Neonatal Cardiogenic Shock and Acute Kidney Injury Associated with a Compressive Retroperitoneal Suprarenal Mass Successfully Managed with Peritoneal Dialysis
Neonatal retroperitoneal masses presenting with multisystem collapse represent a critical clinical emergency. We report the case of a term male neonate who presented on Day 0 of life in profound shock, severe lactic acidosis (pH 6.9, lactate 15 mmol/L), hypoglycemia, and severe biventricular dysfunction (LVEF 20%). Clinical progression was complicated by anuric acute kidney injury (peak serum creatinine 3.7 mg/dL) and feed intolerance. Abdominal ultrasonography revealed a vascular right retroperitoneal suprarenal mass compressing the right renal pelvis, suspicious for congenital neuroblastoma, accompanied by marked hyperferritinemia, elevated LDH (4,488 U/L), and severe activation of the renin-angiotensin-aldosterone axis (renin >500 pg/mL, aldosterone >100 ng/dL). Prompt implementation of acute peritoneal dialysis (PD), hemodynamic stabilization, and mechanical ventilation led to full renal recovery (discharge creatinine 0.94 mg/dL) and clinical stabilization prior to oncologic transfer.
Introduction
Congenital retroperitoneal and suprarenal tumors, predominantly neuroblastoma and congenital mesoblastic nephroma, account for a significant portion of neonatal abdominal neoplasms. While many are diagnosed incidentally on antenatal ultrasonography, a subset presents acutely in the immediate postnatal period with life-threatening complications, including shock, compression of vital renal vasculature, and paraneoplastic or metabolic derangements.
Acute kidney injury (AKI) requiring renal replacement therapy in the first week of life presents significant technical and physiological challenges. This report describes the diagnosis, multidisciplinary stabilization, and successful use of peritoneal dialysis in a neonate with critical multiorgan dysfunction secondary to a compressive retroperitoneal mass.
Case Presentation
Patient information and initial presentation
A 0-day-old, term male neonate weighing 3.00 kg was delivered via normal vaginal delivery and initially roomed-in with the mother. Within the first hours of life, he developed severe apnea, central cyanosis, and lethargy. He was evaluated by a primary pediatrician and urgently transferred to the neonatal intensive care unit (NICU).
On admission, the neonate was in impending respiratory failure and profound shock:
- Vitals & physical exam: cold peripheries, gasping respiration (respiratory rate 36/min), heart rate 100 bpm with feeble peripheral pulses, SpO₂ 70% despite oxygen support, and unresponsiveness to painful stimuli.
- Abdominal exam: soft abdomen with palpable hepatosplenomegaly.
- Initial blood gas & labs: severe mixed metabolic-lactic acidosis with pH 6.90, pCO₂ 18 mmHg, HCO₃⁻ 3.2 mmol/L, base excess −30 mmol/L, and blood lactate 15 mmol/L. Blood glucose testing confirmed severe hypoglycemia.
Diagnostic assessment
- Echocardiography (Day 2): severe biventricular dysfunction with moderate pulmonary arterial hypertension (PAH) and a left ventricular ejection fraction (LVEF) of 20%.
- Brain MRI (Day 3): normal study with no evidence of hypoxic-ischemic encephalopathy (HIE) or intracranial hemorrhage.
- Abdominal ultrasonography (Day 5): a vascular, hyperechoic mass in the right retroperitoneum/suprarenal region causing extrinsic compression on the right renal pelvic region, associated with minimal ascites — highly suspicious for neuroblastoma.
Biochemical & tumor markers · Day 6
Table 1 · Serial laboratory trends
| Date (DOL) | Hb g/dL | TLC /µL | Platelets /µL |
Creatinine mg/dL | Urea mg/dL | Na mEq/L | K mEq/L |
Coagulation / key markers |
|---|---|---|---|---|---|---|---|---|
| 04/05 (DOL 1) | 14.6 | 20,110 | 54,000 | — | — | — | — | pH 6.9, BE −30, lactate 15 |
| 05/05 (DOL 2) | 15.1 | 15,190 | 110,000 | 1.84 | — | 135 | — | PT 26.6 s, INR 2.0, CRP 7 |
| 06/05 (DOL 3) | — | — | — | 2.96 | 56.0 | 132 | 4.0 | INR 1.32 |
| 07/05 (DOL 4) | 12.9 | 8,930 | 66,000 | 3.50 | 80.0 | 135 | 3.7 | PD started |
| 08/05 (DOL 5) | 13.3 | 13,590 | 51,000 | 3.60 | 87.0 | 137 | 3.2 | USG confirms mass |
| 09/05 (DOL 6) | 12.7 | 16,560 | 20,000 | 3.70 | 76.0 | 139 | 3.8 | LDH 4,488, ferritin 3,087 |
| 10/05 (DOL 7) | 11.7 | 17,440 | 110,000 | 3.29 | 71.0 | 138 | 3.6 | Improved urine output |
| 14/05 (DOL 11) | 10.5 | 15,680 | 205,000 | 3.60 | 103.0 | 128 | 2.8 | Resolution of uremia |
| 17/05 (DOL 14) | 9.5 | 19,440 | 432,000 | 1.88 | 62.0 | 134 | 5.7 | Significant renal recovery |
| 20/05 (DOL 17) | 9.2 | 15,970 | 497,000 | 0.94 | 20.5 | 141 | 4.9 | Normalized parameters |
Hospital Course & Therapeutic Interventions
Resuscitation and cardiorespiratory support
Immediate endotracheal intubation and mechanical ventilation were initiated upon admission. Fluid resuscitation with crystalloid boluses and fresh frozen plasma (FFP) was followed by continuous inotropic infusions. Inotropic support was required for 48 hours and successfully weaned following hemodynamic stabilization and restoration of left ventricular function. The patient was extubated after 4 days of invasive mechanical ventilation and transitioned smoothly to room air.
