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cbd and renal function

Cbd and renal function

CBD oil has not been shown to cure or prevent chronic kidney disease, but it may relieve some of the symptoms of CKD.

According to the above research, renal function should be closely monitored in those with CKD, and the lowest effective doses of CBD oil should be used.

With this summary in mind, let’s begin by recapping exactly what CBD oil is, so we can better understand its effects on the kidneys.

Does CBD oil have side effects?

According to nurse Lisa Miller Hedin BSN, RN, the potential for cannabis-related products such as CBD oil has been misunderstood by medics and others.

The endocannabinoid system or ECS is a complex cell-signaling system identified in the early 1990s by researchers exploring THC.

Most oils are sold in 30-milliliter (mL) bottles with a dropper cap. There is currently no known ‘correct’ dose of CBD oil.

Can CBD oil actively assist in kidney diseases?

Speaking at The American Nephrology Nurses Association’s National Symposium recently, she told attendees that it has great potential for treating patients with chronic kidney disease.

Most CBD oil available is a mix of CBD and carrier oil.

Cbd and renal function

Other pain medications — such as acetaminophen or opiate medications — are metabolized by the liver and eliminated through the kidneys. These drugs have been shown to cause damage to the sensitive cells making up the kidneys, which can lead to a worsening of the condition.

Here’s how you can get started using CBD oil today.

With that said, many people with kidney disease are turning to CBD as an adjunctive treatment option along with other medications and diet/lifestyle modifications.

Royal CBD

Using this information, you can calculate what a low dose, medium dose, or high dose of CBD may look like.

But there are some limitations to be aware of.


We recommend starting at the low-strength dose and build up slowly over time to the medium or high-strength doses.

There’s evidence that CBD and other related cannabinoids can support the health of the kidneys during both acute and chronic kidney disease in mice — though this has yet to be confirmed with research on humans.

Cbd and renal function

In other rodent models of CKD, similar protection of the glomerulus was observed in kidneys from rats with diet-induced obesity by blocking the CB1 receptor (21). In addition to the improvement in glomerular function, blockade of the CB1 receptor has been shown to reduce the progression of renal fibrosis in the unilateral ureteral obstruction mouse model (29). The mechanism by which the CB1 receptor antagonism reduces protein excretion may involve VEGF production, which is known to be linked to nephrin expression. In addition, CB1 antagonism may also improve renal function through reduced glomerular and proximal tubular apoptosis (1, 16, 31), although further in vivo studies are needed to confirm these initial in vitro observations.

The mechanism by which CB1 and CB2 receptors regulate tubular epithelial cell survival and/or recovery following sublethal damage remains to be fully determined. On a molecular level, renal CB1 mRNA (39) and protein (39, 55) or CB2 protein (55) were not significantly altered using multiple rodent models of AKI. However, biopsied kidney samples from humans with acute interstitial nephritis showed increased CB1 receptor mRNA (29). These molecular differences may be related to the type of AKI and the species from which the kidneys were obtained. Furthermore, although there may be overlap in the distribution of the CB receptors between specific cell types, the physiological outcome of CB receptor activation is likely dependent upon a number of other factors, such as the expression level of CB1 and CB2 receptors relative to each other, the G proteins associated with them, and the type of accessory proteins that are in close proximity of the receptors, which can amplify or dampen the signaling output.

Table 1 provides a summary of the studies describing CB1 or CB2 expression changes and localization in the kidneys from mice, rats, and humans. In human kidneys, CB1 receptor protein has been detected in proximal convoluted tubules, distal tubules, and intercalated cells of the collecting duct (27). In rodents, CB1 receptor protein was also detected in isolated thick ascending limbs of loop of Henle (53), podocytes in the glomerulus (3, 22), and resistance (i.e., afferent and efferent) arterioles (26). In cultured mesangial and endothelial cells, the expression of CB1 and CB2 mRNA has also been detected. Furthermore, CB2 receptor expression has been reported in cultured proximal tubule (17, 18) or glomerular mesangial cells (6) and sporadically in glomerular podocytes (3, 27). In addition, there are pharmacological studies that have shown that endocannabinoids in the renal vasculature can promote vasodilation via a non-CB1 receptor mechanism, and this may be one possible mechanism responsible for promoting the vascular effects of CB ligands in the kidney (61).

