Related Disciplines > Nephrology
You are looking at 41 - 50 of 53 items
Search for other papers by Runa Acharya in
Google Scholar
PubMed
University of Iowa, Carver College of Medicine, Iowa City, Iowa, USA
Medicine and Endocrinology, University of Iowa, Iowa City, Iowa, USA
Des Moines University, Des Moines, Iowa, USA
Search for other papers by Udaya M Kabadi in
Google Scholar
PubMed
Summary
Diabetic ketoacidosis (DKA) is commonly encountered in clinical practice. The current case is a unique and rare presentation of DKA as the initial manifestation of Cushing’s disease secondary to ACTH-secreting pituitary adenoma. Appropriate management as elaborated in the article led to total remission of diabetes as well as the Cushing’s disease.
Learning points:
-
DKA is a serious and potentially life-threatening metabolic complication of diabetes mellitus.
-
Some well-known precipitants of DKA include new-onset T1DM, insulin withdrawal and acute illness.
-
In a patient presenting with DKA, the presence of a mixed acid–base disorder warrants further evaluation for precipitants of DKA.
-
We present a rare case of DKA as an initial manifestation of Cushing’s disease secondary to ACTH-producing pituitary adenoma.
Search for other papers by Marlene Tarvainen in
Google Scholar
PubMed
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland
Search for other papers by Satu Mäkelä in
Google Scholar
PubMed
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland
Search for other papers by Jukka Mustonen in
Google Scholar
PubMed
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland
Division of Internal Medicine, Seinäjoki Central Hospital, Seinäjoki, Finland
Search for other papers by Pia Jaatinen in
Google Scholar
PubMed
Summary
Puumala hantavirus (PUUV) infection causes nephropathia epidemica (NE), a relatively mild form of haemorrhagic fever with renal syndrome (HFRS). Hypophyseal haemorrhage and hypopituitarism have been described in case reports on patients with acute NE. Chronic hypopituitarism diagnosed months or years after the acute illness has also been reported, without any signs of a haemorrhagic aetiology. The mechanisms leading to the late-onset hormonal defects remain unknown. Here, we present a case of NE-associated autoimmune polyendocrinopathy and hypopituitarism presumably due to autoimmune hypophysitis. Thyroid peroxidase antibody seroconversion occurred between 6 and 12 months, and ovarian as well as glutamate decarboxylase antibodies were found 18 months after acute NE. Brain MRI revealed an atrophic adenohypophysis with a heterogeneous, low signal intensity compatible with a sequela of hypophysitis. The patient developed central (or mixed central and peripheral) hypothyroidism, hypogonadism and diabetes insipidus, all requiring hormonal replacement therapy. This case report suggests that late-onset hormonal defects after PUUV infection may develop by an autoimmune mechanism. This hypothesis needs to be confirmed by prospective studies with sufficient numbers of patients.
Learning points:
-
Pituitary haemorrhage resulting in hypopituitarism has been reported during acute HFRS caused by PUUV and other hantaviruses.
-
Central and peripheral hormone deficiencies developing months or years after HFRS have also been found, with an incidence higher than that in the general population. The pathogenesis of these late-onset hormonal defects remains unknown.
-
This case report suggests that the late-onset hypopituitarism and peripheral endocrine defects after HFRS could evolve via autoimmune mechanisms.
-
The sensitivity of current anti-pituitary antibody (APA) tests is low. A characteristic clinical course, together with typical brain MRI and endocrine findings may be sufficient for a non-invasive diagnosis of autoimmune hypophysitis, despite negative APAs.
Search for other papers by Bilal Katipoglu in
Google Scholar
PubMed
Search for other papers by Ihsan Ates in
Google Scholar
PubMed
Search for other papers by Fatih Acehan in
Google Scholar
PubMed
Search for other papers by Ayşenur Meteris in
Google Scholar
PubMed
Search for other papers by Nisbet Yılmaz in
Google Scholar
PubMed
Summary
Hypothyroidism is a wide clinical spectrum disorder and only a few cases in literature show this. Rhabdomyolysis and acute renal impairment can be seen concurrently in a hypothyroid state. We report a case of severe hypothyroidism with poor drug compliance leading to rhabdomyolysis and acute kidney injury.
Learning points:
-
Hypothyroidism is a rare cause of acute kidney injury.
-
In this case report, we studied a rare occurrence of acute renal impairment due to hypothyroidism with poor drug compliance, which induced rhabdomyolysis.
-
Our report emphasized that thyroid status should be evaluated in patients with unexplained acute renal impairment or presenting with the symptoms of muscle involvement.
