; support vascular health. Prefer cold-milled or especially sprouted and fermented forms to enhance digestibility. omega-3 fatty acids in foods like fatty fish, flaxseeds, and walnuts, help reduce inflammation, lower triglyceride levels, and improve endothelial function. these also inhibit pro-inflammatory cytokines, modulate eicosanoid production, and enhance nitric oxide bioavailability, (reducing the enormous CKD risk of cardiovascular disease). 4. Resistant Starch & Fiber Foods Green banana flour, cooked-cooled rice, oats: these feed friendly gut Bifidobacteria that lowers circulating uremic toxins (p-cresol sulfate, indoxyl sulfate). Jerusalem artichoke (inulin): Enhances microbiome-derived SCFA that protect the tubules via AMPK activation. Fiber is made of non-digestible carbohydrates and lignin (intrinsic to plant cell walls). Dietary fiber can be classified into two main types. Soluble fiber dissolves in water to form a gel-like substance (found in foods such as oats, beans, lentils, apples, and citrus fruits). Insoluble fiber doesn’t dissolve in water- it adds bulk to the stool and aids digestion. It is abundant in whole grains, nuts, seeds, and vegetables. Both types play crucial roles in maintaining health and preventing various diseases. Dietary fiber is not just a single entity but a complex mixture of multiple phytoconstituents that contribute to its health benefits. Fiber phytoconstituents work synergistically to provide various pharmacological activities that contribute to overall health and well-being. 5. Natural Phosphate Binders Organic garlic and onions: Contain allicin and sulfur compounds binding phosphate and reducing FGF-23 signaling. That means bones and blood vessels are supported to respond positively to adaptive efforts to self heal at a cellular level. Mushrooms (shiitake, maitake): Provide β-glucans that enhance immune tolerance and may modulate phosphate retention without synthetic binders. 6. Kidney-Protective Beverages Hibiscus and rooibos tea: Mildly diuretic, antioxidant, and support uric acid metabolism. Many herbal teas like chamomile and mint etc offer refreshment plus medicinal benefits - Java tea, Chanca piedra, tulsi - that’s another blog post or book !! Cucumber water ( sliced cukes in water ) Fermented drinks - home made lacto-ferments or kombucha Organic green tea (matcha micro-dosed): Inhibits oxidative DNA damage in tubular mitochondria (EGCG effect). Foods to Limit Even When Organic High-oxalate greens like spinach, beet greens, Swiss chard (must be limited, avoided or balanced with calcium citrate or magnesium foods.) Choose arugula instead - low oxalate and low potassium-plus it’s the best food to optimize nitric oxide (benefits blood vessels so gracefully). Processed “plant-based” products with hidden phosphates, emulsifiers, and potassium additives - big nope ! Fruit juices and dried fruits due to concentrated sugars and potassium load Sugar - so many better suited choices - and yes in our sugar-flooded world it’s a challenging choice to break up with sugar Functional Food & the Role of the Microbiome Functional foods work through the microbiome. Polyphenols, inulin, and resistant starch shift gut fermentation toward protective metabolites (SCFAs, tryptophan derivatives) that down-regulate renal inflammation and fibrosis markers such as KIM-1 and NGAL. That means progression is slowed down or reversed -the goal of RENOLOGY! Probiotics are primarily bacteria and yeasts - essential microorganisms found in fermented foods like yogurt, kefir, and sauerkraut and crucial for maintaining gut health and overall wellness in ckd (which induces its own unique form of uremic dysbiosis). Lactobacillus and Bifidobacterium each have unique health benefits. Probiotics interact with phytoconstituents in their environment, enhancing their effectiveness or providing additional health benefits. Practical Takeaways for CKD Nutrition Dignified self loving willingness and intention to eat what will help not harm us the spiritual practice of the kidney yogi! Flexible willingness reaps benefits ! Prioritize organic, seasonal, low-phosphate foods. Emphasize diverse plant colors — 🌈 each reflects a different nephro-protective phytochemical. Use slow cooking, steaming, and fermentation to enhance bioavailability and reduce potassium and phosphorus load. This means using cronometer.com and monitoring - everyone is unique and has personalized needs- know yours! Combine wise kidney eating with hydration, timing, and circadian eating patterns to optimize tubular recovery. Exercise, toxin elimination, stress reduction and time in nature and sunshine are obligatory synergists to pave the path to kidney success. Be cautious about eating out ( hidden inflaming oils and pesticides etc are not uncommon and our cells are not happy ) - bring your own food and order tea!! Conclusion - kidney success This is a truly brief introduction to the reality that kidney success can only happen with personal commitment - that loving yourself by making wise choices is a healing modality that’s free and comes with the unit!! For those who want to learn more about this - I recommend reading this 2025 paper by Shirodkar et al, #6 reference below. Bon apetite!! References Rysz J. Nutrients. 