Suture-free polyglactin 910 mesh repair of kidney graft rupture: A case report and review of literature

Abstract

BACKGROUND

Transplantectomy has long been considered the preferred treatment for spontaneous renal graft rupture, prioritizing patient safety over kidney salvage. In the last decade, there has been an increasing number of reports showing that, in selected scenarios, conservative management through graft repair represents a feasible option, challenging traditional approaches.

CASE SUMMARY

We describe the case of a 37-year-old sensitized XY patient who experienced early spontaneous graft rupture after receiving his second deceased donor kidney transplant. Following temporary hemodynamic stabilization and abdominal contrast enhanced computed tomography scan assessment, the recipient was brought back to theatre for surgical exploration. Possible causes of irreversible graft damage were immediately ruled out. The fractured upper pole of the transplanted kidney was repaired using a fibrin sealant, external compression, and a tailored polyglactin 910 mesh wrapped around the graft. The post-operative course was uneventful. After 20 months of follow up, the patient is doing very well, with excellent renal function and complete reabsorption of the mesh, as demonstrated by serial ultrasound evaluations of the graft.

CONCLUSION

Amid organ shortages and sensitized patients, graft nephrectomy is reserved for severe injuries; repair using sealants and mesh is effective.

Key Words: Kidney transplant; Graft rupture; Graft repair; Surgical complications; Mesh; Imaging; Management; Outcome; Case report

Core Tip: Spontaneous kidney graft rupture represents a life-threatening surgical complication, typically presenting with abdominal pain, impaired renal function, and shock. Contrast-enhanced computed tomography scan is the gold standard imaging modality for diagnosis, while aggressive resuscitation and prompt surgical exploration are key factors for optimized recipient and transplant outcomes. For many years, first-line graft nephrectomy has been considered the standard of care. However, there is now evidence supporting a more conservative approach. Indeed, recent reports show that suture-free repair offers several advantages over direct suturing and extended graft manipulation. We describe a case successfully repaired with sealants application and resorbable mesh wrapping.

INTRODUCTION

Spontaneous graft rupture (SGR), though rare, is a critical condition that can result in kidney transplant (KT) loss or death[1]. More often, this dreadful complication arises in the peri-operative course, but delayed presentations have also been recorded[2,3]. Main contributing factors include antibody- or cell-mediated rejection, severe acute tubular necrosis, and renal vein thrombosis[4]. While transplant nephrectomy has been considered the default response for many years, there is now evidence that conservative approaches are feasible in selected clinical scenarios[5]. We herein describe a case of SGR in a sensitized deceased donor KT recipient. The rupture was successfully managed with external compression, application of a fibrin sealant, and tailored resorbable mesh wrapping.

CASE PRESENTATION

Chief complaints

A 37-year-old XY subject with end-stage renal disease secondary to bilateral cystic dysplasia was admitted to our center for a deceased donor KT in April 2023. The very early post-transplant course was uneventful, with excellent urinary output (> 2000 mL/day) and rapid amelioration of renal function (serum creatinine concentration, 2.3 mg/dL). Three days after the procedure, the patient reported a sudden-onset, sharp, left-sided abdominal pain, mainly located above the surgical incision and unresponsive to analgesics. There were no fluids flowing out from the drain placed in the surgical site and no signs of hemodynamic instability were detected.

History of present illness

The patient was hospitalized as a KT candidate. The kidney donor was a 50-year-old XY individual who had died from intra-cranial hemorrhage. The donor and recipient were blood group compatible and had six human leukocyte antigen mismatches. Pre-operative class-I and class-II panel reactive antibody tests were both 50%. Complement dependent cytotoxicity and flow cytometry assays were negative. Macroscopically, the kidney was normal and medium sized, with two arteries, one vein, and one ureter. It was extra-peritoneally transplanted into the left iliac fossa. The procedure was carried out smoothly, with neglectable blood loss, optimal graft reperfusion, and immediate urinary output. Cold and warm ischemia time were seven hours and 45 minutes, respectively. As induction, the patient received intravenous thymoglobulin 5/mg/kg total-dose and methylprednisolone 500 mg/day for three days. Maintenance immunosuppression consisted of oral lifecycle pharma-tacrolimus (0.15 mg/kg/day), mycophenolic acid 2000 mg/day, and prednisone 20 mg/day.

History of past illness

The comorbidities of the recipient included chronic kidney disease (bilateral cystic dysplasia) on renal replacement therapy (hemodialysis), systemic hypertension, secondary hyperparathyroidism, and previous KT failed due to Pseudomonas aeruginosa deep surgical site infection, further complicated by right external iliac arteritis, right external iliac vein thrombosis, and massive bleeding requiring multiple transfusions, graft nephrectomy, local debridement, and endovascular stenting.