Search for other papers by Elizabeth M Madill in
Google Scholar
PubMed
Search for other papers by Shamil D Cooray in
Google Scholar
PubMed
Department of Medicine (Alfred), Monash University, Melbourne, Victoria, Australia
Search for other papers by Leon A Bach in
Google Scholar
PubMed
Summary
Thyrotoxicosis is an under-recognised but clinically important complication of parathyroidectomy. We report a case of a 37-year-old man with tertiary hyperparathyroidism who initially developed unexplained anxiety, diaphoresis, tachycardia, tremor and hyperreflexia one day after subtotal parathyroidectomy. Thyroid biochemistry revealed suppressed thyroid stimulating hormone and elevated serum free T4 and free T3 levels. Technetium-99m scintigraphy scan confirmed diffusely decreased radiotracer uptake consistent with thyroiditis. The patient was diagnosed with thyrotoxicosis resulting from palpation thyroiditis. Administration of oral beta-adrenergic antagonists alleviated his symptoms and there was biochemical evidence of resolution fourteen days later. This case illustrates the need to counsel patients about thyroiditis as one of the potential risks of parathyroid surgery. It also emphasises the need for biochemical surveillance in patients with unexplained symptoms in the post-operative period and may help to minimise further invasive investigations for diagnostic clarification.
Learning points
-
Thyroiditis as a complication of parathyroidectomy surgery is uncommon but represents an under-recognised phenomenon.
-
It is thought to occur due to mechanical damage of thyroid follicles by vigorous palpation.
-
Palpation of the thyroid gland may impair the physical integrity of the follicular basement membrane, with consequent development of an inflammatory response.
-
The majority of patients are asymptomatic, however clinically significant thyrotoxicosis occurs in a minority.
-
Patients should be advised of thyroiditis/thyrotoxicosis as a potential complication of the procedure.
-
Testing of thyroid function should be performed if clinically indicated, particularly if adrenergic symptoms occur post-operatively with no other cause identified.
Search for other papers by Ling Zhu in
Google Scholar
PubMed
Search for other papers by Sueziani Binte Zainudin in
Google Scholar
PubMed
Search for other papers by Manish Kaushik in
Google Scholar
PubMed
Search for other papers by Li Yan Khor in
Google Scholar
PubMed
Search for other papers by Chiaw Ling Chng in
Google Scholar
PubMed
Summary
Type II amiodarone-induced thyrotoxicosis (AIT) is an uncommon cause of thyroid storm. Due to the rarity of the condition, little is known about the role of plasma exchange in the treatment of severe AIT. A 56-year-old male presented with thyroid storm 2months following cessation of amiodarone. Despite conventional treatment, his condition deteriorated. He underwent two cycles of plasma exchange, which successfully controlled the severe hyperthyroidism. The thyroid hormone levels continued to fall up to 10h following plasma exchange. He subsequently underwent emergency total thyroidectomy and the histology of thyroid gland confirmed type II AIT. Management of thyroid storm secondary to type II AIT can be challenging as patients may not respond to conventional treatments, and thyroid storm may be more harmful in AIT patients owing to the underlying cardiac disease. If used appropriately, plasma exchange can effectively reduce circulating hormones, to allow stabilisation of patients in preparation for emergency thyroidectomy.
Learning points
-
Type II AIT is an uncommon cause of thyroid storm and may not respond well to conventional thyroid storm treatment.
-
Prompt diagnosis and therapy are important, as patients may deteriorate rapidly.
-
Plasma exchange can be used as an effective bridging therapy to emergency thyroidectomy.
-
This case shows that in type II AIT, each cycle of plasma exchange can potentially lower free triiodothyronine levels for 10h.
-
Important factors to consider when planning plasma exchange as a treatment for thyroid storm include timing of each session, type of exchange fluid to be used and timing of surgery.
Search for other papers by Soledad Bell in
Google Scholar
PubMed
Search for other papers by Gabriela Alejandra Sosa in
Google Scholar
PubMed
Search for other papers by Ana del Valle Jaen in
Google Scholar
PubMed
Search for other papers by María Fabiana Russo Picasso in
Google Scholar
PubMed
Summary
Thyroid lipomatosis is a rare disease, as a total of 20 cases have been described in the literature. It is characterized by diffuse infiltration of the stroma by mature adipose tissue and by progressive growth that produces different degrees of compressive symptoms. Our aim is to present the case of a 36-year-old woman who consulted because of dyspnea caused by a multinodular goiter. She underwent surgery with the presumptive diagnosis of a malignant neoplasia, but the pathological examination of the surgical specimen established the diagnosis of thyroid lipomatosis.
Learning points
-
Thyroid lipomatosis is a rare, benign disease characterized by diffuse infiltration of the stroma by mature adipose tissue.
-
The pathophysiology of diffuse proliferation of adipose tissue in the thyroid gland is unclear.
