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Kidney Damage from High Blood Pressure Leads to New Lymphatic Vessel Formation

Scientists have discovered that in rodents, hypertension- or aging-induced kidney injury and inflammation leads to the development of new lymphatic vessels in the kidneys. Hypertension (high blood pressure) is a leading cause of chronic kidney disease and kidney failure. Previous research has shown that a type of immune cell, called the macrophage, accumulates in the kidney and contributes to inflammation—a process that can lead to hypertension, which in turn increases risk for kidney disease. In a new study, researchers examined the effects of hypertension on lymphatic vessels, which drain fluid, immune cells (such as macrophages), and waste products away from tissues. Hypertension can lead to the formation of new lymphatic vessels, a process known as lymphangiogenesis, in various organs. However, lymphangiogenesis can either be harmful or beneficial depending on various factors, such as the timing of the inflammatory response. Because lymphatic vessels have been implicated in kidney disease, the scientists hypothesized that hypertension could affect the dynamics of their formation in the kidneys.

The researchers used well-studied rat models, including two types of rats that spontaneously develop hypertension, referred to as SHR (for spontaneously hypertensive rat). One of these types of hypertensive rats also develops kidney damage (a strain called SHR-A3), while the other does not (called SHR-B2). These two strains were compared with a third that does not develop high blood pressure under similar conditions (called WKY). By examining molecular signals of lymphangiogenesis from kidney biopsies, the researchers found that kidneys of male SHR-A3 rats (prone to kidney damage) had a higher density of lymphatic vessels and increased lymphangiogenesis than did the kidneys of male rats without hypertension (WKY). By contrast, male SHR-B2 rats’ kidneys had fewer lymphatic vessels and reduced lymphangiogenesis compared to kidneys from WKY rats. Molecular signals indicating the presence of macrophages and inflammation were stronger in SHR-A3 rats’ kidneys than in kidneys from SHR-B2 or WKY rats, suggesting that immune cells had invaded the injured kidneys.

The researchers then examined the effect of aging on lymphangiogenesis in the kidneys. They used Fischer 344 rats, which spontaneously develop kidney disease over time, but not hypertension. When 4-month old male rats were compared to 20- and 24-month old rats, the scientists found that kidney injury from aging led to lymphangiogenesis and increased immune cell invasion, similar to the SHR-A3 strain.

These findings suggest that kidney damage, due to either a hypertensive state or the course of aging, can lead to increased macrophage-induced inflammation and density of lymphatic vessels in the kidney. However, the rodent models in the study were used because they exhibit particular traits (e.g., strong resistance to hypertension or kidney damage) that may not represent a real-world situation in people. A more likely explanation in patients, the scientists suggest, is that hypertension induces subtler kidney inflammation, injury, and lymphangiogenesis than is seen in these animal models, consistent with the slower progression of the disease that is often observed in chronic kidney disease. Additional research would help determine whether lymphatic vessels could be useful targets for the development of therapeutic strategies to reduce risk for hypertension and kidney disease.

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