Personal and family history

Besides the comorbidities, the personal and family history was unremarkable.

Physical examination

Physical examination upon admission did not identify any abnormal findings.

Laboratory examinations

Laboratory tests performed to assess the post-operative abdominal pain showed a substantial decrease in hemoglobin levels (9.6 g/dL).

Imaging examinations

After a brief bedside assessment with a Doppler ultrasound (US) scan (showing a well-perfused graft surrounded by a large retro-peritoneal fluid collection), the recipient underwent immediate contrast-enhanced computed tomography (CT) evaluation. The imaging study demonstrated a large (9.6 cm × 4.3 cm × 17 cm), retro-peritoneal hematoma (Figure 1A) with features of active bleeding from the upper pole of the transplanted kidney (Figure 1B). A focal laceration of the renal cortex not involving the calyceal system and a 3.8-cm-wide area of parenchymal hypoperfusion were noticed in proximity to the blushing spot (Figure 1C). Therefore, a plan was made for surgical exploration.

Figure 1 Urgent abdominal contrast-enhanced computed tomography scan. A: Large, retro-peritoneal hematoma (orange arrow); B: Rupture in the upper pole of the transplanted kidney (orange arrow); C: Area of parenchymal hypoperfusion just below the fracture (orange arrow).

FINAL DIAGNOSIS

Intra-operatively, we found a voluminous, partially organized, retro-peritoneal hematoma surrounding the graft, displacing the bladder, and tearing the fascia of the homolateral psoas muscle. Overall, the kidney appeared viable and well perfused, with a 3-cm-wide and 2-cm-deep laceration in the upper pole. There were no signs of leakage at the vascular or ureteral anastomotic sites. The renal vein was patent as much as the two renal arteries. Besides, we noticed a thrombotic occlusion of a superior branch of the main renal artery, likely determining the ischemic area detected by the CT scan.

TREATMENT

Relevant bleeding and oozing sources located in the surgical site were easily controlled using bi-polar electrocautery and topical hemostats. The parenchymal injury of the graft was managed as follows. The edges and the bottom of the laceration were covered and filled up with a fibrin sealant (Tisseel^®, Baxter International, Deerfield, Illinois). After that, we applied a gentle compression on the edges of the lesion. As shown in Figure 2, the surface of the kidney was sprinkled with a fibrin sealant and wrapped in a tailored polyglactin 910 knitted mesh (Vicryl^™ Knitted Mesh, Ethicon Inc., Raritan, New Jersey). The mesh was cut in the center and trimmed to let the renal vessels perfectly fit in the gap (Figure 3A). The extremities of the mesh were gradually tightened and tied together with multiple polydioxanone sutures (Figure 3B), avoiding vascular compression while achieving the desired hemostatic effect. The entire procedure took 245 minutes, with an estimated blood loss of 250 mL.

Figure 2  Intra-operative photograph showing the kidney graft covered by a fibrin sealant and wrapped with a tailored polyglactin 910 knitted mesh.

Figure 3 Intra-operative photographs. A: Tailored polyglactin 910 knitted mesh cut in the center and trimmed to let the renal graft vessels to perfectly fit in the gap; B: Extremities of the mesh tightened and tied together with absorbable polydioxanone sutures.

OUTCOME AND FOLLOW-UP

Following the operation, the patient was transferred to the ward with stable vital parameters, reassuring hemoglobin levels, normal urinary output, and excellent renal function. No further complications were recorded, and he was safely discharged from the hospital 14 days after the transplant. At 20 months of follow up, the recipient is doing very well, with a serum creatinine concentration of 1.17 mg/dL. As demonstrated by serial US scans of the surgical site, the polyglactin 910 mesh was gradually reabsorbed, disappearing within six months of implantation. Relevantly, we observed that the prosthetic device did not preclude the possibility of thoroughly evaluating the vascularization of the graft with doppler US techniques (Figure 4).

Figure 4 Serial post-operative ultrasound scans of the kidney graft showing progressive resorption of the polyglactin 910 knitted mesh. A: After seven days (white arrow); B: After three months (white arrow); C: After six months.