Table 2.

Consumption of cannabis and various related products (cannabinoids) for both medicinal and recreational use is gaining popularity. Furthermore, regulatory changes are fostering a cultural shift toward increasing liberalization of cannabis use, thereby increasing the likelihood of even larger numbers of individuals being exposed in the future. The two different types of receptors (CB1 and CB2) that are activated by the pharmacologically active ingredients of cannabis are found in numerous tissues, including the kidneys. Experimental studies suggest that stimulation of these receptors using pharmacologic agents or their naturally occurring ligands could have both deleterious and beneficial effects on the kidneys, depending on receptor distribution, type of renal insult, or the timing of the activation during acute or chronic states of kidney injury. To date, the mechanisms by which the CB1 or CB2 receptors are involved in the pathology of these renal conditions remain to be fully described. Furthermore, a better understanding of the impact of exocannabinoids and endocannabinoids on the renal system may lead to the development of new drugs to treat kidney disease and its complications. Given the increasing public health relevance of cannabis exposure, it is clear that more research is necessary to clarify the various physiological and pathophysiological effects of cannabis and related analogs on the kidney. This will help limit the deleterious effects of these substances while promoting their potential beneficial impact on renal function in various types of kidney diseases.

Cannabinoid receptor signaling in renal glomerular and tubular epithelial cells. Cannabinoid 1 (CB1) receptor activation activates distinct pathways in the podocytes/mesangial cells of the glomerulus (A), proximal tubule (B), and thick ascending limb of Henle (C). ROS, reactive oxygen species; NOX, NADPH oxidase; CARM1, coactivator-associated arginine methyltransferase 1; AMPK, 5′ AMP-activated protein kinase; ERK, extracellular signal-regulated kinase; PPARγ, peroxisome proliferator-activated receptor gamma; IL-1β, interleukin-1β; SOCS3, suppressor of cytokine signaling 3; ICAM-1, intercellular adhesion molecule 1; TNF-α, tumor necrosis factor-α; NO, nitric oxide; NOS, nitric oxide synthase; iNOS, inducible nitric oxide synthase; TGF-β, transforming growth factor-β; CCR2, C-C motif chemokine receptor 2; PARP, poly ADP ribose polymerase; BK, bradykinin receptor; AT-1, angiotensin type 1 receptor; PKC, protein kinase C; PKA, protein kinase A; PA, palmitic acid; PLA2, phospholipase A2; BV, blood vessels; TRPV1, transient receptor potential vanilloid 1; DAG, diacylglycerol; PIP2, phosphatidylinositol 4,5-bisphosphate; IP3, inositol 1,4,5-trisphosphate.

Effects of Cannabinoids on Human Acute Kidney Injury and Chronic Kidney Disease

Prevalence of cannabis use worldwide in 2014. Modified from United Nations Office on Drugs and Crime, United Nations Office on Drugs and Crime., accessed on March 27, 2017.

In a mouse model of chemically induced diabetic nephropathy, proteinuria was markedly reduced through the preservation of glomerular podocytes following administration of a selective CB1 receptor antagonist (AM251) (1). Similar findings were observed using genetic rodent models of diabetic nephropathy (22, 43). In db/db mice, chronic blockade of the CB1 receptor resulted in a reduction in microalbuminuria and decreased expansion of mesangial cells in the glomerulus (43). In Zucker diabetic obese rats, CB1 inverse agonist, JD5037, improved renal function and reduced albuminuria after long-term chronic administration (22). On the other hand, activation of the CB2 receptor has been shown to play a protective role in the diabetic nephropathy (3, 20). Functionally, CB2 receptor stimulation using AM1241 has been shown to ameliorate albuminuria, restore podocyte protein expression, and decrease expression of profibrotic markers (collagen type IV and TGF-β) in diet-induced obese rats (20). Similar findings were observed in a study using streptozotocin-treated mice (3).