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\begin{document}

\title{Subcapsular renal transplant hematoma mimicking acute tubular necrosis}



\author[1]{Rhea Akel}%
\author[1]{Elias El-Haddad}%
\author[1]{Kamal Hachem}%
\affil[1]{Hotel-Dieu De France}%


\vspace{-1em}



  
  \date{May 27, 2024}


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\textbf{Subcapsular renal transplant hematoma mimicking acute tubular
necrosis}

\textbf{Introduction}

Kidney transplantation is the treatment of choice for patients with
end-stage renal disease. However, it is associated with serious
potential complications. In the immediate posttransplant period,
ultrasound (US) is considered to be one of the major imaging tools in
the evaluation of early graft complications. In fact, it is a
noninvasive, nonionizing, effective and reliable imaging modality that
is accessible and portable, and provides immediate results.

We discuss two cases of patients who underwent a living-donor kidney
transplantation, complicated by subcapsular hematoma mimicking acute
tubular necrosis (ATN) on Color Doppler Ultrasonography Study (CDUS).

\textbf{Case presentation}

Patient A is a 32-year-old woman, who was admitted to undergo an
elective living-donor kidney transplant. Medical history includes
end-stage renal disease due to focal segmental glomerulosclerosis
(confirmed by histology) treated with conservative management, 8-year
history of chronic hypertension and pre-eclampsia.

Family history includes a brother who underwent a living-donor kidney
transplant as a treatment for end-stage renal disease secondary to
membranous nephropathy.

Preoperative medical assessment was unremarkable. Vital signs were
within normal limits, except for a blood pressure of 152/89 mmHg.
Laboratory results showed a baseline serum creatinine levels of 877
\selectlanguage{greek}μ\selectlanguage{english}mol/L.

The surgery was performed without per-operative complications, and the
patient was transferred to the intensive care unit for observation.

Within 24 hours of admission, the patient presented an acute oliguria,
nonresponsive to fluid resuscitation. Physical examination showed a soft
and nontender abdomen. Vital signs were normal. Serial laboratory
results showed a progressive increase in serum creatinine levels, after
reaching a nadir of 284 \selectlanguage{greek}μ\selectlanguage{english}mol/L. Acute renal rejection was suspected.

A Color-Doppler sonography of transplant kidney performed urgently
revealed a renal graft of normal size, measuring 10.8cm, located in the
right iliac fossa, with normal echostructure and without hydronephrosis.
Subcapsular renal hematoma of 22 mm thickness, extending on a length of
9 cm, with an estimated volume between 50 -- 76 ml (Figure 1),
responsible of a compression on the major part of the renal parenchyma,
was noted. CDUS showed a high resistive flow, without a diastolic
component, with a resistive index (RI) of 1 (Figure 2). Diastolic reflux
was noted. The graft vessels were patent, with no stenosis or thrombosis
detected. Due to these findings, ATN was suspected.

Following these results, the patient underwent an emergent surgical
evacuation of the subcapsular renal hematoma. Subsequently and
immediately, the diuresis was back to normal. A prompt repeat CDUS
revealed complete resolution of the subcapsular hematoma (Figure 3) with
a normal RI, between 0.56 and 0.6 (Figure 4). Serial laboratory results
showed a continuous decline in serum creatinine levels until reaching
normal levels of 80 \selectlanguage{greek}μ\selectlanguage{english}mol/L within two days only.

Thereafter, the patient had an uncomplicated in-hospital stay, and was
discharged home one week later.

Patient B is a 40-year-old woman, who was admitted to undergo an
elective living-donor kidney transplant. Medical history includes
end-stage renal disease due to bilateral vesicoureteral reflux with
recurrent urinary tract infections treated with bilateral ureteral
reimplantation. Family history was negative.

Preoperative medical assessement was unremarkable. Vital signs were
within normal limits. Laboratory results showed a baseline serum
creatinine levels of 687 \selectlanguage{greek}μ\selectlanguage{english}mol/L.

The surgery was performed without per-operative complications, and the
patient was transferred to the intensive care unit for observation.

Within 24 hours of admission, the patient presented an acute oliguria,
nonresponsive to fluid resuscitation. Physical examination showed a soft
and nontender abdomen. Vital signs were normal. Serial laboratory
results showed a progressive increase in serum creatinine levels, after
reaching a nadir of 273 \selectlanguage{greek}μ\selectlanguage{english}mol/L. Acute renal rejection was suspected.

A Color-Doppler sonography of transplant kidney performed urgently
revealed a renal graft of normal size, measuring 10.7cm, located in the
right iliac fossa, with normal echostructure and without hydronephrosis.
Subcapsular renal hematoma of 20 mm thickness, extending on a length of
7.1 cm (Figure 1'), responsible of a compression on the major part of
the renal parenchyma, was noted. CDUS showed a high resistive flow,
without a diastolic component, with a resistive index (RI) of 1 (Figure
2'). Diastolic reflux was noted. The graft vessels were patent, with no
stenosis or thrombosis detected. Due to these findings, ATN was
suspected.

