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Updated: May 20, 2026

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
Published on: June 2, 2022
Acute calciphylaxis precipitated by the initiation of hemodialysis
Insights
Calciphylaxis (CUA) can acutely develop after starting hemodialysis (HD) due to calcium-phosphate imbalances. Careful management of calcium levels and dialysate composition during initial HD is crucial for prevention.
Area of Science:
- Nephrology
- Vascular Medicine
- Dermatology
Background:
- Calciphylaxis (calcific uremic arteriopathy) involves calcification of small arteries, leading to skin necrosis, often in end-stage renal disease (ESRD) patients.
- Elevated serum calcium × phosphorus (Ca × P) product is a key risk factor, and its normalization is critical for CUA management.
Observation:
- A novel case of acute calciphylaxis (CUA) is presented in a Stage-5 chronic kidney disease (CKD) patient immediately following the initiation of hemodialysis (HD).
- This iatrogenic CUA is hypothesized to result from rapid calcium influx from dialysate and acidosis correction, creating a favorable environment for Ca-P complex formation during the first HD session.
Findings:
- This is the first reported instance of hemodialysis-associated acute iatrogenic calciphylaxis (CUA).
- The study highlights the potential for rapid CUA development in CKD patients with high Ca × P product upon commencing HD.
Implications:
- Initiating HD in high Ca × P product patients requires strategies to prevent CUA, including adequate hydration, lower calcium dialysate, and avoidance of vitamin D analogues and calcium-based medications.
- Empiric use of sodium thiosulfate during initial HD sessions may be a promising strategy to prevent Ca-P precipitation and mitigate the risk of potentially fatal CUA.
Abstract:
Calciphylaxis, or calcific uremic arteriopathy (CUA), is characterized by metastatic calcification in the media of small arteries and arterioles leading to cutaneous necrosis. It is most commonly seen in patients with end stage renal disease who have elevated serum calcium × phosphorus (Ca × P) product. Normalization of Ca × P product is considered paramount in the prevention and treatment of CUA. We describe a novel presentation of CUA in which a Stage-5 CKD patient developed signs and symptoms of CUA immediately after initiation of hemodialysis (HD). We postulate that an influx of calcium from the dialysate into the patient's blood, in addition to correction of her acidosis, led to abundant substrate in a favorable milieu for Ca-P complex formation at the time of her first HD session. Our case is the first reported case of HD associated iatrogenic acute CUA. To avoid this complication, we should maintain adequate hydration,use lower calcium dialysate, and avoid vitamin D analogues and calcium-containing medications when initiating HD in patients with high Ca-P product. Since sodium thiosulfate is known to prevent precipitation of Ca-P complexes, its empiric use during initial HD treatments may be effective in preventing CUA, a potentially fatal disease.
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