How does hyperparathyroidism affect the kidneys

The derangements in calcium and phosphate that result from rHPT may accelerate vascular calcification, including coronary artery calcification. Calcification of the cardiovascular tissue can affect the myocardium, atrial-ventricular conduction, and valvular function. Some studies have suggested that FGF may induce arterial smooth muscle myocytes to change into osteoblast-like cells that lead to vascular calcification. There is an association between CKD and medial calcification in the arterioles of the skin and soft tissue leading to vascular compromise and ulceration.

This constellation of complications was formerly called calciphylaxis but is now termed calcific uremic arteriolopathy, and it is associated with an eight-fold increase in mortality rate. In tumoral calcinosis, the patient can develop soft-tissue calcium deposits that can appear to be soft-tissue malignant tumors on imaging studies Figure 3.

The frequency of monitoring for serum calcium, phosphorus, and PTH are listed in Table 1. Summary of National Kidney Foundation guidelines on evaluation of calcium and phosphorus metabolism and parathyroid hormone.

The initial management of rHPT follows a stepwise approach with the goal of optimizing serum phosphorus and calcium levels through a combination of a low phosphorus diet, phosphate binders, vitamin D derivatives, and calcimimetic medications. Unfortunately, this is very difficult given the high prevalence of phosphorus in Western diets. Dietary phosphorus comes from 2 sources: 1 protein-rich food groups such as meat and milk; and 2 phosphorus additives, which are used to process meats and cheeses.

Phosphorus used as an additive is often only implied in the ingredients list, and not individually reported on the food label. Therefore, the true amount of phosphorus contained in a product may be underestimated. However, it should be noted that there is a paucity of good quality data regarding dietary phosphorus restriction and outcomes in CKD. Because of the difficulty in maintaining a low phosphorus diet, phosphate binders are usually an essential part of medical therapy for patients with CKD.

Phosphate binders have been shown to decrease serum phosphorous and PTH levels. Several phosphate binders are available, including aluminum hydroxide, calcium salts, sevelamer hydrochloride, sevelamer carbonate, and lanthanum carbonate. In general, aluminum hydroxide should be limited to a short period because of the risk of aluminum toxicity. Newer agents such as lanthanum have unknown long-term effects of bone deposition. Iron-based binders such as sucroferric oxyhydroxide are also available to lower serum phosphorous.

The Kidney Disease Outcomes Quality Initiative recommends for patients with CKD stages 3 and 4, that phosphate binders be used if phosphorus levels cannot be controlled within the target range despite dietary phosphorus restriction. In patients who remain hyperphosphatemic despite initiation of a single phosphate binder, combination therapy can be used.

Although observational studies have suggested improved survival in patients treated with vitamin D analogs, a meta-analysis showed no difference in mortality, bone pain, vascular disease, or rate of parathyroidectomy when comparing patients on vitamin D analogs versus those not taking vitamin D.

The Kidney Disease: Improving Global Outcomes work group recommends that in patients with CKD stages 3 to 5 not on dialysis , attempts to control hyperphosphatemia, hypocalcemia, and vitamin D deficiency be made first. If PTH remains elevated or is progressively rising, treatment with calcitriol or vitamin D analogs is suggested. Close attention must be paid to serum levels of calcium and phosphorus, which if greater than In patients with CKD stage 5 on dialysis, active vitamin D sterols such as calcitriol, paricalcitol, or doxercalciferol are used to control hyperparathyroidism.

Cinacalcet HCL is a calcimimetic agent that exhibits allosteric modulation of the calcium receptor on the parathyroid gland, increasing sensitivity to extracellular calcium and thereby suppressing PTH secretion. Combined analysis of these studies showed that cinacalcet decreases rates of parathyroidectomy, fractures, and cardiovascular hospitalization. Patients receiving cinacalcet treatment rather than placebo also have improvements in self-reported physical function and less bodily pain.

In , the Evaluation of Cinacalcet Hydrochloride Therapy to Lower Cardiovascular Events Trial randomized patients with ESRD and moderate to severe rHPT to cinacalcet or placebo and found that cinacalcet did not significantly reduce overall or cardiovascular mortality. High-quality studies are currently lacking to evaluate which patients might benefit from parathyroidectomy.

In lieu of such data, the National Kidney Foundation recommends that the criteria in the Sidebar: Indications for Consideration for Parathyroidectomy be used to merit referral to an experienced surgeon for evaluation.

The three most common surgical procedures used in the treatment of rHPT are total parathyroidectomy TPX alone, TPX with auto-transplantation, and subtotal parathyroidectomy. TPX involves identification and removal of all parathyroid glands. This operation may be associated with the lowest rate of recurrent hyperparathyroidism. In TPX with autotransplantation, all 4 glands are removed, followed by autologous reimplantation of 20 mg to 70 mg of the most normal-appearing gland into the sternocleidomastoid muscle, pectoralis major muscle, or forearm brachioradialis muscle.

