Plaque is the French term for “plate,” which is relevant because lesions frequently resemble small (dirty) plates. Randall plaques are subepithelial calcifications of the renal papilla that are 2 mm in their largest diameter. They are thought to be a risk factor for the development of renal stones because they serve as a foundation for calcium oxalate crystals.
The minute deposits of calcium phosphate that makeup Randall’s plaques are found in the underlying membranes of the narrow loops of Henle. It is believed that these plaques have a significant role in the development of calcium oxalate stones in a subset of patients because they serve as anchoring nucleation sites for the creation of calcium oxalate crystals.
These plaques are rarely found in medical kidney biopsies because they are in a place that is not often biopsied. It is believed that these plaques constitute the starting point for the production of urinary stones. A lot of Randall’s plaque is only found in people who get calcium oxalate stones for no apparent reason.
Randall’s Plaque Symptoms
In most cases, there are no symptoms, and stone development does not always happen in the case of Randall’s Plaque. Randall’s plaque starts in the basement membranes of Henle’s thin loops. The loops of Henle’s basement membrane were typically where calcification developed, from which it spread into the interstitium in the direction of the urothelium. It has been discovered that the collecting ducts and vasa recta are closely related to subepithelial Randall’s plaque.
Randall’s Plaque Causes
Urine frequency and urinary content have been two important parameters linked to the development of Randall’s plaque. The development of CaP crystals, which can combine to form plugs and plaques inside the renal space or be discharged in the urine, is stimulated by elevated urinary calcium. The remaining plaques in the renal space have the ability to penetrate the papillary epithelium and infiltrate the interstitium before coming into contact with CaOx crystals, macromolecules, and proteins in the urine. Continuous contact with this chemical environment stimulates crystal adhesion and encourages stone development and retention over time.
Randall’s Plaque Diagnosis
On all imaging modalities, these calcifications appear as microscopic foci with at least fifty percent of their surface covered by renal parenchyma. When urine is present all around the foci, calyceal microlithiasis, which is visible inside the calyces, may be the cause. The subepithelial calcification of the renal papilla that occurs in Randall plaques is defined as having the greatest diameter of fewer than 2 millimeters. They are thought to be a risk factor for the development of renal stones because they serve as an anchor for calcium oxalate crystals.
Randall’s Plaque Treatment
The presence of excessive calcium in the urine is referred to as hypercalciuria. It is possible that the condition is secondary, meaning that it is a consequence of another ailment that is creating high amounts of calcium in the bloodstream, or it is possible that the condition is “idiopathic,” meaning that it occurs on its own with normal blood calcium levels.
All studies point to hypercalciuria as a factor that facilitates its occurrence. Low urine volume and pH are additional factors that make the situation worse. As a result, maintaining high urine volume, controlling urine calcium, and possibly even regulating urine pH may all help prevent the development of new plaque.
Allopurinol (Zyloprim, Aloprim) and a medication to maintain your urine alkaline may be recommended by your doctor in order to lower the amounts of uric acid in your blood and urine. Allopurinol with an alkalizing agent may occasionally be used to dissolve uric acid stones.
- Drink plenty of fluids which is a crucial factor to maintain an optimum urine volume.
- Eat moderate amounts of protein.
- Consume less salt (sodium).
- Make sure your diet has the correct quantity of calcium.
- Do not take vitamin C pills.
- Eat fewer meals high in oxalate.
Oxalate levels can be lowered by including calcium-rich foods in meals. The elimination of oxalate through the stool rather than the urine is facilitated by the natural binding of calcium to oxalate, which is accomplished by eating calcium-rich foods at meals.