
































J Nepal Paediatr Soc | VOL 42 | ISSUE 02 |MAY-AUG,  2022 83

Case SeriesSri Lankan patientS with mucopoLySaccharidoSiS type iVaiVa

Acute Kidney Injury Secondary to Abdominal Tuberculosis: A 
Diagnostic Dilemma - A Case Report

Tuberculosis is a serious public health issue in developing countries. 
Hypercalcemia, though reported in granulomatous disease, is mild and 
asymptomatic in tuberculosis. A 16 year old girl female presented with 
significant weight loss, loss of appetite and on examination hepatosplenomegaly. 
Ultrasound abdomen (USG) showed mesenteric and retroperitoneal 
lymphadenopathy with hepatosplenomegaly with mild ascites. We report an 
unusual case of hypercalcemia with renal injury due to abdominal tuberculosis 
in an immunocompetent female.

Abstract

*Corresponding Author
Bharti Yadav
Senior Resident
Department of Paediatrics,
Faculty of Medical and Health Sciences
SGT University, 
Gurgaon-Badli Road Chandu, 
Budhera, Gurugram, 
Haryana 122505, India
Email: bhartiyadav32@gmail.com

Article History 
Received On : 22 Dec, 2021
Accepted On : 17 Aug, 2022

Funding sources: None 

Conflict of Interest: None

Keywords: Acute kidney injury, 
Corticosteroids, Hypercalcemia, 
Tuberculosis

Online Access

DOI: 
https://doi.org/10.3126/jnps.v42i2.41608

Introduction
Tuberculosis is a serious public health issue in developing countries. Hypercalcemia, 
though reported in granulomatous disease is atypical in tuberculosis. It is an immune-
mediated response by the macrophages present in the granulomata which causes 
an increase in reabsorption of calcium from bones and intestine and suppression of 
the parathyroid gland leading to decrease PTH release.1 This leads to an increase in 
calcium levels in the blood. Hypercalcemia can further cause renal injury. We report 
an unusual case of hypercalcemia with renal injury due to abdominal tuberculosis in 
an immunocompetent female.

Case report
A 16 year old girl female presented to our OPD with generalized weakness, loss 
of appetite and weight loss (10 kgs) for three months with no history of fever, 
cough, diarrhea. Her vitals were stable and physical examination did not reveal 
any abnormality except mild pallor. There was mild hepato-splenomegaly with no 
tenderness or fullness in the abdomen. On being investigated, hemoglobin was 10 
gm / dl with a normal total leucocyte count. Her liver function tests were normal.  
Ultrasound abdomen (USG) showed mesenteric and retroperitoneal lymphadenopathy 
with hepatosplenomegaly with mild ascites. Chest radiograph and Mantoux test were 
negative. The rest of the tuberculosis workup was normal. 

After one week of initiation of therapy, she was readmitted with complaints of frequent 
falls. She had stopped taking anti tubercular therapy after two days due to nausea and 
vomiting. On admission her vitals were stable and had no new findings on general 
and systemic examination. The investigations revealed a normal hemogram except 
hemoglobin of 10 gm / dl with a microcytic hypochromic picture. ESR was 75 mm 
and serum calcium level was 15 mg / dl with a corrected calcium of 15.9 mg/
dl. Her phosphorous was 3.87 mg / dl, serum albumin 2.9 g/dl and globulin 3.6 
g / dl with normal liver function tests. However, blood urea was 80 mg / dl and 
serum creatinine 2.5 mg / dl. Urine routine microscopy examination was normal. 
PTH level was 6.18 pg / ml (12 - 72 pg/ml) and Vitamin D was 79.1 ng / ml 
which ruled out hypervitaminosis D. Serum angiotensin converting enzyme level 

Case Report

DOI: 103126/JNPS.V4113

Copyrights & Licensing © 2022 by author(s). This is an Open Access article distribut-
ed under Creative Commons Attribution License (CC BY NC )

Bharti Yadav, Richa, Shikha Sadadiwala, Manimukta Singh

Department of Paediatrics, Faculty of Medical and Health Sciences SGT University, Gurgaon-Badli Road Chandu, Budhera, Gurugram, 
Haryana 122505, India