This implant typically takes 3 to 4 weeks to revascularize and resume function. The advantage of removal and reimplantation of parathyroid tissue into an ectopic site is ease of access in the event of recurrence and reoperation. This avoids the morbidity associated with re-exploration of the neck. This may be associated with an increased risk of injury to the recurrent laryngeal nerve. All 3 operations are accepted surgical treatment options for rHPT, and each is associated with specific advantages and disadvantages.

Successful parathyroidectomy can dramatically improve symptoms, including bone pain, arthralgia, muscle weakness, and psychological disturbances. Several studies have suggested a survival benefit from parathyroidectomy in the treatment of rHPT, including significant reductions in the incidence of major cardiovascular events and all-cause mortality. A range of nonsurgical options are available, including initiating a low phosphorus diet, phosphate binders, vitamin D analogs, and calcimimetic agents, but unfortunately the data on the efficacy of these treatments at improving overall and cardiovascular mortality are mixed.

Some patients require parathyroidectomy, which may improve symptoms and reduce cardiovascular and overall mortality, but it carries the expected risks of surgery. Author Contributions. Noah K Yuen, MD, provided study conception and design and participated in analysis and interpretation of data and writing the manuscript. Shubha Ananthakrishnan, MD, participated in writing the manuscript and in critical revision of the manuscript.

Michael J Campbell, MD, provided study conception and design and participated in analysis and interpretation of data, writing the manuscript, and the decision to submit for publication. Disclosure Statement. About three years ago I found on the thyroid gland … a small organ, hardly as big as a hemp seed, which was enclosed in the same connective tissue capsule as the thyroid, but could be distinguished therefrom by a lighter color.

A superficial examination revealed an organ of totally different structure from that of the thyroid, and with a very rich vascularity. National Center for Biotechnology Information , U.

Journal List Perm J v. Perm J. Published online Jul E-mail: ude. Copyright and License information Disclaimer. This article has been cited by other articles in PMC. Abstract Renal hyperparathyroidism rHPT is a common complication of chronic kidney disease characterized by elevated parathyroid hormone levels secondary to derangements in the homeostasis of calcium, phosphate, and vitamin D.

PTH is probably the most important regulator of calcium metabolism and functions primarily via 3 mechanisms: PTH is thought to stimulate PTH receptors mainly on osteoblasts, which then, through multiple cell-to-cell mechanisms, stimulate osteoclast formation and bone resorption, leading to increased serum calcium and phosphorus levels.

Kidney stones can cause pain, blood in the urine, urinary tract infections, blockage of the ureter, and even kidney damage. Surgery for primary hyperparathyroidism decreases the frequency of developing new kidney stones among those patients with kidney stones and primary hyperparathyroidism. Intermountain Healthcare. While you wait for a kidney stone to pass -- or for stone fragments to pass after a procedure -- y What is a staghorn kidney stone?

Methodist Specialty and Transplant Hospital. They were disappointed to realize that the nephrologist didn't even know what her calcium was-he didn't check. Of course it is high too! Her calcium was Jane has 21 high blood calcium levels documented in the past 11 years, and she has had zero normal calcium levels. Thus Jane has calcified kidneys nephrocalcinosis because her doctor is ignoring her high blood calcium for over a decade. We are unhappy with the primary care doctor who knew her calcium was high, but was "just watching it".

However, we are amazed that the kidney doctor didn't even figure this out. The family had to figure this out with Google's help. The ignorance here is palpable.

This lady has zero component of secondary renal hyperparathyroidism, she has primary hyperparathyroidism which has gone untreated for over a decade and this has killed her kidneys. The nephrologist gave her high dose vitamin D, again, ignorant-you cannot give vitamin D to a person with high calcium-it will make the calcium go higher.

Jane's calcium went to This is a simple problem. The high blood calcium has been ignored for years and it is building up in Jane's tissues, specifically in her kidneys. Jane is dying from un-treated primary hyperparathyroidism and her doctors are watching it happen. Today we removed a huge, 15 year old parathyroid tumor out of Jane's neck. The entire operation took 16 minutes and she went home just over 1 hour later. Her other three parathyroid glands were perfectly normal she had one parathyroid adenoma, like most people with primary hyperparathyroidism.

I told Jane to expect her kidney failure to improve slowly, just a little bit, however it is possible that this parathyroid tumor was removed too late. It is possible that she will need a kidney transplant. High blood calcium kills people. Jane's doctors were worried about her high cholesterol, but high blood calcium is much more deadly than high cholesterol, and it makes her feel bad and takes away the joy of life. It is not normal to have high blood calcium and the longer it is high, the worse damage it will cause.

Adults over 40 should have calcium levels of One final lesson for you all. Nobody is looking out for you but you. If you are reading this, it is very likely that you know more about hyperparathyroidism than your doctor does. Always get a copy of your blood work and laboratory test results. Do NOT rely on your doctors-many of them will let you down.

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