Kidney Week

Abstract: SA-PO0347

AKI After Recreational Melanotan II Use

Session Information

• AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Faradji, Daniel, Methodist Health System, Dallas, Texas, United States

Daniel Faradji, MD

• Dehmami, Farbod, Methodist Health System, Dallas, Texas, United States

Farbod Dehmami, MD, PharmD

• Frangenberg, Alexander M., Methodist Health System, Dallas, Texas, United States

Alexander M. Frangenberg, DO, MS

• Javed, Madeeha, Methodist Health System, Dallas, Texas, United States

Madeeha Javed, DO

Introduction

Melanotan-II is a synthetic melanocortin receptor (MCR) agonist developed alongside afamelanotide (FDA-approved for erythropoietic protoporphyria) but never approved itself. Though discontinued, it has gained rising popularity for recreational tanning use driven by social media. Its renal safety profile remains poorly characterizied with isolated reports of acute kidney injury (AKI) largely attributed to rhabdomyolysis. We report a case of AKI following subcutaneous use in which the degree of kidney injury was disproportional to a modest creatine kinase elevation, suggesting a mechanism beyond pigment-induced tubular injury.

Case Description

A 51-year-old male with a past medical history of hypertension presented 90 minutes following his first subcutaneous melanotan-II injection. Symptoms included muscle cramping, lower-extremity paresthesias, an erection lasting >5 hours, nausea, and chest wall/abdominal pain. His initial blood pressure was 141/82 mmHg with a heart rate of 128; he was diaphoretic and afebrile. Initial studies were significant for a white blood cell count of 21.7 x 10⁹/L, serum creatinine of 2.32 mg/dL (baseline 1.00), serum bicarbonate of 12 mmol/L with an anion gap of 24, and an initial lactate of 7.4 mmol/L. His initial creatine kinase was 363 U/L, peaked at 1301 U/L, and downtrended. A CT of the abdomen and pelvis with and without contrast showed no renal infarction, calculus, or hydronephrosis. Management included volume resuscitation and a sodium bicarbonate infusion. Creatinine improved (2.32 → 1.5 → 1.2 mg/dL) with normalization of lactate, leukocytosis, creatine kinase, and symptom resolution.

Discussion

This patient's symptoms of priapism, gastrointestinal symptoms, and vasoconstrictive features of chest/abdominal pain, and lactic acidosis are consistent with systemic MCR activation. MCRs are expressed in the renal vasculature and can produce renal vasoconstriction and decreased perfusion. The severity of AKI (KDIGO stage 2) in the setting of only mildly elevated CK argues against pigment-induced tubular injury as the primary mechanism, and the concurrent lactic acidosis supports a vasoconstrictive/ischemic etiology. The improvement in serum markers with fluid resuscitation following drug cessation strengthens this association. With increasing recreational use, clinicians should recognize melanotan-II as an emerging cause of vasoconstriction-mediated AKI, distinct from rhabdomyolysis-related injury.