The kidneys are an important system for cardiovascular function and excretion of waste products. Similarly, factors affecting kidney function can indirectly affect other physiological processes Such as blood pressure control, heart rate, sodium excretion. And thus maintain the balance of salt in the body. CB1 and CB2 receptors are widely expressed in the renal system And so endogenous cannabinoids and cannabis can alter their function. From clinical and clinical information, here is what we know about the activation of CB1 and CB2 receptors in the kidneys.
There are few clinical studies in humans. Therefore, little is known about the effects of cannabinoids on healthy or unhealthy kidneys. The difference is that the distribution of CB1 and CB2 receptors is disrupted in the case of pre-existing kidney disease. As in the case of diabetic nephropathy. Sampling of patients showed increased CB1 receptor expression. While in humans and mice, decreased CB2 expression has been reported in this case.
In fact, studies to date have shown that reducing the use of pharmacological agents for CB1 activity and increasing CB2 activity is associated with improved kidney structure and function especially in models of chronic kidney disease. In addition, the administration of cannabidiol (CBD) preserves renal structures when oxygen flow is intermittently reduced. This is related to an animal model with acute kidney damage.
It seems that CBD may have direct effects that protect the structure and function of the kidney. However, the final physiological effect of CB receptor activation is probably not easily predicted.
CBD can indirectly impair kidney function by reducing inflammation. Activation of CB2 receptors has an anti-inflammatory effect. This reduces the penetration of inflammatory cells and the production of cytokines (a molecule that increases inflammation).
While both CB1 and CB2 receptors are expressed in the kidneys, the effects of the endocannabinoid system (ECS) in the kidneys are not well understood. Endocannabinoids, such as anandamide, have been shown to influence renal hemodynamics and tubular sodium reabsorption via CB1 receptor activation. Several animal models of kidney diseases have also demonstrated that an imbalance of cannabinoid receptor signaling with dominant CB1 receptor activation over CB2 receptor activation can lead to deleterious effects such as oxidative stress, inflammation, cell dysfunction, apoptosis, and fibrosis. More importantly, restoration of the imbalance in the ECS via CB1 blockade and CB2 agonism may be renoprotective and counter the effects of metabolic syndrome. In obese insulin-resistant rats, CB1 receptor blockade prevented proteinuria, renal function decline, and reduced both glomerular and tubule interstitial fibrosis in conjunction with improving body weight, fasting glucose, and lipids. Without influencing body weight, CB1 receptor deletion, specifically in the renal proximal tubules, has also been shown to reduce renal lipotoxicity and nephropathy in obese rats, suggesting direct endocannabinoid effects in the kidneys. Similarly, in nondiabetic animal models, excessive CB1 receptor activity resulted in podocyte damage, nephron loss, and proteinuria, and correction of systemic and peripheral imbalance of CB1 and CB2 receptor activation reduced albuminuria and podocin loss in diabetic animals for secondary prevention. The association between endocannabinoid imbalance and diabetic nephropathy has yet to be replicated in human studies; nonetheless, these preliminary findings suggest that CB1 receptor blockade and CB2 receptor agonism may be possible therapeutic targets for the management of diabetic nephropathy. The impact of recreational marijuana on these processes in the kidney, however, is less clear given that concentrations of cannabinoids vary with each strain and the affinity of each cannabinoid can fall along a wide spectrum between agonism and antagonism to each receptor.
Kidney function structure
Conversely, in another study using a mouse model of acute kidney injury, activation of the CB1 receptor is associated with increased oxidative stress, which stimulates inflammation and ultimately leads to cell death. It is on the cardiovascular system. This reduces the overall risk of high blood pressure and stiffness.
In addition, we lack studies on the effects of cannabis (smoked) on healthy or unhealthy populations. However, only one study, involving 647 patients with CRF, showed that smoking cannabis was not associated with decreased renal function. Kidney function markers also remain unchanged, a small prospective trial in which medical cannabis was used to relieve pain. In addition, in 1225 patients who underwent kidney transplantation, the use of medical cannabis did not affect the function of the transplanted kidney.
Therefore, cannabinoid signaling has a therapeutic effect against kidney disease. CBD-rich products appear to have greater drug potential than THC. With the advent of new knowledge about cannabinoids, it will be clear which species and products are beneficial for patients with kidney disease.
Due to limited treatment options, symptom management in patients with CKD can be challenging, and therefore therapeutic alternatives are in high demand. In recent years, medical marijuana has emerged as an attractive therapeutic option, but continues to be used for a variety of unsubstantiated indications with minimal guidance on known risks, particularly with respect to the altered physiological state of patients with kidney disease. At this time, the supportive evidence for using nonsynthetic cannabinoids for symptom management is limited to the treatment of chronic neuropathic pain, with promising potential when used topically for the treatment of uremic pruritus.