-
Thyroid lipomatosis is clinically manifested by a progressive enlargement of the thyroid that can involve the airway and/or upper gastrointestinal tract, producing dyspnea, dysphagia, and changes in the voice.
-
Given the rapid growth of the lesion, the two main differential diagnoses are anaplastic carcinoma and thyroid lymphoma.
-
Imaging studies may suggest a differential diagnosis, but a definitive diagnosis generally requires histopathological confirmation after a thyroidectomy.
Search for other papers by Yael R Nobel in
Google Scholar
PubMed
Search for other papers by Maya B Lodish in
Google Scholar
PubMed
Search for other papers by Margarita Raygada in
Google Scholar
PubMed
Search for other papers by Jaydira Del Rivero in
Google Scholar
PubMed
Search for other papers by Fabio R Faucz in
Google Scholar
PubMed
Search for other papers by Smita B Abraham in
Google Scholar
PubMed
Search for other papers by Charalampos Lyssikatos in
Google Scholar
PubMed
Search for other papers by Elena Belyavskaya in
Google Scholar
PubMed
Search for other papers by Constantine A Stratakis in
Google Scholar
PubMed
Johns Hopkins University School of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Baltimore, Maryland, 21287, USA
Suburban Hospital, Bethesda, Maryland, 20814, USA
Search for other papers by Mihail Zilbermint in
Google Scholar
PubMed
Summary
Autosomal recessive pseudohypoaldosteronism type 1 (PHA1) is a rare disorder characterized by sodium wasting, failure to thrive, hyperkalemia, hypovolemia and metabolic acidosis. It is due to mutations in the amiloride-sensitive epithelial sodium channel (ENaC) and is characterized by diminished response to aldosterone. Patients may present with life-threatening hyperkalemia, which must be recognized and appropriately treated. A 32-year-old female was referred to the National Institutes of Health (NIH) for evaluation of hyperkalemia and muscle pain. Her condition started in the second week of life, when she was brought to an outside hospital lethargic and unresponsive. At that time, she was hypovolemic, hyperkalemic and acidotic, and was eventually treated with sodium bicarbonate and potassium chelation. At the time of the presentation to the NIH, her laboratory evaluation revealed serum potassium 5.1 mmol/l (reference range: 3.4–5.1 mmol/l), aldosterone 2800 ng/dl (reference range: ≤21 ng/dl) and plasma renin activity 90 ng/ml/h (reference range: 0.6–4.3 ng/ml per h). Diagnosis of PHA1 was suspected. Sequencing of the SCNN1B gene, which codes for ENaC, revealed that the patient is a compound heterozygote for two novel variants (c.1288delC and c.1466+1 G>A), confirming the suspected diagnosis of PHA1. In conclusion, we report a patient with novel variants of the SCNN1B gene causing PHA1 with persistent, symptomatic hyperkalemia.
Learning points
-
PHA1 is a rare genetic condition, causing functional abnormalities of the amiloride-sensitive ENaC.
-
PHA1 was caused by previously unreported SCNN1B gene mutations (c.1288delC and c.1466+1 G>A).
-
Early recognition of this condition and adherence to symptomatic therapy is important, as the electrolyte abnormalities found may lead to severe dehydration, cardiac arrhythmias and even death.
-
High doses of sodium polystyrene sulfonate, sodium chloride and sodium bicarbonate are required for symptomatic treatment.
Search for other papers by Asma Deeb in
Google Scholar
PubMed
Search for other papers by Hana Al Suwaidi in
Google Scholar
PubMed
Search for other papers by Salima Attia in
Google Scholar
PubMed
Search for other papers by Ahlam Al Ameri in
Google Scholar
PubMed
Summary
Combined17α-hydroxylase/17,20-lyase deficiency is a rare cause of congenital adrenal hyperplasia and hypogonadism. Hypertension and hypokalemia are essential presenting features. We report an Arab family with four affected XX siblings. The eldest presented with abdominal pain and was diagnosed with a retroperitoneal malignant mixed germ cell tumour. She was hypertensive and hypogonadal. One sibling presented with headache due to hypertension while the other two siblings were diagnosed with hypertension on a routine school check. A homozygous R96Q missense mutation in P450c17 was detected in the index case who had primary amenorrhea and lack of secondary sexual characters at 17 years. The middle two siblings were identical twins and had no secondary sexual characters at the age of 14. All siblings had hypokalemia, very low level of adrenal androgens, high ACTH and high levels of aldosterone substrates. Treatment was commenced with steroid replacement and puberty induction with estradiol. The index case had surgical tumor resection and chemotherapy. All siblings required antihypertensive treatment and the oldest remained on two antihypertensive medications 12 years after diagnosis. Her breast development remained poor despite adequate hormonal replacement. Combined 17α-hydroxylase/17,20-lyase deficiency is a rare condition but might be underdiagnosed. It should be considered in young patients presenting with hypertension, particularly if there is a family history of consanguinity and with more than one affected sibling. Antihypertensive medication might continue to be required despite adequate steroid replacement. Breast development may remain poor in mutations causing complete form of the disease.
