Is Nattokinase Good for Kidneys? Potential Benefits Explained

Nattokinase, an enzyme derived from fermented soybeans, has gained attention for its cardiovascular and circulatory benefits. Given the kidneys’ reliance on proper blood flow and filtration, researchers are exploring how it may influence renal health.

Understanding its effects requires examining its role in circulation, blood components, and filtration mechanisms.

Fibrinolytic Role in Renal Circulation

Nattokinase is known for its fibrinolytic properties, meaning it helps break down fibrin, a protein involved in blood clot formation. This has significant implications for renal circulation, as the kidneys require unobstructed blood flow for optimal filtration and waste removal. Impaired fibrinolysis has been linked to microvascular thrombosis, which can compromise renal perfusion and contribute to chronic kidney disease (CKD) progression. By promoting fibrin degradation, nattokinase may help maintain balance between coagulation and fibrinolysis in the renal microvasculature, reducing clot-related obstructions.

The renal vasculature is particularly susceptible to fibrin deposition due to its extensive capillary network and high-pressure filtration system. Excessive fibrin accumulation in glomerular capillaries can lead to endothelial dysfunction, increased vascular resistance, and reduced glomerular filtration rate (GFR). A 2020 study in Thrombosis Research found that nattokinase enhances endogenous fibrinolysis by upregulating plasmin activity, a key enzyme in fibrin breakdown. This suggests supplementation could mitigate fibrin-related vascular impairments, potentially preserving renal function in individuals at risk of thrombotic complications.

Beyond its fibrinolytic effects, nattokinase also influences blood viscosity, which affects renal hemodynamics. Increased viscosity is associated with reduced renal perfusion and heightened glomerular stress, particularly in those with hypertension or diabetes. Research in The Journal of Nutritional Biochemistry indicated that nattokinase lowers plasma fibrinogen levels, a major determinant of blood viscosity. By reducing fibrinogen, nattokinase may enhance microcirculatory flow in the kidneys, ensuring nephrons receive adequate oxygen and nutrients while efficiently clearing waste.

Effects on Blood Components Relevant to Kidney Function

The composition and behavior of blood components significantly impact renal health, as the kidneys rely on stable hemodynamics and balanced biochemical interactions for filtration. Nattokinase has been shown to influence fibrinogen, platelets, and erythrocytes, all of which are relevant to kidney function.

One of its most studied effects is reducing circulating fibrinogen, which correlates with lower blood viscosity. Elevated fibrinogen has been linked to renal microvascular damage and glomerular sclerosis. A 2021 meta-analysis in Frontiers in Pharmacology found that nattokinase supplementation reduced fibrinogen by 10-15%, potentially improving renal perfusion and lowering the risk of clot-related microangiopathies.

Nattokinase also affects platelet aggregation, a process that, when dysregulated, can contribute to renal vascular complications. Platelet hyperactivity has been implicated in CKD progression, particularly in individuals with metabolic disorders like diabetes, where endothelial dysfunction exacerbates platelet adhesion in renal capillaries. A clinical trial in Thrombosis and Haemostasis found that nattokinase reduced platelet aggregation markers, suggesting a role in preventing thrombotic events that impair renal microcirculation. This is particularly relevant for those with hypertension, as platelet-driven vascular inflammation can increase glomerular pressure and nephron damage.

Erythrocyte deformability, or the ability of red blood cells to change shape while navigating renal microvasculature, is another factor influenced by nattokinase. Reduced flexibility has been observed in conditions like diabetic nephropathy, where rigid red blood cells contribute to vascular resistance and impaired oxygen delivery to renal tissues. A study in Clinical Hemorheology and Microcirculation reported that nattokinase improved erythrocyte deformability by enhancing nitric oxide bioavailability, which supports vascular elasticity. This may help optimize renal oxygenation, reducing the risk of hypoxia-induced tubular injury and fibrosis.

Interactions With Renal Tissues and Filtration Pathways

Nattokinase’s influence on renal tissues extends beyond circulation, affecting the kidney’s filtration system. The glomerular basement membrane (GBM), a critical barrier within the nephron, regulates the passage of proteins and solutes. Disruptions in this membrane contribute to proteinuria, a hallmark of kidney dysfunction. Research suggests that nattokinase may support GBM permeability by modulating extracellular matrix turnover. A study in The American Journal of Physiology-Renal Physiology highlighted how proteolytic enzymes similar to nattokinase regulate matrix metalloproteinases (MMPs), which are involved in collagen remodeling within the GBM. By preventing excessive extracellular matrix accumulation, nattokinase could support filtration efficiency and reduce protein leakage.

Tubular function also plays a key role in kidney health, as renal tubules reabsorb essential nutrients while excreting waste. Sodium transport mechanisms, vital for electrolyte balance and blood pressure regulation, may be influenced by enzymatic activity in the renal microenvironment. Some preliminary findings indicate that nattokinase interacts with sodium-potassium ATPase activity, a key regulator of tubular sodium reabsorption. Alterations in this enzyme’s function have been linked to hypertensive nephropathy, where excess sodium retention exacerbates kidney strain. While direct clinical data on nattokinase’s effect on sodium transport remain limited, experimental models suggest that proteolytic enzymes can modulate tubular ion exchange, potentially improving renal electrolyte handling.