DISCUSSION

SGR, marked by an overt parenchymal laceration without pre-existing macroscopic evidence of tissue injury at the time of organ retrieval, benching, or transplantation, represents an uncommon yet potentially fatal surgical complication[1]. Reported incidence varies from 0.4% to 9.6%, depending on the series[6,7]. Rejection is currently recognized as the leading cause of atraumatic graft rupture. Less frequent etiologies include renal vein thrombosis, severe acute tubular necrosis, ischemic or hemorrhagic infarction of the renal cortex, ureteral obstruction with hydronephrosis, pyelonephritis, renal abscess, and neoplasms[2,8]. In our case, the rupture, located in the upper pole of the kidney, was likely caused (or perhaps favored) by the thrombotic event involving the superior branch of the main renal artery. To date, no specific donor- or recipient-related risk factors have been identified[3,9]. However, it has been shown that delayed graft function (defined as the need for dialysis within seven days of transplant) is associated with a substantial increase in the risk of rupture (unadjusted risk ratio, 3.0, 95% confidence interval 2.4-3.8; P < 0.001)[3].

As herein reported, SGR mostly occurs within the first two post-transplant weeks, but later cases have been recorded[4,10]. Common clinical features are sudden-onset abdominal pain with possible irradiation to the lumbar region, sweating, reduced urinary output, tachycardia, hypotension, and hemorrhagic shock[5]. US scan certainly represents the preferred first-line imaging modality for the evaluation of the transplanted kidney. Nevertheless, in the emergency setting, contrast-enhanced CT scan remains the gold standard technique[11]. Typical radiological findings include kidney enlargement, cortical oedema, parenchymal disruption, active pooling of contrast material within or around the graft, and hematoma-like fluid collections located in the retro-peritoneal space.

Prompt diagnosis and aggressive fluid resuscitation represent key factors for optimized recipient management. While immediate transplant nephrectomy was once considered the preferred strategy for SGR, recent evidence supports a more conservative approach, showing excellent salvage rates and long-term graft survivals. According to our literature review (Table 1), from 1973 to 2024, 383 cases of SGR have been reported, with 163 immediate transplant nephrectomies and 220 surgical repairs. Among the latter, 34 attempts eventually failed, leading to a concerning overall record of 197 graft losses and 13 deaths. However, sorting the cases of SGR for publication era (1973-1990, 1991-2010, and 2011-2024), it can be noticed that, over the last 50 years, there has been a paradigm shift in the treatment of SGR, as much as a substantial improvement in repair-related outcomes (Figure 5). Indeed, with all the due limitations of a merely descriptive analysis performed on summaries based on individual cases, comparing overall graft losses (immediate graft nephrectomies plus graft nephrectomies following failed repairs) between the three publication eras, we can observe a striking difference in the relative number of successful graft salvages: 36/115 (1973-1990) vs 116/230 (1991-2010) vs 34/38 (2011-2024). Therefore, in current clinical practice, it appears as first-line graft nephrectomy can be justified only by refractory hemodynamic instability, disseminated intravascular coagulation, irreversible rejection, or complex graft injuries with very limited chances of recovery. The graft salvage attempt should be also guided by the specific characteristics of the recipient, including age, comorbidities, and future transplant options. Relevantly, the latest reports show that recurrent rupture, the most dreadful complication of attempted graft repair, occurs in less than 10% of the patients and does not compromise the prognosis.

Figure 5  Flow diagrams summarizing and comparing the main outcomes of the episodes of spontaneous kidney graft rupture reported in the literature and sorted in different publication eras: 1973-1990, 1991-2010, and 2011-2024.

Table 1 Case reports and case series describing episodes of spontaneous kidney graft rupture published between 1973 and 2024.