Following these results, the patient underwent an emergent surgical
evacuation of the subcapsular renal hematoma. Subsequently and
immediately, the diuresis was back to normal. A prompt repeat CDUS
revealed complete resolution of the subcapsular hematoma (Figure 3')
with a normal RI, between 0.62 (Figure 4'). Serial laboratory results
showed a continuous decline in serum creatinine levels until reaching
normal levels of 64 \selectlanguage{greek}μ\selectlanguage{english}mol/L within two days only.

Thereafter, the patient had an uncomplicated in-hospital stay, and was
discharged home one week later.

\textbf{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 period\textsuperscript{1}. 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 injury\textsuperscript{1}.

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 phase\textsuperscript{2}.

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 death\textsuperscript{3}, 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\%\textsuperscript{4}.

The signs and symptoms of subcapsular hematoma in renal allograft vary
depending on the duration and severity of the
bleeding\textsuperscript{5}.~The clinical presentation of patients with
a single kidney and renal allografts includes flank pain/tenderness,
decreased urine output or acute renal failure\textsuperscript{5}, 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 stages\textsuperscript{1}.

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
threatening\textsuperscript{5}. 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.

\textbf{Conclusion}

Despite the low incidence of postoperative renal hematoma following
kidney transplantation, it can have serious complications affecting the
outcome of the graft and even the patient. When the renal hematoma is
subscapular with a mass effect on the renal parenchyma and intrarenal
hyperpressure, CDUS can show a falsely elevated RI, that can mimic ATN.

The mainstay of the treatment would be the emergent evacuation of the
hematoma with postoperative imaging control.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Figure 1: Patient A: Axial (a) and sagittal (b) view of the renal graft
showing a well-differentiated kidney with an echogenic collection (*)
encircling and deforming the parenchyma, compatible with a subcapsular
hematoma.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Figure 1': Patient B: Axial (a) and sagittal (b) view of the renal graft
showing a well-differentiated kidney with an echogenic collection (*)
encircling and deforming the parenchyma, compatible with a subcapsular
hematoma.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

Figure 2: Patient A: Spectral waveform of intrarenal arteries showing a
resistive flow with no diastolic component and diastolic reflux.
Resistive index was evaluated at 1.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

Figure 2': Patient B: Spectral waveform of intrarenal arteries showing a
resistive flow with no diastolic component and diastolic reflux.
Resistive index was evaluated at 1.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

Figure 3: Patient A: Sagittal (a) and axial (b) view of the renal graft
showing complete resolution of the subcapsular hematoma and its mass
effect.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}

Figure 3': Patient B: Sagittal (a) and axial (b) view of the renal graft
showing complete resolution of the subcapsular hematoma and its mass
effect.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image7/image7}

\end{center}
\end{figure}

Figure 4: Patient A:

(a) Spectral waveform of intrarenal arteries showing complete return to
normal of the resistive index, evaluated at 0.58.

(b) Sagittal view of the graft showing complete resolution of the mass
effect and normal Color Doppler vascularization of the renal parenchyma.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image8/image8}

\end{center}
\end{figure}

Figure 4': Patient B:

(a) Spectral waveform of intrarenal arteries showing complete return to
normal of the resistive index, evaluated at 0.62.

(b) Sagittal view of the graft showing complete resolution of the mass
effect and normal Color Energy vascularization of the renal parenchyma.

1. Irshad, A. \emph{et al.} A review of sonographic evaluation of renal
transplant complications. \emph{Curr. Probl. Diagn. Radiol.}\textbf{37}
, 67--79 (2008).

2. S, N. \emph{et al.} Doppler-based renal resistive index for
prediction of renal dysfunction reversibility: A systematic review and
meta-analysis. \emph{Journal of critical
care}https://pubmed.ncbi.nlm.nih.gov/25746587/ (2015).

3. Hachem, L. D. \emph{et al.} Postoperative surgical-site hemorrhage
after kidney transplantation: incidence, risk factors, and
outcomes.\emph{Transpl. Int.} \textbf{30} , 474--483 (2017).

4. Yap, R., Madrazo, B., Oh, H. K. \& Dienst, S. G. Perirenal fluid
collection after renal transplant. \emph{Am. Surg.} \textbf{47} ,
287--290 (1981).

5. Yar, A., Iqbal, N., Khan, R., Sheikh, A. A. E. \& Mahmud, U. S.
Oliguria due to extensive subcapsular hematoma in renal graft: does
surgical intervention ensure better outcomes? \emph{CEN Case
Rep.}\textbf{8} , 147--150 (2019).\selectlanguage{english}
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