The question of whether delta-9-tetrahydrocannabinol (THC), the primary psychoactive compound in cannabis, can cause kidney stones is a growing public concern. As cannabis use expands globally, researchers are working to understand its full physiological impact on major organs, including the kidneys. Kidney stone disease, also known as nephrolithiasis, is a common condition affecting approximately one in eleven people in their lifetime. This exploration reviews the current evidence and theoretical mechanisms regarding THC’s relationship with stone formation.
Current Evidence on THC and Kidney Stones
Direct clinical evidence establishing a causal link between THC consumption and the formation of kidney stones is currently lacking in the medical literature. No large-scale, long-term epidemiological studies have definitively shown that cannabis users are at a higher risk of developing the condition compared to the general population. The current research focuses mostly on observational data, which can only show association, not causation.
One major cross-sectional study analyzed data from the National Health and Nutrition Examination Survey (NHANES) and found a surprising inverse correlation in a specific demographic. Regular marijuana use was associated with a lower likelihood of reporting a history of kidney stones in male users, particularly those consuming cannabis one to seven times per week. This suggests that THC itself is not an established primary risk factor.
The protective hypothesis suggests that cannabinoids may promote diuresis, or increased urine output, which shortens the time mineral crystals remain in the kidney. However, the relationship is complex, and an indirect risk exists for some chronic, heavy users. Cannabinoid hyperemesis syndrome (CHS), involving recurrent episodes of severe nausea and vomiting, leads to significant dehydration and electrolyte imbalances. Since dehydration is an established cause of kidney stones, CHS could indirectly increase stone risk in vulnerable individuals.
Mechanisms of Kidney Stone Formation
Kidney stones are solid masses that form from crystallized substances found in urine. The most common type is the calcium oxalate stone, accounting for about 80% of all cases, with others including uric acid, struvite, and cystine stones. The formation process begins when urine becomes supersaturated, meaning the concentration of stone-forming salts and minerals exceeds their ability to remain dissolved.
This state of supersaturation drives the second stage, known as nucleation, where the dissolved ions precipitate out of the solution to form microscopic crystal seeds. Nucleation can occur homogeneously in the fluid or heterogeneously on existing surfaces within the renal tubules. Following nucleation, the crystals undergo aggregation, where they stick together and accumulate additional components to grow into a clinically significant size.
A final factor is crystal retention, where the small aggregates become fixed within the kidney, often on the renal papillae, allowing for continued growth into a mature stone. Established risk factors that promote these steps include consistently low urine volume due to dehydration, a diet high in sodium or oxalate, and genetic predispositions. Changes in urine pH are also important, as the solubility of certain stone constituents, like uric acid, is highly dependent on the urine’s acidity.
THC’s Interaction with Renal Function
The theoretical basis for THC’s influence on kidney stone formation lies in its interaction with the endocannabinoid system (ECS), a regulatory network found throughout the body, including the kidneys. Cannabinoid receptors, specifically CB1 and CB2, are present in renal tissues, suggesting a role in modulating kidney function. The ECS helps control renal hemodynamics, which is the flow of blood through the kidney, and the reabsorption of sodium and water.
The body’s own endocannabinoids, such as anandamide (AEA), can affect the glomerular filtration rate (GFR), which measures how well the kidneys filter blood. AEA has been shown in animal models to decrease GFR by causing the efferent arterioles to dilate more significantly than the afferent arterioles. This mechanism highlights the ECS’s direct involvement in regulating urine concentration and flow.
THC itself has been shown in some studies to increase urine output, a diuretic effect that could theoretically reduce the residence time of crystals in the nephron. Conversely, dysregulation of the ECS, particularly the upregulation of the CB1 receptor, has been linked to detrimental effects in kidney disease models, including inflammation and fibrosis. These theoretical pathways suggest that THC’s complex interaction with renal physiology may influence the delicate balance of fluid and electrolyte management that prevents stone formation.