Related Experiment Video
Updated: Aug 19, 2026

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
Published on: June 2, 2022
Cutaneous necrosis by calcific uremic arteriolopathy
Ricardo Luis Galimberti1, Eduardo Dos Ramos Farias, Isabel Hidalgo Parra
1Department of Dermatology, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. ricardo.galimberti@hospitalitaliano.org.ar
Insights
Calcific uremic arteriolopathy, a severe vascular condition in dialysis patients, may improve with early diagnosis and treatment of distal lesions. Survival appears linked to diagnosis timing and lesion location, not solely treatment type.
Area of Science:
- Nephrology
- Vascular Medicine
- Dermatology
Background:
- Calcific uremic arteriolopathy (CUA) is a rare, severe condition causing arterial calcification and tissue ischemia.
- CUA predominantly affects patients with chronic renal failure undergoing dialysis or those with secondary hyperparathyroidism post-renal transplant.
Observation:
- Six end-stage renal disease patients (five on hemodialysis, one on peritoneal dialysis) presented with painful livedo reticularis and limb skin necrosis.
- All observed patients had secondary hyperparathyroidism and elevated calcium-phosphorus product.
- Clinical features included white race, hypoalbuminemia, diabetes, and obesity.
Findings:
- Subtotal parathyroidectomy was performed in three patients, resulting in one survival and two deaths.
- Aggressive wound care with hemodialysis and phosphorus binders improved lesions in one patient.
- Local wound care alone also led to lesion improvement in another patient.
- Early diagnosis, distal lesions, and normal serum albumin correlated with survival, independent of treatment modality.
Implications:
- Early diagnosis and management of specific clinical factors are crucial for improving outcomes in calcific uremic arteriolopathy.
- Further research into the pathogenesis and optimal treatment strategies for CUA is warranted.
- This study highlights the importance of a multidisciplinary approach in managing complex renal disease complications.
Background:
Calcific uremic arteriolopathy is a rare and serious disorder characterized by systemic medial calcification of the arteries and tissue ischemia. Most often it is found in patients with chronic renal failure on dialysis and in renal transplant recipients with secondary hyperparathyroidism.
Methods:
We report six patients with end-stage renal disease [five on hemodialysis (one with a nonfunctioning renal graft) and one on peritoneal dialysis] who developed painful livedo reticularis and skin necrosis of the limbs. All had secondary hyperparathyroidism and elevated calcium-phosphorus product. Our patients presented with the following clinical features: white race (six patients), hypoalbuminemia (three patients), diabetes (one patient), and obesity (four patients).
Results:
Subtotal parathyroidectomy was performed in three cases. Despite this procedure, two patients died; one patient survived and his lesions healed. One patient was treated with aggressive wound care and hemodialysis (with low dialysate calcium concentration and Renagel phosphorus binders) and one patient received only local wound care, both with improvement of their lesions. In one case, no therapy was performed because the patient died immediately after diagnosis.
Conclusions:
The three patients who survived (Cases 4, 5 and 6) had distal lesions, normal serum albumin, and an early diagnosis. There was a relationship between the outcome of the patients and these factors, rather than the type of treatment received.
Related Concept Videos
Cellular Injury IV: Necrosis
Diabetic Foot Ulcer
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation
Necrosis
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Peripheral Artery Disease I: Introduction
Acute Kidney Injury II: Pathophysiology
