Understanding Kidney Health Together

We provide support and information for those affected by chronic kidney disease and IgA nephropathy to enhance their quality of life.

Testimony

Committed to raising awareness and providing resources for individuals and families dealing with chronic kidney diseases, including IgA nephropathy.

My name is Aileen P. For many years, I have been taking the blood pressure medication amlodipine, a calcium channel blocker. This medicine blocks the entrance of calcium into the cells, causing vasodilation and reducing blood flow. In the short term, it can help lower your blood pressure. However, over time, my uric acid levels gradually increased. After one year, they went up from 5.0 mg/dL to 6.0, then after two years, they rose further to 7, 8, 10, and even 13.0 mg/dL after 10 years of taking amlodipine. It is already well-known that all blood pressure medications can cause an elevation in uric acid levels.

After ten years, I was diagnosed with IgA Nephropathy and end-stage renal disease (ESRD). Was it caused by amlodipine? Most doctors would say no, attributing it to genetics. But what exactly is IgA Nephropathy? It is a genetic mutation, specifically involving mutations in the gene, which affects the production of IgA. It is also scientifically proven that uric acid can produce reactive oxygen species, which can trigger mutations. Therefore, the doctors I consulted were wrong. Amlodipine's elevation of uric acid likely triggered a mutation in the gene.

With the aid of turmeric and a low-carbohydrate diet, I was able to slow down the progression of the disease for two years. However, I still ended up needing dialysis. My point is that lifestyle changes really helped delay the disease progression by two years. Who can survive for two years with a GFR of 9.0 without dialysis? I did.

Aileen P.