Introduction
Primary hyperparathyroidism commonly manifest by hypercalcaemia and increased level of parathyroid hormone (PTH). Secondary hyperparathyroidism such as due to renal disease or vitamin D deficiency may present with normocalcaemia or low calcium. But primary hyperparathyroidism in presence of renal failure is diagnosed only when it is suspected. (Cusano et al., 2013). Classic Primary hyperparathyroidism usually present as a symptomatic disorder with kidney stone, abdominal or bone pain. But in the absence of hypercalcaemia usually PTH level is not measured and screening for the parathyroid adenoma or hyperplasia is not investigated (Rao et al., 1988). Again if the clinical features of Primary hyperparathyroidism are only constipation and depression in presence of chronic disease like chronic kidney disease (CKD) usually it may be mistaken as a case of secondary hyperparathyroidism. However in presence of renal condition like nephrocalcinosis or renal tubular acidosis primary hyperparathyroidism used to be investigated. In this report our aim is to present a case of normocalcaemic Primary hyperparathyroidism with unusual features (constipation, depression) in presence of mild renal failure and nephrocalcinosis. It is important to diagnose because surgical treatment may be required (Cusano et al., 2013).

Case presentation
A 60 years old nondiabetic, normotensive, menopaused woman was asymptomatic until October,2014 besides complaints of low back pain for one month without any red flag signs. She had no bladder complaints but complained of constipation for several months. She looked depressed and was clinically pale. She had regular sinus rhythm with 88/min and a normal blood pressure. She had neither bony tenderness nor edema or skin changes. Fundoscopic examination was normal. There were no organomegaly as well as no features of spondyloarthropathy or osteoporosis. Her x-ray lumbosacral spine revealed osteoarthrosis with normal C- reactive protein (CRP). Complete Blood Count (CBC) confirmed anaemia (Hb% 10 gm/dl) which was microcytic hypochromic on peripheral blood film. Urine routine and microscopic examination showed trace albuminuria, pyuria (plenty of pus cells/ HPF) and hematuria (3-5RBC/ HPF). Urine culture confirmed growth of E. coli. What came out on routine assessment of renal function was renal impairement (S. creatinine 1.5 mg/dl) which guided us to do sonology of both kidneys (Figure 1). It revealed bilateral nephrocalcinosis which was also evident in plain x-ray abdomen too. Her intravenous urography  excluded ureteric stone. Then she was advised to do serum calcium, inorganic phosphate and serum PTH which  revealed normal calcium and phosphate level along with elevated PTH level (611.8 ng/ml). Thereafter we focused on her neck glands. Ultrasonogram(USG) of neck (Figure 2a) showed solitary hypervascular nodule near lower pole of right thyroid (1.8x1.4 cm) with CT scanning (Figure 2b) later on showing the nodule to be a parathyroid adenoma (2x1 cm). It was nonmetastatic although some prominent cervical lymph nodes were there, mostly reactive. Parathyroid scintigraphy (sestamibi scan) concluded it was parathyroid adenoma or hyperplasia and simultaneously they advised to rule out hot nodule of thyroid. So we ran thyroid function test which was quite normal. Her urine calcium & urine calcium-creatinine ratio was found to be elevated which excluded familial hypocalciuric hypercalcaemia. To find out any skeletal changes owing to hyperpara- thyroidism we performed x-ray of both hands and skull which were normal. But Dual Energy X-ray Absorptiometry (DEXA) showed T score of AP spine, femur and radius below -2.5. Her endoscopy of upper GIT was also normal. 

Figure 1 Ultrsonogram of whole abdomen

Figure 2 USG(a)  and CT scan(b) of neck

Discussion
Normocalcaemic Primary hyperparathyroidism was first recognized in 2008 (Bilezikian et al., 2009). Prevalance of Primary hyperparathyroidism varies from 0.5% to 16.7% in various series. (Charopoulas et al., 2006). Whether there is masking of hypercalcaemia due to presence of renal failure it is unknown. Again why the biphasic nature of nomocalcaemic primary hyperparathyroidism doesn’t change in presence of chronic kidney disease is also unknown. Our patient has educed GFR (43 ml/min/1.73 m² BSA) with increased parameters of bone resorption. It is essential to screen such a patient from apparently normal population (Bilezekian et al., 2010). In conclusion it is appeared that even in a patient with nephrocalcinosis, renal failure and normocalcaemia, Primary hyperparathyroidism should be evaluated as early as possible.

Author’s contribution
PKD: designed and managed the patient
NJ: took the history and collected all the investigations
PKD & AHMTM: finalized and drafted the article
All authors read and approved final manuscript.

Acknowledgement
We pay our thanks to the patient and our humble gratitude to the director of Chittagong Medical College Hospital for giving us the opportunity to report this case.

References
Bilezikian J.P., Khan A.A., and Potts Jr., 2009, Guidelines for the management of Primary hyperparathyroidism: summary statement from the third international workshop, The Journal of Clinical Endocrinology and Metabolism, 94: 335-339
http://dx.doi.org/10.1210/jc.2008-1763

Bilezekian J.P., and Silverberg S.J., 2010, Normocalcaemic Primary hyperparathyroidism, Arq Bras EndocrinolMetab, 54: 106-109
http://dx.doi.org/10.1590/S0004-27302010000200004

Charopoulas I., Tournis S., Trovas G., Raptou P., Kalrymides P., Skrandavos G., Katnalira K., and Lyritin G.P., 2006, Effect of primary hyperparathyroidism on volumetric bone mineral density & bone geometry assessed by peripheral quantitative computed tomography in postmenopausal women, The Journal of Clinical Endocrinology and Metabolism, 91: 1748-1753
http://dx.doi.org/10.1210/jc.2005-2102 

Cusano N.E., Silverberg S.J., and John P. Bilezikian, 2013, Normocalcaemic primary hyperparathyroidism, Journal of Clinical Densitometry, 16(1): 33-39
http://dx.doi.org/10.1016/j.jocd.2012.12.001

Rao D.S., Wilson R.J., Kleerekoper M., and Parfitt A.M., 1988, Lack of biochemical progression or continuation of accelerated bone loss in mild asymptomatic primary hyperparathyroidism: evidence for biphasic disease course, The Journal of Clinical Endocrinology and Metabolism, 67: 1294-1298
http://dx.doi.org/10.1210/jcem-67-6-1294