Endocrine Abstracts

Background: Nephrocalcinosis is characterized by the deposition of calcium products in kidney parenchyma and tubules. It may cause acute or chronic kidney injury or be incidentally detected radiographically in a patient with normal kidney function. Most patients with nephrocalcinosis do not progress to end-stage kidney disease, but with certain underlying conditions, may be associated with progressive kidney dysfunction.

Methods: The patient was diagnosed with primary hiperparathyroidism on the basis of blood analysis, biochemical analysis, schintigraphy, calcium levels and parathyroid hormone (PTH).

Case presentation: A 70 year old female patient came to the Emergency Unit with fatigue, diffuse abdominal pain, vomiting, diarrhea and decrease in the amount of urination. Laboratory analysis revealed hyperkalemia, hyponatremia, high azotemia (266 mg/dl) and creatinemia (7.2 mg/dl), high uricemia and phosphatemia. PTH =832 g/d (high), 25-hidroxyVit D=8.3 mg/dl (low), total Ca=9 mg/dl(normal). Cell blood count showed normocromic normocytic anemia. Diuresis was 1 liter/24 hours (low) and diagnosis of acute renal failure was made. Hemodyalisis was started and after first session dhe patient was hospitalized to nephrology department. The patient was well known for a 20 years of recidivant renal calculosis and has had three interventions of renal calculus, which ended successfully. She suffered from chronic renal failure as well. Levels of calcium and PTH raised progressively from 2016 to 2021. Actual abdominal echography showed calculus and multiple cysts. Parathyroid schintigraphy showed hyperfixation of 99 mTc MIBI 20 mCi that leads to the conclusion of parathyroid adenoma. During hospitalization the patient underwent hemodyalisis. She was planned for three and half gland parathyroidectomy.

Conclusion: Medullary nephrocalcinosis is a well known manifestation of primary hyperparathyroidism. When this happens, hyperplasia of parathyroid gland also occur and if primary hyperparathyroidism wasn’t diagnosed, tertiary hyperparathyroidism can develop and differential diagnosis become very difficult. In our case, nephrocalcinosis is a strong evidence of primary hyperparathyroidism and correlates with schintigraphy, but raising values of PTH during years also suggests secondary hyperparathyroidism due to chronic renal failure. In this scenario tertiary hyperparathyroidism can also happen. Treatment of choice is three and a half parathyroidectomy wich is a definitive solution for adenoma (primary vs tertiary), and calcium lowering therapy even in the background of parathyroid hyperplasia.Keywords Medullary nephrocalcinosis, primary hyperthyroidism, parathyroid adenoma, calcium, PTH, kidney, parathyroid glands, calcul, chronic renal faiure.