Subcapsular renal hematomas (SRHs) are rare but significant findings that carry potential risks in both acute and chronic settings. These crescentic fluid collections, confined by the renal capsule, can exert pressure on the underlying renal parenchyma and may be accompanied by perinephric hemorrhage. SRH can manifest with various clinical symptoms, including anemia, pain, infection, kidney injury, and hypertension. While the etiology of spontaneous hematomas remains unclear, traumatic causes can result from physical injury or accidents, while iatrogenic causes are associated with postprocedural complications.

In a comprehensive 10-year retrospective review, a total of 97 patients with acute SRH in the native kidney were included. The etiologies of SRH were classified into 3 categories: traumatic (21%), spontaneous (32%), and iatrogenic (47%), as seen in the Table. Notably, spontaneous SRH cases often lacked clear underlying causes, with less than half of patients having associated cystic or solid masses. Renal biopsy was the most common iatrogenic etiology (18/28), followed by nephrostomy placement/exchange (7/28) and percutaneous nephrolithotomy (PCNL; 7/28).

Complications associated with SRH were observed in several patients. Three patients developed Page kidney phenomenon, with hypertension secondary to renin-angiotensin-aldosterone system activation. Among these patients, 2 had solitary kidneys, necessitating new hemodialysis or open hematoma evacuation. The Page kidney with a contralateral functional kidney was managed conservatively. Additionally, 6 patients developed infected perinephric hematomas, requiring interventions such as image-guided drainage (n=5) or nephrectomy (n=1) on day 85, on average. Perinephric bleeding occurred in 21 patients, with 17 of them undergoing renal artery embolization. Of the 17 patients requiring renal artery embolization, 4 presented with trauma, 7 after iatrogenic causes, and 6 were spontaneous (3 with renal masses). While rare, an additional 2 cases required operative hematoma evacuation due to severe pain and abdominal compartment syndrome.

Prompt recognition of the SRH in addition to recognition of the cause of the bleed may be impactful to predicting outcomes. Perhaps the most common etiology of SRH is renal biopsy, as seen in our cohort (19%). A prospective study of 471 patients by Manno et al reported a 33% rate of postbiopsy SRH in native kidneys. However, 90% of these hematomas were clinically silent.¹ Our study noted that 55% of postbiopsy hematomas required intervention ranging from multiple transfusions to renal artery embolization.

Iatrogenic renal subcapsular hematoma from routine urological cases traditionally has been described regarding percutaneous stone extraction (PCNL) and extracorporeal shock wave lithotripsy. In our study, PCNL (7/46) and extracorporeal shock wave lithotripsy (6/46) were the most common iatrogenic causes of SRH. Additionally, placement or exchange of nephrostomy tube had a similar incidence (7/46). SRH after ureteroscopic lithotripsy is detailed in relatively few case reports. Our study reports 4 SRHs in the setting of ureteroscopy. A systematic review by Whitehurst et al in 2017 of 9,000 patients who underwent ureteroscopic lithotripsy found the incidence of SRH to be 0.45%.² It has been postulated that SRHs are more likely to form after ureteroscopy in the setting of hydronephrosis leading to deformed vasculature and loss of parenchymal elasticity. In addition, trauma from the guidewire and prolonged high-pressure flow in the pelvicaliceal system may be attributed to the risk of SRH.

About one-third of the hematoma cases in our study were spontaneous bleeds, unrelated to trauma or iatrogenic etiology. Of the 31 spontaneous SRHs, 8 were related to renal masses and 4 to polycystic kidneys. Wunderlich syndrome describes the acute onset of spontaneous, nontraumatic renal hemorrhage into the subcapsular and perirenal spaces. It is traditionally characterized by Lenk’s triad: acute flank pain, flank mass, and hypovolemic shock. More than half of these patients in our study were clinically silent. However, 3 of 97 (3%) of the total SRH cases developed Page kidney, all from spontaneous hematomas, 1 of which was related to an underlying renal mass.

The natural history of the SRH timeline to resolution has not been elucidated in the current literature. Our study included patients with at least 3 follow-up cross-sectional imaging series. Among the 94 patients who underwent follow-up imaging within 10 months, 20 of them (21%) demonstrated complete hematoma resolution. Further imaging between 10 and 15 months was conducted on 18 patients, with an additional 8 patients (44%) showing resolved hematomas. On average, the complete resolution of the hematoma took approximately 368 days. Although our study lacks complete follow-up for each patient, it may be recommended that patients with SRH expect follow-up for 1.5 to 2 years until resolution.

There is currently no evidence-based guideline for the management of SRH. The study’s findings shed light on the natural history, clinical course, and management of SRHs. Early recognition is key, especially in the setting of solitary or allograft kidney, to prevent progressive ischemic organ damage. Indications for intervention as seen in our study include severe anemia and hemodynamic instability, intolerable pain, infected hematoma intractable to antibiotic therapy, and Page kidney.