From Ovarian Hyperstimulation Syndrome (OHSS) to Cortical Necrosis: A Rare Renal Catastrophe

Introduction: Ovarian hyperstimulation syndrome (OHSS) is a known complication of assisted reproduction. While typically mild and self-limiting, critical OHSS can cause anasarca and multi-organ dysfunction. Acute kidney injury (AKI) is an uncommon complication of OHSS, with cortical necrosis being even rarer. We present a case of critical OHSS leading to acute cortical necrosis in a young woman with no prior comorbidities, highlighting the importance of early detection and aggressive supportive care. Case Description: A 26-year-old woman with primary infertility underwent controlled ovarian stimulation using rFSH, hCG, and cetrorelix. Seven oocytes were retrieved. Within three days, she developed abdominal pain, distension, and respiratory distress and presented to our center with oliguria and multi-organ dysfunction. Examination showed pallor, pedal edema, hypotension, & hypoxia. Labs revealed severe thrombocytopenia, metabolic acidosis, renal dysfunction, elevated transaminases, & hypoalbuminemia. Ultrasound showed bilaterally enlarged echogenic kidneys and gross ascites. She was managed with IV albumin, supportive care, and intermittent hemodialysis. Inotropes were tapered in 48 hours, with clinical improvement over a week, though she remained oligo-anuric. A diagnosis of critical OHSS was made with differentials of acute tubular necrosis (ATN) and thrombotic microangiopathy (TMA). Sepsis, infections, TMA, and autoimmune causes were ruled out. Renal biopsy confirmed acute cortical necrosis. She remains on RRT and is under OPD follow-up, with plans for renal transplantation. Discussion: Critical OHSS, seen in 0.1–2% of cases, can be fatal due to cytokine-mediated vascular permeability, causing edema, hemoconcentration, and organ hypoperfusion. ATN or prerenal factors primarily cause AKI in OHSS. In reproductive-age females, cortical necrosis is typically obstetric in origin—septic abortion, eclampsia, or sepsis—making OHSS a rare cause. This case is notable as it developed without typical risk factors like high estradiol, early pregnancy, or prior OHSS. Only two prior cases of OHSS-related cortical necrosis have been reported. Prompt initiation of fluids, albumin, vasopressors, and RRT is critical for managing this condition. With the increasing use of assisted reproduction, vigilant monitoring during ovarian stimulation is vital to prevent such outcomes.

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Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025n4775kbh
Primary Topic
Ovarian function and disorders
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article
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article

From Ovarian Hyperstimulation Syndrome (OHSS) to Cortical Necrosis: A Rare Renal Catastrophe

Arunkumar Subbiah, Dipankar Bhowmik, Eshwar Chowdari Kolluru
Journal of the American Society of Nephrology
Ovarian function and disorders
article

From Ovarian Hyperstimulation Syndrome (OHSS) to Cortical Necrosis: A Rare Renal Catastrophe

Arunkumar Subbiah, Dipankar Bhowmik, Eshwar Chowdari Kolluru
article en

Abstract

Introduction: Ovarian hyperstimulation syndrome (OHSS) is a known complication of assisted reproduction. While typically mild and self-limiting, critical OHSS can cause anasarca and multi-organ dysfunction. Acute kidney injury (AKI) is an uncommon complication of OHSS, with cortical necrosis being even rarer. We present a case of critical OHSS leading to acute cortical necrosis in a young woman with no prior comorbidities, highlighting the importance of early detection and aggressive supportive care. Case Description: A 26-year-old woman with primary infertility underwent controlled ovarian stimulation using rFSH, hCG, and cetrorelix. Seven oocytes were retrieved. Within three days, she developed abdominal pain, distension, and respiratory distress and presented to our center with oliguria and multi-organ dysfunction. Examination showed pallor, pedal edema, hypotension, & hypoxia. Labs revealed severe thrombocytopenia, metabolic acidosis, renal dysfunction, elevated transaminases, & hypoalbuminemia. Ultrasound showed bilaterally enlarged echogenic kidneys and gross ascites. She was managed with IV albumin, supportive care, and intermittent hemodialysis. Inotropes were tapered in 48 hours, with clinical improvement over a week, though she remained oligo-anuric. A diagnosis of critical OHSS was made with differentials of acute tubular necrosis (ATN) and thrombotic microangiopathy (TMA). Sepsis, infections, TMA, and autoimmune causes were ruled out. Renal biopsy confirmed acute cortical necrosis. She remains on RRT and is under OPD follow-up, with plans for renal transplantation. Discussion: Critical OHSS, seen in 0.1–2% of cases, can be fatal due to cytokine-mediated vascular permeability, causing edema, hemoconcentration, and organ hypoperfusion. ATN or prerenal factors primarily cause AKI in OHSS. In reproductive-age females, cortical necrosis is typically obstetric in origin—septic abortion, eclampsia, or sepsis—making OHSS a rare cause. This case is notable as it developed without typical risk factors like high estradiol, early pregnancy, or prior OHSS. Only two prior cases of OHSS-related cortical necrosis have been reported. Prompt initiation of fluids, albumin, vasopressors, and RRT is critical for managing this condition. With the increasing use of assisted reproduction, vigilant monitoring during ovarian stimulation is vital to prevent such outcomes.

Journal of the American Society of NephrologyVol. 36(10S)
All India Institute of Medical Sciences (IN)
Openalex Percentile: Top 52%
Ovarian function and disorders
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