Fluoride Action Network

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Patient SK, a 40-yr-old female, resident of Bhagalpur village in Bihar, India, was operated for gallstones 3 years previously. On pre-operative checkup, mild renal dysfunction was detected. She was asymptomatic for renal disease with serum creatinine of 159 mmol/l (1.8mg/dl), bland urinary sediment and small echo-genic kidneys on ultrasound. She was put on conservative management for chronic renal failure (CRF) and was doing well till 1 year ago. Since then she developed back pain, which increased on walking. Pain was dull in character without any radiation. There were no systemic complaints. In the past month when her pain increased substantially, causing discomfort in day-to-day activities. On investigation she was found to have moderate renal failure with blood urea nitrogen (BUN) of 11.8mmol/l and serum creatinine of 309m mol/l (3.5mg/dl). Other labs showed serum calcium of 2.4mmol/l, phosphorus 1.1mmol/l, alkaline phosphatase 243U/l, uric acid 381 mmol/l and intact parathyroid hormone (iPTH) of 182.0pg/ml. X-rays of bilateral forearms, pelvis and spine were taken (Figures 1–3, respectively), which revealed generalized increase in bone density, degenerative changes with osteophytes in lumber vertebra, calcification of bilateral iliolumbar and sacrospinous ligaments and interosseous membrane calcification in forearms. Definitive diagnosis was reached with estimation of fluoride levels in blood and urine, which were 0.291 mg/l and 0.962 mg/l (15.3 and 50.6 mmol/l), respectively. Her drinking water source, ground water from a tubewell, was found to contain 3.910mg/l (205.9 mmol/l) of fluoride. She was diagnosed to have fluorosis with moderate CRF and was advised to use domestic reverse-osmosis-treated water for cooking and drinking.

Main sources of fluoride include food and water. About 50–70% of fluoride is excreted by the kidneys [1]. Individuals with kidney disease have decreased ability to excrete fluoride in urine and are at risk of developing fluorosis even at normal recommended limit of 0.7 to 1.2mg/l (37–63 mmol/l) of fluoride in drinking water [2]. In fluorosis with normal renal function, urine fluoride rises above 0.5–4.48mg/l (26–236 mmol/l) and may reach 1.5–13.0mg/l (79–685 mmol/l) [3]. Serum fluoride rises to 0.04–0.28mg/l (2.1–14.7 mmol/l) in such patients [1]. Fluoride is bone-seeking due to its high affinity for calcium phosphate and therefore accumulates in bone. Radiological changes can be quite similar to changes of renal osteodystrophy, and therefore the diagnosis may be missed unless specifically investigated.


1. Reddy DR, Deme SR, Fluorosis . In: Chopra JS, Sawhney IMS eds. Neurology in Tropics, B.I. Churchill Livingstone, New Delhi, India: 1999; 82–92.

2. Arnala I, Alhava EM, Kauranen P. Effects of fluoride on bone in Finland. Histomorphometry of cadaver bone from low and high fluoride areas. Acta Orthop Scand 1985; 56: 161–166

3. Sesikaran B, Rao SM, Krishnamurti D, Reddy DR. Studies in sural nerve biopsies in endemic skeletal fluorosis. Fluride [sic, Fluoride] 1994; 27: 189–193.