Learning points
-
Endocrine hypertension due to rarer forms of CAH should be considered in children and adolescents, particularly if more than one sibling is affected and in the presence of consanguinity.
-
17α-hydroxylase/17,20-lyase deficiency is a rare form of CAH but might be underdiagnosed.
-
Blood pressure measurement should be carried out in all females presenting with hypogonadism.
-
Anti-hypertensive medications might be required despite adequate steroid replacement.
-
Initial presenting features might vary within affected members of the same family.
-
Adverse breast development might be seen in the complete enzyme deficiency forms of the disease.
Search for other papers by Reiner Jumpertz von Schwartzenberg in
Google Scholar
PubMed
Search for other papers by Ulf Elbelt in
Google Scholar
PubMed
Search for other papers by Manfred Ventz in
Google Scholar
PubMed
Search for other papers by Knut Mai in
Google Scholar
PubMed
Search for other papers by Tina Kienitz in
Google Scholar
PubMed
Search for other papers by Lukas Maurer in
Google Scholar
PubMed
Search for other papers by Thomas Rose in
Google Scholar
PubMed
Search for other papers by Jens C Rückert in
Google Scholar
PubMed
Search for other papers by Christian J Strasburger in
Google Scholar
PubMed
Search for other papers by Joachim Spranger in
Google Scholar
PubMed
Parathyroid carcinoma is a rare disease leading to severe hypercalcemia due to hyperparathyroidism. Surgery is the primary treatment option. A more progressive form of the disease is characterized by parathyrotoxicosis, and subsequent hypercalcemia is the most common cause of death. We report a case presenting with severe hypercalcemia due to parathyrotoxicosis from parathyroid carcinoma treated for the first time using the monoclonal antibody denosumab as a rescue therapy and present long-term follow-up data. The 71-year-old patient presented with severe hypercalcemia due to metastatic parathyroid carcinoma. Despite undergoing treatment with bisphosphonates, cinacalcet hydrochloride, and forced diuresis, the patient`s condition deteriorated rapidly due to resistant hypercalcemia. Surgery performed because of spinal metastasis and forced diuresis lowered calcium levels, albeit they remained in the hypercalcemic range and significantly increased when forced diuresis was stopped. Considering a palliative situation to overcome hypercalcemia, we decided to administer denosumab, a monoclonal antibody that binds to the receptor activator of nuclear factor-kappa B ligand. After a single subcutaneous administration of 60 mg denosumab, calcium levels normalized within one day. Subsequent denosumab injections led to permanent control of serum calcium for more than 2 years despite rising parathyroid hormone levels and repeated surgeries. Together with recent cases in the literature supporting our observation, we believe that denosumab is relevant for future trials and represents an effective tool to control hypercalcemia in patients with advanced stages of parathyroid cancer.
Learning points
-
Severe hypercalcemia is the most common cause of death in patients with parathyroid carcinoma.
-
The monoclonal antibody denosumab rapidly lowered severely elevated serum calcium levels due to parathyrotoxicosis.
-
Denosumab was effective in the long-term treatment of hypercalcemia despite progression of parathyroid carcinoma.
Search for other papers by Jiman Kim in
Google Scholar
PubMed
Search for other papers by Eulsun Moon in
Google Scholar
PubMed
Search for other papers by Seungwon Kwon in
Google Scholar
PubMed
Summary
Diabetic nephropathy, a microvascular complication of diabetes, is a progressive kidney disease caused by angiopathy of the capillaries in the kidney glomeruli. Herein, we report a case of a 62-year-old patient with a 30 year history of diabetes, who showed a substantial improvement in diabetic nephropathy on administration of 30 g of Astragalus membranaceus extract per day. After 1 month, estimated glomerular filtration rate increased from 47 to 72 ml/min per 1.73 m2 and was subsequently maintained at the 1-month follow-up. Urinary protein levels also decreased following treatment. Herein, we present and discuss the evidence and mechanism of A. membranaceus on diabetic nephropathy in this patient.
Learning points
-
Diabetic nephropathy is a progressive kidney disease.
-
Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are currently used to prevent and delay the progression of diabetic nephropathy. However, their effects are not sufficient to prevent a decline in kidney function.
-
Furthermore, combination therapy with an ACE inhibitor and an ARB can produce adverse effects without additional benefits.
-
In the early phase of diabetic nephropathy, administration of Astragalus membranaceus can be a therapeutic option.