International Journal of Clinical Case Reports 2015, Vol.5, No. 39, 1-3
1
Case report Open Access
Normocalcaemic Primary Hyperparathyroidism with Nephrocalcinosis in early
Chronic Kidney Disease: a Case Report
Dutta P.K.
1
, Nishat Jahan
2
, Tharakul Mazid A.H.M.
2
1. Professor of Nephrology, Department of Nephrology, Chittagong Medical College, Chittagong, Bangladesh
2. Honorary Medical Officer, Chittagong Medical College, Chittagong, Bangladesh
Corresponding author email
International Journal of Clinical Case Reports, 2015, Vol.5, No.39 doi: 10.5376/ijccr.2015.05.0039
Received: 29 Jun., 2015
Accepted: 30 Jul., 2015
Published: 07 Sep., 2015
Copyright
©
2015 Dutta et al., This is an open access article published under the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original work is properly cited.
Preferred citation for this article:
Dutta P. K., Nishat Jahan and Tharakul Mazid A. H. M., 2015, Normocalcaemic Primary Hyperparathyroidism with Nephrocalcinosis in early Chronic Kidney
Disease: a Case Report, International Journal of Clinical Case Reports, 5(39): 1
-
3 (doi
Abstract
The clinical findings of hyperparathyroidism may be due to hypercalcaemia or involvement of the renal system as well as
skeletal and haemopoietic system. Most patient with Primary hyperparathyroidism show few evidence of kidney diseases such as
nephrocalcinosis, renal tubular acidosis and mild renal failure. But usually in these cases hypercalcaemia is evident. This case being
presented is of interest due to normocalcaemia with renal involvement with primary hyperparathyroidism.
Keywords
Chronic kidney disease; Nephrocalcinosis; Normocalcaemia; Primary hyperparathyroidism
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