2021;13(3):843 — Functional foods in CKD. Hsu CN, Tain YL. Int J Mol Sci. 2021;22(3):1180 — Nrf2 foods in renal programming. Vaziri ND et al. Kidney Int. 2016;90(4):853-865 — Gut microbiome modulation in CKD. Chiu YH et al. Clin Nutr. 2020;39(8):2510-2518 — Organic diet and reduced cadmium load. Hara Y. Biochem Pharmacol. 2018;154:298-305 — EGCG and tubular oxidative stress Shirodkar, Sanket, et al. “Role of Functional Foods and Nutraceuticals in Nutrition and Health.” Academia Nutrition and Dietetics, vol. 2, no. 2, Academia.edu Journals, 2025,
- "Leaky Kidney" & Tight Junctions: a new way to look at kidney decline
by Robin Rose MD October 9, 2025 The conversation about leaky gut has become very commonplace - we have learned about this aspect of dysbiosis, what it is, and what to do. DID YOU KNOW THERE ARE TIGHT JUNCTIONS IN KIDNEY TUBULES? Tight junctions [TJs] are multi-protein complexes that seal the space between epithelial [lining] cells. There are many: claudins, occludin, ZO-1/2/3 [zonulin], JAMS. (Start learning more: https://pmc.ncbi.nlm.nih.gov/articles/PMC4214347/ ) IN RENAL TUBULES these junctions are specialized according to the segment they are from. Let's first take a look at the normal and then explore how it becomes damaged. The TJs are gatekeepers of renal polarity and selectivity - they prevent the back-leak of solutes filtered in the glomerulus - maintaining reabsorptive efficiency and protecting the tubules from toxin diffusion. Understand that resorption means.... after the glomerulus filters all of the blood, the tubules must discern what must be brought back into the body [resorbed] and what must be “secreted” as in discarded [aka urine]. Proximal tubule [PCT] - is where this reabsorption action starts - the discernment to choose what to keep and what to eliminate. In PCT, claudin-2 and claudin-10a are involved. Leaky epithelium is a normal process that allows controlled paracellular Na+, Ca++, and water to be reabsorbed back into the blood. From Netter CIBA Collection volume 6 1973 p10 Thick ascending limb [TAL] has claudin-16 and claudin-19, offering tight selectivity for Mg++ and Ca++ reabsorption. Distal Tubule & Collecting Duct use Claudin-3, -4, -8 which offers a tight barrier, maintaining ionic gradients, preventing backleak of solutes. Netter p 15 LEAKY KIDNEY?!! Yes! Like leaky gut, there is a disruption of the tubular epithelial tight junctions - leading to increased para-cellular permeability - called tubular barrier dysfunction. What Causes This? Oxidative stress & Inflammation - via NF-kB, TNF-a, IL-6, ROS Toxins & Drugs - like lithium, cisplatin, contrast dye, heavy metals, glyphosate, fluoride etc. Protein overload - dietary awareness is critical, and albuminuria is itself pro-inflammatory Hyperglycemia/diabetes - tubular damage precedes glomerular injury as glucotoxicity Ischemia-reperfusion or hypoxia - affecting the PCT and TAL especially Uremic toxins - there are hundreds of substances induced by chronic kidney decline - some have been studied and reported, like p-cresol sulfate and indoxyl-sulfate Dysbiosis --::> endotoxemia - systemic lipopolysaccharides [LPS} also disrupt renal TJs Phosphate toxicity - a known hazard starting in early kidney decline Aging - energy deficit + chronic oxidative/inflammatory injury + loss of protective factors → progressive tubular atrophy and interstitial fibrosis, even with normal glomeruli. What are the Consequences of TJ Damage in Tubules? This idea of “leaky kidney” is not metaphorical — it’s an early driver of chronic tubular pathology. Let's look at what happens when the tubular tight junctions break down: Backleak of filtrate: when solutes and small proteins re-enter the tubule lumen or interstitium → inefficient reabsorption occurs, with resultant tubular wasting syndromes . This is a failure to reclaim what's been filtered in the glomerulus, including nutrients - which leads to excessive loss in the urine ["wasting"] of electrolytes, amino acids, glucose, phosphate, bicarbonate [even with normal glomerular filtration]. This is a topic that deserves its own blog. Interstitial inflammation: leaky paracellular flow allows inflammatory mediators and toxins to get into peritubular space → tubulointerstitial nephritis [TIN] - a bad outcome. Tubular cell de-differentiation & Epithelial-Mesenchymas Transition [EMT] : loss of the TJ polarity triggers this unfortunate process as cells change in this epithelial-mesenchymal transition → fibrosis. Loss of selective ion handling: TAL's TJ disruption → hypo-magnesemia , hyper-calciuria [seen in claudin-16/19 mutations, a hereditary prototype of “leaky tubule”]. Mutations of CLDN16 or CLDN19 genes lead to loss of function of these tight junction channels [called familial hypomagnesemia with hypercalciuria and nephrocalcinosis - FHHNC]. PCT's TJ disruption → phosphate, amino acid, glucose losses [Fanconi-like states]. Accelerated CKD progression: TJ injury activates TGF-β/Smad , NF-κB , β-catenin , promoting fibrosis and loss of nephron integrity. THE MECHANISMS INVOLVED Oxidative stress ROS damages occludin and ZO-1, increasing permeability. Inflammatory cytokines TNF-α, IL-1β, IL-6 internalize TJ proteins. Uremic toxins / LPS Reduce claudin-2 expression; increase leakiness. Phosphate overload Increases calciprotein particles → oxidative and TJ injury. Hyperglycemia Activates PKC and RAGE → TJ disassembly. Mitochondrial dysfunction Energy deficit impairs cytoskeletal anchoring of TJ. TESTING & BIOMARKERS While there’s no direct “leaky kidney” panel, there are functional biomarkers that reflect tubular integrity, guiding us to suspect patterns of decline. β₂-Microglobulin PCT dysfunction / leakiness. NAG (N-acetyl-β-D-glucosaminidase) Lysosomal enzyme → tubular cell injury. KIM-1 Dedifferentiation marker — early tubular damage. NGAL Distal/collecting duct stress. Urinary LDH or mitochondrial DNA Cell death / permeability. Microalbuminuria May reflect both glomerular and tubular barrier leak. RENOLOGY PREVENTATIVE WISDOM START WITH THE LOW HANGING FRUIT Lifestyle & Functional Medicine Control systemic inflammation (periodontal, gut, obesity, toxin avoidance. Dietary willingness - lower protein and salt, plant based organic food, with precision & personalized care based on labs. Exercise, stress reduction, time in nature, confront stress Avoid nephrotoxins: lithium, NSAIDs, glyphosate, silica, fluoride etc. Optimize hydration and bicarbonate reserve - alkalinize! Ensure sufficient quality sleep / circadian repair: pineal -melatonin–Klotho–mitochondrial alignment restores epithelial polarity. Address dysbiosis: endotoxemia is a major indirect disruptor of renal TJs. Nutraceutical & Natural Interventions Antioxidants NAC, l-carnosine, alpha-lipoic acid, CoQ10, astaxanthin Reduce ROS, preserve TJ proteins. Anti-inflammatory polyphenols Curcumin, resveratrol, quercetin Block NF-κB and TGF-β activation; increase claudin/occludin. Melatonin Improves TJ stability in renal ischemia models; links to Klotho axis. Omega-3s (EPA/DHA) Lower cytokines, restore ZO-1/claudin-2 balance. Probiotics / Gut-kidney axis Reduce systemic LPS and endotoxin-mediated TJ injury. Magnesium citrate / PLADO diet Stabilize phosphate and acid-base balance to prevent TJ stress. Cellular Medicine and Peptide & Bioregulation Care Pielotax [kidney cytomax bioregulator peptide]: shown in Khavinson studies to restore tubular epithelial polarity and improve TJ integrity in CKD models. Vesugen or Ventfort [blood vessel bioregulator peptides]: shown to restore tubular polarity and support anti-EMT effect Epithalon [pineal bioregulator peptide] upregulates ZO-1 and occludin expression [studied in gut and kidney epithelium]. SS-31 (Elamipretide): stabilizes mitochondrial cardiolipin → prevents energy failure that destabilizes TJs. ARA-290 [EPO-derived peptide - without influence on EPO's blood effects ]: reduces TNF-α, restores TJ proteins in diabetic nephropathy models. NOW WE KNOW This is a lot of fascinating detail that illustrates what is happening. The tubules are very precious Protectors of Life. Our self-loving obligation of offering tender loving care for our kidneys starts with the awareness of how these tubules look, how they work, how they break, and now we have many strategies to start with reciprocating and protecting them back! References Hou J et al. Nature Reviews Nephrology 2013;9(6):367-381.– “Claudins and the kidney barrier: from molecules to disease.” Günzel D & Yu AS. Physiological Reviews 2013;93:525-596. Kimura K et al. Am J Physiol Renal Physiol 2020;318(4):F816-F828.– “Tight junction dysfunction in tubulointerstitial fibrosis.” Zhang L et al. Front Pharmacol 2022;13:867389.– “Oxidative stress disrupts renal tubular tight junctions via mitochondrial dysfunction.” Khavinson V et al. Bulletin of Experimental Biology and Medicine 2015;159(3):388-392.– “Short peptides normalize renal epithelial barrier and morphology in aging models.”
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