Discussion
Kidney transplant is the treatment of choice for patients with end-stage renal disease, however it is classified as an intermediate-high-risk surgery with serious potential complications. Examples of surgical and vascular complications include wound infection, hematoma, acute renal failure due to ATN, perirenal abscess, renal artery or vein thrombosis, urine leak, and many more.
ATN is the most common cause of impaired renal function in the early post-transplantation period1. It represents necrosis of tubular cells that commonly slough into the tubular lumen. The initial cause of ATN in transplant patients is usually related to the process of the transplant itself that causes ischemia to the kidney. In addition, reperfusion after the transplant may lead to oxygen free radical injury1.
The diagnosis of post-transplantation ATN is based on either inadequate and slow reduction of the serum creatinine level or oliguria through early post-operative phase2.
Our patient suffered from acute oliguria during the early post-operative phase and rising serum creatinine levels, raising the suspicion of ATN.
A CDUS was performed on postoperative day 1, and revealed a RI of 1 with a diastolic reflux, compatible with the diagnosis of ATN.
However, a subcapsular hematoma encircling the renal graft was concurrently seen, responsible of a compression on the major part of the renal parenchyma, causing a mass effect and hyperpressure on the intrarenal vessels.
While the incidence of postoperative surgical‐site hemorrhage in kidney transplantation is relatively low, it may be associated with an increased risk of graft loss or death3, thus, explaining the importance of early detection and adequate treatment.
The overall incidence of significant postoperative hematomas from renal transplant varies from 4 to 8%4.
The signs and symptoms of subcapsular hematoma in renal allograft vary depending on the duration and severity of the bleeding5. The clinical presentation of patients with a single kidney and renal allografts includes flank pain/tenderness, decreased urine output or acute renal failure5, all of which were present in our two patients.
The subcapsular hematoma of our patient was totally evacuated in the operative room. Rapid clinical and biological improvements were noted. The diuresis was back to normal and serum creatinine levels reached normal values.
Only two days after complete evacuation of the hematoma, a repeat CDUS of the renal graft showed a normal RI, between 0.56 an 0.6, alongside complete resolution of the subcapsular hematoma.
Usually, ATN occurs right after the transplantation and resolves within two weeks, but can last for up to three months. About 10%–30% of these patients require dialysis in the early stages1.
The rapid return to normal of the RI postoperatively, in addition to the rapid clinical and biological improvement within only two days of surgical evacuation of the hematoma, excludes the diagnosis of ATN. Thus, we can assume that the mass effect and the intrarenal hyperpressure caused by the subscapular renal hematoma was responsible of the abnormally elevated RI at 1, mimicking ATN.
Subcapsular renal hematomas can be managed conservatively. However, many case reports showed conservative line of therapy to be life threatening5. In fact, it could continue to increase with time and cause a renal vein thrombosis. Surgical management should be in the first line of therapy when it comes to subcapsular renal hematomas with hemodynamic changes, in order to avoid any further complications and save the graft.