QJM Advance Access published July 4, 2014 Q J Med doi:10.1093/qjmed/hcu138
Advance Access Publication 26 June 2014
Clinical picture The utility of magnetic resonance imaging in the diagnosis of chronic lithium nephropathy stabilize renal function. The extent of renal recovery is dependent on the degree of fibrosis and scarring.1,2 Lithium-induced hypercalcaemia (LAH) occurs in 25–30% of patients but is not influenced by duration of therapy.1,5 LAH is thought to unmask previously undiagnosed primary hyperparathyroidism. In the majority of cases, hyperparathyroidism results from a solitary parathyroid adenoma.5 With long-term therapy, hyperparathyroidism also occurs from diffuse parathyroid tissue hyperplasia and increased parathyroid mass can be seen on ultrasound.5 Ultrasound scanning of the kidneys may be used to detect lithium-induced changes such as echogenic foci related to areas of fibrosis and microcysts.3,6 However, ultrasonography findings are not specific to lithium-induced structural damage. T2-weighted MRI is superior to ultrasound and CT scanning in distinguishing chronic lithium
Figure 1. MRI microcysts.
illustrates
multiple
bilateral
renal
! The Author 2014. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: [email protected] Page 1 of 2
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A 66-year-old woman with a long family history of bipolar affective disorder presented to the renal clinic with renal impairment and hypercalcaemia. She had been taking lithium therapy continuously for 28 years following her first and only significant episode of depression (she had also been taking thyroxine continuously from 6 months after starting lithium). She had polydipsia and polyuria, with nocturia up to three times per night. Significant findings on examination were a soft systolic murmur at the apex and a raised blood pressure of 175/98. Urinalysis was unremarkable; serum creatinine was 157 mmol/l (estimated glomerular filtration rate of 30 ml/min/1.73 m2), serum calcium 2.86 mmol/l (normal range 2.2–2.6 mmol/l) and parathyroid hormone 18.1 pmol/l. A parathyroid adenoma was subsequently identified and surgically removed. The electrocardiogram was normal and echocardiogram revealed mild global ventricular hypertrophy. Ultrasound scan of the renal tract revealed multiple anechoic cysts in both kidneys with blurred renal outlines, making renal size measurements difficult. Coronal T2-weighted magnetic resonance imaging (MRI) revealed multiple microcysts measuring 2–3 mm in size throughout both kidneys. The kidneys were normal in size with preserved parenchymal thickness. No hepatic cysts were demonstrated (Figure 1). Nephrogenic diabetes insipidus is a common complication of chronic lithium therapy.1,2 It is also associated with acute kidney injury after acute lithium intoxication and chronic kidney disease (CKD), which may progress to end-stage renal disease.2,3 CKD usually occurs after 10–20 years of lithium therapy.1 Renal biopsies of patients with lithium nephropathy show chronic tubulointerstitial nephritis associated with other abnormalities including tubular dilatation and atrophy, interstitial fibrosis, cortical and medullary cyst formation and focal segmental glomerulosclerosis.1–4 The withdrawal of lithium does not always improve or
Clinical Picture nephropathy, with a characteristic pattern of multiple symmetrical and uniform corticomedullary microcysts (usually
Advance Access Publication 26 June 2014
Clinical picture The utility of magnetic resonance imaging in the diagnosis of chronic lithium nephropathy stabilize renal function. The extent of renal recovery is dependent on the degree of fibrosis and scarring.1,2 Lithium-induced hypercalcaemia (LAH) occurs in 25–30% of patients but is not influenced by duration of therapy.1,5 LAH is thought to unmask previously undiagnosed primary hyperparathyroidism. In the majority of cases, hyperparathyroidism results from a solitary parathyroid adenoma.5 With long-term therapy, hyperparathyroidism also occurs from diffuse parathyroid tissue hyperplasia and increased parathyroid mass can be seen on ultrasound.5 Ultrasound scanning of the kidneys may be used to detect lithium-induced changes such as echogenic foci related to areas of fibrosis and microcysts.3,6 However, ultrasonography findings are not specific to lithium-induced structural damage. T2-weighted MRI is superior to ultrasound and CT scanning in distinguishing chronic lithium
Figure 1. MRI microcysts.
illustrates
multiple
bilateral
renal
! The Author 2014. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: [email protected] Page 1 of 2
Downloaded from by guest on December 11, 2014
A 66-year-old woman with a long family history of bipolar affective disorder presented to the renal clinic with renal impairment and hypercalcaemia. She had been taking lithium therapy continuously for 28 years following her first and only significant episode of depression (she had also been taking thyroxine continuously from 6 months after starting lithium). She had polydipsia and polyuria, with nocturia up to three times per night. Significant findings on examination were a soft systolic murmur at the apex and a raised blood pressure of 175/98. Urinalysis was unremarkable; serum creatinine was 157 mmol/l (estimated glomerular filtration rate of 30 ml/min/1.73 m2), serum calcium 2.86 mmol/l (normal range 2.2–2.6 mmol/l) and parathyroid hormone 18.1 pmol/l. A parathyroid adenoma was subsequently identified and surgically removed. The electrocardiogram was normal and echocardiogram revealed mild global ventricular hypertrophy. Ultrasound scan of the renal tract revealed multiple anechoic cysts in both kidneys with blurred renal outlines, making renal size measurements difficult. Coronal T2-weighted magnetic resonance imaging (MRI) revealed multiple microcysts measuring 2–3 mm in size throughout both kidneys. The kidneys were normal in size with preserved parenchymal thickness. No hepatic cysts were demonstrated (Figure 1). Nephrogenic diabetes insipidus is a common complication of chronic lithium therapy.1,2 It is also associated with acute kidney injury after acute lithium intoxication and chronic kidney disease (CKD), which may progress to end-stage renal disease.2,3 CKD usually occurs after 10–20 years of lithium therapy.1 Renal biopsies of patients with lithium nephropathy show chronic tubulointerstitial nephritis associated with other abnormalities including tubular dilatation and atrophy, interstitial fibrosis, cortical and medullary cyst formation and focal segmental glomerulosclerosis.1–4 The withdrawal of lithium does not always improve or
Clinical Picture nephropathy, with a characteristic pattern of multiple symmetrical and uniform corticomedullary microcysts (usually