Ref.	SGR/KT (n)	P.O. day (range)	Follow up (months)	Graftectomy	Repair	Repair technique	Graft salvage	Death
Lord et al[1], 1973	1/280	14	< 1	1	0	-	-	1
Ghose et al[20], 1973	6/71	-	-	3	3	Porcine skin gelatin + sutures	3	0
Fjeldborg et al[21], 1974	7/200	-	-	4	3	-	1	2
Libertino et al[22], 1974	1/-	1	32	1	0	-	-	0
Anderson et al[23], 1976	1/-	5	9	0	1	Autogenous musculofascial tissue + sutures	1	0
Van Cangh et al[24], 1977	9/325	-	-	6	3	Autogenous fat bolster + sutures	0	0
Brekke et al[12], 1978	16/448	-	-	10	6	Direct sutures	1	0
Goldman et al[25], 1978	1/-	8	1	1	0	-	-	0
Susan et al[26], 1978	4/474	5-16	15	0	4	Oxidized cellulose + sutures	2	0
Prompt et al[27], 1979	8/327	2-11	< 1	6	2	-	0	0
Dryburgh et al[6], 1979	9/93	1-18	22	7	2	-	1	2
van der Vliet et al[28], 1980	1/211	-	-	1	0	-	-	0
Goldman et al[29], 1982	7/350	3-7	58	3	4	-	4	0
Thukral et al[13], 1982	3/100	6-8	60	0	3	Direct sutures or direct sutures + oxcel mesh	3	0
Ajao et al[2], 1984	1/-	1475	1	1	0	-	-	1
Yadav et al[30], 1985	11/152	7-14	30	3	8	Porcine skin gelatin + sutures	8	3
Serrallach et al[31], 1985	5/66	4-10	15	0	5	Compression + lyophilized human dura	5	0
Schwartz et al[32], 1986	5/80	5-17	-	4	1	-	0	1
Chopin et al[33], 1989	4/85	5-32	12	0	4	Synthetic glue + polyglactin 910 mesh	3	0
Richardson et al[34], 1990	15/791	3-14	72	9	6	Topical hemostatic agent + sutures	4	1
Odocha et al[35], 1991	1/-	5	-	1	0	-	-	0
Robertson et al[36], 1992	6/384	4-38	43	0	6	Oxidized cellulose + sutures	6	0
Rosario et al[37], 1993	3/571	2-4	-	0	3	Polyglycolic acid mesh	3	0
Yadav et al[38], 1994	15/237	-	120	4	11	Gelatin matrix + sutures	11	-
Said et al[39], 1994	3/75	4-11	10	2	1	Oxidized cellulose + sutures	1	0
Heimbach et al[18], 1995	8/238	8-17	94	1	7	Fibrin sealant + collagen foam + polyglactin 910 mesh	7	0
Guleria et al[17], 1995	1/-	5	-	0	1	-	1	0
Azar et al[3], 1996	12/331	4-21	-	12	0	-	-	1
Zadrozny et al [40], 1997	8/112	-	-	2	6	Fibrin sealant + polyester mesh or cyanoacrylate + polyester mesh or gelatin matrix + sutures	3	0
Pontones Moreno et al[41], 1998	21/868	-	-	4	16	Lyophilized human dura or autogenous fascia lata or lyophilized human dura + autogenous fascia lata or polyglycolic acid mesh	16	0
Szenohradszky et al[42], 1999	53/628	-	-	37	16	-	16	-
Chan et al[43], 1999	1/-	5	1	0	1	Collagen sheets coated with hemostats	1	0
Philipneri et al[44], 2000	1/-	7	< 1	0	1	-	1	0
Ramos et al[45], 2000	11/934	2-13	-	10	1	Fibrin sealant + collagen foam	1	0
Millwala et al[46], 2000	4/145	-	6	2	2	Porcine skin gelatine + polyglycolic acid mesh or collagen foam + fibrin sealant + lyophilized human dura	2	1
Ahmed et al[8], 2001	1/-	1099	3	0	0	-	-	0
Hochleitner et al[4], 2001	14/1811	3-23	111	5	9	Direct sutures or fibrin sealant + infrared and/or laser coagulation or absorbable mesh	9	0
Zakir et al[10], 2003	1/-	644	< 1	1	0	-	-	0
Guleria et al[47], 2003	3/172	5-7	-	0	3	Autogenous muscle patch (transversus abdominis/internal oblique muscle)	3	0
He et al[48], 2003	38/1000	-	60	2	31	Sutures + external oblique aponeurosis pledgets	29	0
Sanchez de la Nieta et al[9], 2004	10/657	1-10	-	5	5	Direct sutures or Polyglycolic acid mesh	3	0
Busi et al[49], 2004	4/778	4-13	< 1	3	1	-	1	0
Shahrokh et al[7], 2005	6/1682	4-13	60	3	3	Autogenous fat bolster + sutures or oxidized cellulose + sutures	2	0
Basaran et al[50], 2009	5/1379	6-32	-	5	0	-	-	-
Askandarani et al[51], 2011	1/-	1950	-	1	0	-	-	-
McCausland et al[52], 2011	1/-	11	7	0	1	Human thrombin and animal gelatin + fibrin sealant	1	0
Han et al[15], 2012	26/1851	-	78	0	26	Autogenous fat bolster + resorbable bundle or autogenous muscle patch + resorbable bundle or sutures + autologous cubic muscle pledgets or sutures + external oblique aponeurosis pledgets	26	0
Lai et al[53], 2014	1/-	9	24	0	1	Oxidized cellulose + sutures + hem-o-lok	1	0
Sin et al[54], 2014	1/-	20	-	1	0	-	-	0
Almarastani et al[55], 2014	1/-	4	1	0	1	Human fibrinogen and thrombin + bovine albumin-glutaraldehyde	1	0
Favi et al[5], 2015	1/-	4	96	0	1	Human thrombin and animal gelatin + polyglactin 910 mesh	1	0
Ray et al[56], 2017	1/-	6	< 1	0	1	Human fibrinogen and thrombin + sutures + hem-o-lok	1	0
Ko et al[57], 2019	1/-	6	20	0	1	Human thrombin and animal gelatin + oxidized cellulose	1	0
Fazeli et al[58], 2021	1/-	5	< 1	0	1	Sutures + fat bolster	1	0
Montali et al[59], 2022	1/-	14	2	1	0	-	-	0
Godara et al[60], 2022	1/-	7	-	-	1	Sutures + oxidized cellulose	1	0
Konopa et al[61], 2024	1/-	4	30	1	0	-	-	0

