Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...
Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations01:26

Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations

Renal calculi, commonly termed kidney stones, are crystalline solid masses that form in the kidneys but can occur at any point within the urinary system, encompassing the kidneys, ureters, bladder, and urethra.The pathophysiology of renal stones involves several key factors: supersaturation of the urine with stone-forming constituents, changes in urine pH, a decrease in urine volume, and the presence of substances that promote or inhibit stone formation.Supersaturation of Urine: This is the...
Ascites01:19

Ascites

DefinitionAscites is the buildup of fluid inside the peritoneal cavity. It occurs when fluid moves out of the vascular system faster than the peritoneal lymphatics can remove it. This fluid shift is most commonly seen in liver cirrhosis but can also appear in several other systemic disorders.EtiologyCirrhosis remains the leading cause of ascites. Other conditions that can contribute include:Heart failureConstrictive pericarditisAbdominal cancersNephrotic syndromeSevere protein–calorie...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Retraction of "Acetyl-l-carnitine increases artemin level and prevents neurotrophic factor alterations during neuropathy" [Neuroscience 167(4) (2010) 1168-1174].

Neuroscience·2024
Same author

The evaluation of the intracavitary effusions by a bedside ultrasound examination.

Clinical hemorheology and microcirculation·2022
Same author

Bilateral spontaneous renal artery dissection and antiphospholipid antibodies.

British journal of biomedical science·2020
Same author

Lag3<sup>+</sup> regulatory T lymphocytes in critical carotid artery stenosis.

Clinical and experimental medicine·2019
Same author

In vitro fertilization and autoimmunity: Evidence from an observational study.

European journal of obstetrics, gynecology, and reproductive biology·2019
Same author

Systemic lupus erythematosus and myelofibrosis: A case report and revision of literature.

Leukemia research reports·2018
Same journal

Association of systemic lupus erythematosus with 90-day readmission following heart failure hospitalization: A national readmission database (NRD) analysis, 2016-2017.

Lupus·2026
Same journal

Association of GPX4 rs713041 and rs4807542 polymorphisms and serum GPX4 levels in Chinese patients with systemic lupus erythematosus.

Lupus·2026
Same journal

Giant cell myocarditis in an 18-year-old patient with new-onset systemic lupus erythematosus: A fatal case of rapidly progressing heart failure.

Lupus·2026
Same journal

An evidence-based specialist nursing protocol for children with hypoprothrombinemia-lupus anticoagulant syndrome (HLAS) and its application research.

Lupus·2026
Same journal

T-bet expression in B cell subsets: Association with T peripheral helper cells and clinical activity in systemic lupus erythematosus.

Lupus·2026
Same journal

Autonomic dysfunction in systemic lupus erythematosus and systemic sclerosis.

Lupus·2026
See all related articles

Related Experiment Video

Updated: Jun 4, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Hypercalcaemia in systemic lupus erythematosus.

F Del Porto1, M Proietta, A Koverech

  • 1Università degli Studi di Roma "La Sapienza", II Facoltà di Medicina e Chirurgia, Dipartimento di Medicina Clinica e Molecolare, Ospedale Sant'Andrea, Roma, Italia. flavia.delporto@uniroma1.it

Lupus
|February 2, 2011
PubMed
Summary
This summary is machine-generated.

Hypercalcaemia, a common complication of primary hyperparathyroidism and malignancies, can rarely be linked to Systemic Lupus Erythematosus (SLE). This report details the 10th patient with SLE and hypercalcaemia, highlighting a rare but significant association.

Related Experiment Videos

Last Updated: Jun 4, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Area of Science:

  • Endocrinology
  • Rheumatology
  • Internal Medicine

Background:

  • Hypercalcaemia is a frequent finding in primary hyperparathyroidism and malignancies.
  • Various other conditions, including vitamin D hypervitaminosis, sarcoidosis, granulomatous diseases, certain drugs, and endocrine disorders, can also cause hypercalcaemia.
  • Systemic Lupus Erythematosus (SLE) is a rare cause of hypercalcaemia.

Observation:

  • Nine cases of hypercalcaemia in patients with SLE, without evidence of primary hyperparathyroidism, have been previously documented.
  • This paper presents the 10th such case, adding to the limited literature on this association.

Findings:

  • The 10th patient with Systemic Lupus Erythematosus (SLE) presented with hypercalcaemia.
  • No evidence of primary hyperparathyroidism was found in this patient.
  • This case reinforces the rare association between SLE and hypercalcaemia.

Implications:

  • Recognizing hypercalcaemia as a potential complication of SLE is crucial for accurate diagnosis and management.
  • Further research may elucidate the mechanisms linking SLE and hypercalcaemia.
  • This finding may prompt earlier investigation for hypercalcaemia in SLE patients presenting with relevant symptoms.