How To Avoid Kidney Damage Due To Gout
As in other parts of the body, the adverse effects of gout arise as a result of the formation of crystals of urate and uric acid. By watching out for the specific foods to avoid with gout it is possible to reduce uric acid levels to a more normal healthy level.
The kidney is particularly susceptible to such problems because so much urate passes through the kidney in its elimination from the body and because a major function of the kidney is to concentrate the fluid passing through it.
Three important factors in urate crystallization are the concentration of urate, the pH or acidity of the fluid, and the presence or absence of solubilising factors that maintain urate in solution. The normal function of the kidney increases the first two of these factors that promote crystal formation: the kidney acts to concentrate most constituents of the fluid passing through it, including urate, and it increases its acidity as the tubular fluid passes from the cortex of the kidney down toward the medulla and into the kidney pelvis.
When, in previous centuries, gout was severe and untreatable, repeated attacks of gout would lead to the formation of tophi, and some of these tophi would form within the kidney.
The cellular response at the sites of crystal formation could lead to kidney disease, causing high blood pressure (hypertension). The hypertension resulting from tophi forming within a kidney could then aggravate the tendency to vascular disease, which could go on to cause further kidney disease. Thus, in the untreated state, the development of tophi in the kidney could lead to hypertension, and both the tophi and the hypertension could aggravate the underlying kidney disease or kidney failure. In general, the risk of developing this type of kidney disease was proportional to the severity or the degree of hyperuricemia. Thus, in times past, many patients with severe tophaceous gout would develop kidney disease and could proceed to develop kidney failure with vascular disease, with all the potential complications that affect the heart and blood vessels.
That was before effective treatments became available. Today, many patients with gout still worry that their gout will progress to cause kidney disease, so it cannot be emphasized too much that if gout is treated effectively, and the serum urate is restored to normal, the risk of formation of tophi within the kidney becomes negligible. If the serum urate in a gouty patient is normal, that patient is at no greater risk of kidney disease than a person without gout. Kidney disease of this type is currently seen only in patients with tophaceous gout who, for one reason or another, do not achieve a normal serum urate concentration.
Our studies of patients with both gout and kidney disease suggest that kidney disease does not develop in patients with primary gout until patients have had an average of 20 attacks of gout over a period of 5-10 years. However, the patient with gout may have other risk factors for cardiovascular disease, and these may persist even when the serum urate is normal and may, in themselves, contribute to the development of kidney disease on a vascular, or blood vessel, basis.Others | No Comments »