Renal management and peritoneal dialysis
On DOL 1, urine output was severely restricted (<20 mL/24 h) with non-responsiveness to loop diuretic challenges (furosemide). Serum creatinine rose steadily from 1.84 mg/dL to a peak of 3.70 mg/dL. Following pediatric nephrology consultation, acute peritoneal dialysis (PD) was initiated on DOL 4. PD was maintained continuously for 4 days, resulting in steady clinical resolution of fluid overload, resumption of spontaneous diuresis, and gradual normalization of renal chemistry (serum creatinine reached 0.94 mg/dL by DOL 17).
Infection control and transfusion support
Given clinical sepsis and coagulopathy, empirical intravenous antibiotic therapy (meropenem and Megnova) was administered for 10 days, alongside fluconazole (Syscan) prophylaxis for 7 days. Blood cultures yielded no bacterial growth. Transfusion support included 2 units of FFP and 1 unit of packed red blood cells (PRBC).
Gastrointestinal and nutritional management
Initial enteral feedings resulted in feeding intolerance and vomiting, requiring temporary bowel rest. Feedings were reintroduced incrementally and advanced to 15–20 mL boluses via nasogastric tube, supported by prokinetic and anti-reflux therapy (domperidone, ondansetron, and lansoprazole).
Outcome and Follow-up
By DOL 18 (21/05/2026), the patient was clinically stable, maintaining normal room-air saturations, with recovered urine output and resolved azotemia. Definitive contrast-enhanced CT of the abdomen and core needle/excisional biopsy were deferred during the acute renal failure phase to prevent contrast-induced nephrotoxicity.
The infant was electively transferred to a tertiary pediatric hematology-oncology center for:
- Contrast-enhanced CT abdomen and tumor biopsy for definitive histopathological typing.
- Staging and management of the suprarenal mass (neuroblastoma workup).
- Neurodevelopmental, visual (ROP), and audiological (OAE) screening at 1 month of corrected age.
Discussion
Neonatal presentations of abdominal masses with concurrent multi-organ failure are rare and associated with significant mortality. The initial clinical picture in this patient was characterized by cardiogenic shock, profound lactic acidosis, and pulmonary hypertension. The markedly elevated renin (>500 pg/mL) and aldosterone (>100 ng/dL) levels suggest that the mass caused extrinsic mechanical compression of the renal parenchyma and vascular pedicle, triggering localized renal hypoperfusion and compensatory activation of the renin-angiotensin system.
Differential diagnosis
The differential diagnosis for a hypervascular, compressive retroperitoneal/suprarenal mass in this age group includes:
- Congenital neuroblastoma: the most common neonatal malignancy, supported in this case by the vascular retroperitoneal localization, elevated ferritin (3,087 ng/mL), and elevated LDH (4,488 U/L).
- Neonatal adrenal hemorrhage: can mimic neuroblastoma on ultrasonography, though it typically causes a rapid decline in hemoglobin and lacks internal vascular flow on Doppler interrogation.
- Congenital mesoblastic nephroma: the most frequent congenital renal tumor, capable of causing secondary renin-mediated systemic complications.
This case highlights the life-saving role of acute peritoneal dialysis in neonates with severe, medically refractory AKI. Timely initiation of PD effectively cleared metabolic waste products, alleviated uremia, and bridged the patient through the acute phase of renal shutdown without complications related to vascular access or hemodynamic instability.
Furthermore, delaying contrast administration until renal function normalized (creatinine <1.0 mg/dL) was critical to prevent secondary tubulotoxic injury in a solitary functioning or compromised renal bed.
Learning Points
- Vascular compression cascades: neonatal retroperitoneal masses can present with profound systemic collapse, mediated by severe compression of renal vessels, massive renin-angiotensin activation, and secondary cardiac dysfunction.
- Efficacy of early neonatal PD: peritoneal dialysis remains an effective, safe modality for managing acute anuric renal failure in unstable neonates with multiorgan failure.
- Staged diagnostic approach: in critically ill neonates with retroperitoneal tumors and AKI, contrast imaging should be judiciously deferred until baseline renal function is restored through supportive interventions.