Hyperparathyroidism (HPT) occurs when one or more of the four parathyroid glands produce an excessive amount of parathyroid hormone (PTH). This overproduction is usually caused by a non-cancerous growth, known as an adenoma. The answer to whether this hormonal imbalance affects the kidneys is a yes, as HPT is a cause of various kidney problems. Excess PTH disrupts the body’s mineral balance, leading to damaging consequences for the renal system, ranging from the formation of deposits to permanent reduction in kidney function.
How Hyperparathyroidism Disrupts Kidney Function
The primary function of parathyroid hormone is to regulate the body’s levels of calcium and phosphorus. When PTH is released in excess, it signals the bones to release stored calcium and the kidneys to reabsorb more calcium back into the bloodstream. This physiological response leads to hypercalcemia, which is an abnormally high concentration of calcium in the blood. The kidneys are simultaneously tasked with filtering and excreting the excess mineral load.
The constant calcium overload results in a high concentration of calcium filtered into the urine, known as hypercalciuria. The tubules within the kidneys, which reabsorb water and other substances, become stressed processing this mineral-rich fluid. Prolonged exposure to high calcium concentrations causes physical damage to the kidney tissue and filtering structures. This metabolic strain compromises the kidney’s filtering capacity.
Specific Kidney Conditions Caused by HPT
The most common consequence of HPT is the formation of kidney stones (nephrolithiasis). These stones develop when high levels of calcium and phosphate in the urine crystallize within the collecting ducts. Stones can obstruct urine flow, potentially leading to infections and pressure damage within the kidney.
A less frequent complication is nephrocalcinosis, involving the deposition of calcium directly into the kidney tissue. Unlike stones that pass through the urinary tract, these deposits build up within the parenchyma, the functional part of the kidney. This internal calcification causes inflammation and scarring, impairing the kidney’s ability to filter waste.
Untreated HPT and persistent hypercalcemia can lead to the development or progression of chronic kidney disease (CKD). Prolonged injury from stones and calcification causes permanent scarring, reducing the number of functional filtering units (nephrons). This decrease in functional tissue lowers the Glomerular Filtration Rate (GFR), the measure of overall kidney function. Untreated HPT destroys the kidney’s capacity until irreversible CKD is established.
Diagnosing and Tracking Kidney Damage
Physicians use laboratory and imaging studies to confirm HPT-related kidney damage. Blood tests measure primary metabolic markers, including serum calcium and PTH levels. Doctors also monitor creatinine and blood urea nitrogen (BUN) levels, which are waste products that build up when the kidneys are not filtering effectively. Elevated creatinine indicates reduced kidney function.
A 24-hour urine collection test quantifies the amount of calcium excreted over a full day. This measurement confirms hypercalciuria, showing the extent of the calcium overload the kidneys are managing. The results help determine disease severity and the risk of future stone formation.
Imaging studies visualize the physical consequences of the disease within the renal structure. An ultrasound or computed tomography (CT) scan detects the presence, size, and location of kidney stones (nephrolithiasis). These scans also reveal nephrocalcinosis, where mineral deposits appear as bright spots embedded in the kidney tissue.
Reversing or Managing Kidney Damage
The most effective treatment for primary hyperparathyroidism is a surgical procedure called parathyroidectomy. This involves removing the overactive parathyroid gland, immediately halting excessive PTH production and normalizing calcium levels. This surgery resolves the hormonal imbalance and removes the root cause of the kidney’s mineral overload.
Successful parathyroidectomy often results in a rapid decrease in calcium excreted in the urine. For patients with early-stage kidney damage, this intervention halts injury progression and may allow for some improvement in kidney function. If surgery is not feasible, or in cases of secondary HPT, certain medications can be used.
Calcimimetics, such as Cinacalcet, increase the sensitivity of calcium-sensing receptors on the parathyroid glands, prompting them to produce less PTH. This helps manage calcium levels and slows the progression of damage. The prognosis for kidney function is tied to the timing of the intervention, as early treatment provides the best chance of preventing irreversible scarring associated with advanced chronic kidney disease.