J Nepal Paediatr Soc | VOL 42 | ISSUE 02 |MAY-AUG,  202284

Case Report Acute Kidney injury SecondAry to AbdominAl tuberculoSiS

was (60.7 U/L) which was within normal limits. The Myeloma 
panel showed no evidence of monoclonal gammopathy. 24-hour 
urinary calcium level and urinary calcium creatinine ratio were 
also normal. Whole body positron emission tomography CT (PET 
CT) showed a lesion with high fluorodeoxyglucose uptake in the 
terminal ileum. [Fig 1] A diagnostic laparoscopy with biopsy was 
done. [Fig 2] Microscopically, the lesion showed granuloma. 
It consisted mainly in the recruitment at the infectious stage of 
macrophages, highly differentiated cells such as multinucleated 
giant cells, epithelioid cells, and foamy cells, all these cells being 
surrounded by a rim of lymphocytes and caseous necrosis in the 
center [Fig 3]. Gene Xpert (Cepheid, made in USA) from the 
biopsy sample was positive. Hence a diagnosis of abdominal 
tuberculosis causing hypercalcemia and acute kidney injury 
was made. The patient was rehydrated with isotonic saline. 
Bisphosphonates and corticosteroids – Prednisolone 40 mg daily 
for two weeks, tapered 5 mg weekly was also given. The patient 
improved symptomatically as her serum calcium and creatinine 
levels decreased and was given anti tubercular therapy for six 
months with regular follow-ups. After two months, her general 
condition and lab parameters improved. 

Figure 1. Showing a PET CT image of the abdomen suggestive 
of high FDG uptake in the terminal ileum

Figure 2. Showing diagnostic laparoscopy and biopsy: 
Small whitish tubercles over visceral and parietal peritoneum, 
inflammatory adhesions on the visceral and peritoneal surface, 
thickening, hyperemia, and retractions of the greater omentum.

Figure 3. Shows histopathology of the specimen: showing 
granuloma with multinucleated giant cells, epithelioid cells, and 
Foamy cells, surrounded by a rim of lymphocytes and caseous 
necrosis in the center

Discussion
Worldwide 1% to 3% gastrointestinal (GI) tuberculosis (TB) cases 
are present.2 The ileocecal region is the most commonly involved 
region but it can involve any part of the gastrointestinal tract.3,4 
Diagnosis is difficult because of its non-specific presentation.

 GI TB responds well to standard antituberculous drugs. Surgery is 
only needed in cases that develop complications such as strictures 
or obstruction, or do not respond to medical therapy. High 
clinical suspicion, early introduction of anti-tubercular therapy, 
and involvement of an interprofessional team are necessary for 
reducing morbidity and mortality.

The first step in the evaluation of a patient with hypercalcemia is 
to assess whether it is parathyroid dependent or independent. A 
normal or low parathyroid hormone level would mean a parathyroid 
independent pathology. Common granulomatous disorders like 
tuberculosis and sarcoidosis are commonly associated with 
hypercalcemia but they are rarely symptomatic.5 Various studies 
have noted the incidence of hypercalcemia in tuberculosis to be 
between 2.3% and 28%.6,7 The manifestations of hypercalcemia 
include polyuria, polydipsia, vomiting, dehydration, constipation, 
and reduced level of alertness in absence of neurological disease. 
ECG findings suggested shortened QT interval.

The pathophysiology of hypercalcemia in tuberculosis and 
sarcoidosis is due to the extrarenal conversion of 25 hydroxyvitamin 
D3 to the active form 1, 25 dihydroxy vitamin D3 by the activated 
macrophages in the granuloma.8 This occurs due to the increased 
production of 1 hydroxylase which is independent of PTH. 
The active form of Vitamin D results in increased reabsorption 
of calcium from bone and intestine leading to hypercalcemia. 
The renal injury associated with hypercalcemia occurs due to 
various mechanisms. It may be due to vomiting and dehydration 
or hypercalciuria can itself give rise to nephrocalcinosis and 
nephrolithiasis. Direct renal vasoconstriction can also reduce the 
GFR. These patients are managed with isotonic saline with loop 
diuretics followed by calcitonin. Dietary modifications are also 
required which include low calcium, low oxalate, and elimination 



J Nepal Paediatr Soc | VOL 42 | ISSUE 02 |MAY-AUG,  2022 85

Case ReportAcute Kidney injury SecondAry to AbdominAl tuberculoSiS

of vitamin D supplements. Bisphosphonates and glucocorticoids 
are the mainstay of treatment. They induce osteoclast apoptosis 
directly and reduce osteoclastic bone resorption. Bisphosphonates 
affect proliferation and differentiation of osteoblasts and prevent 
their apoptosis, whereas they also neutralize the RANKL-mediated 
stimulation of osteoclasts.9 Steroids decrease 1 hydroxylase 
activity thereby reducing the level of 1,25 dihydroxy Vitamin D3 
levels. This leads to reduced calcium absorption. 

It has also been observed that ketoconazole a general inhibitor of 
P450 enzymes decreases calcitriol production hence decreasing 
calcium levels. An antimalarial drug such as chloroquine, 
or  hydroxychloroquine can also be used as it decreases the 
inflammatory activity of the disease. 10

Conclusions
Symptomatic hypercalcemia with acute kidney injury is rarely a 
presenting complaint in granulomatous disorders like tuberculosis. 
It should be promptly managed with isotonic saline, loop diuretics, 
and corticosteroids. The incidence of hypercalcemia due to 
tuberculosis is between 2.3% and 28%.

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9. Viereck V, Emons G, Lauck V, Frosch KH, Blaschke S, 
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