SGR: Spontaneous graft rupture; KT: Kidney transplant; P.O.: Post-operative day.

In this specific case, we opted for graft repair for the following reasons: (1) The quality of the kidney was above average; (2) Considering the past surgical history of the patient and the previous immunization, the chances of receiving another transplant were relatively low; (3) The recipient was young, fit (no diabetes mellitus, no cardiac conditions, no autoimmune disorders), hemodynamically stable, and with no signs of coagulopathy at the time of the second operation; (4) As shown by the contrast-enhanced CT scan performed before surgery, the laceration was in the upper pole of the graft, with a neglectable risk of post-operative ureteral ischemia or necrosis; (5) The imaging study demonstrated that the rupture was superficial (limited to the renal cortex), without involvement of the calyceal system (minimal risk of post-operative urinary leakage); (6) Intra-operatively, the kidney appeared viable and well perfused, with no signs of vascular thrombosis or ureteral leakage; (7) As suggested by the CT scan (area of parenchymal hypoperfusion close to the bleeding spot), and in line with the intra-operative findings (thrombotic occlusion of a small superior branch of the main renal artery), the rupture did not recognize an immunological cause (severe rejection episode or thrombotic microangiopathy) possibly jeopardizing long-term graft survival or function; (8) All bleeding and oozing sources in the surgical site were easily controlled using bi-polar electrocautery and topical hemostats; (9) The hemorrhage caused by the laceration stopped short after the application of the fibrin sealant and external compression; and (10) During the wrapping maneuver with the polyglactin 910 mesh, there were no signs of recurrent bleeding from the ruptured area of the kidney.

Graft repair techniques have also evolved over time (Table 1). In the past, direct suturing of the ruptured edges of the transplanted kidney was common practice[12,13]. Nowadays, most surgeons prefer avoiding unnecessary manipulation of the graft, opting for the primary use of topical hemostatic agents or sealants[5], such as oxidized regenerated cellulose, absorbable gelatin matrix, microfibrillar collagen, microporous polysaccharide spheres, topical thrombin, fibrin sealant, human thrombin plus animal gelatin, bovine albumin-glutaraldehyde tissue adhesive, and dual polyethylene glycol[14]. As a matter of fact, it has been demonstrated that suture-free repairs are easier, faster, and less traumatic than traditional suture-based techniques, with reduced peri-operative blood loss[15]. Since the graft of our patient was frankly edematous and extremely fragile, in line with current trends, we decided to apply a fibrin sealant at the base of the rupture and over the damaged margins of the graft. To generate and maintain an external compression, we also wrapped the kidney with a polyglactin 910 knitted mesh, anchored to the surface of the organ with a fibrin sealant, and progressively tightened with interrupted resorbable sutures (Supplementary material). Indeed, renal corsetage offers several additional advantages as it supports hemostasis and reduces the risk of further laceration[16]. Reported options include human tissues such as external oblique aponeurosis, fascia lata, and lyophilized dura or synthetic devices like polypropylene, polyglycolic acid, and polyglactin meshes[15,17]. We believe that a polyglactin 910 knitted mesh represents the optimal choice because it is readily available, cheap, flexible, resistant, non-antigenic, non-pyrogenic, and completely resorbable within three to six months of use. Furthermore, compared to non-absorbable synthetic materials, polyglactin 910 entails a reduced risk of infection and it is associated with less scarring[5,18]. These characteristics are particularly relevant in the setting of renal graft repair as transplant patients are more susceptible to infectious complications than the general population[19], are routinely followed up with US scans or graft biopsies and may require further surgical procedures in the long term.

CONCLUSION

SGR represents a serious complication of KT. Most cases occur in the peri-operative course and usually present with abdominal pain and hemorrhagic shock. Contrast enhanced CT scan is the gold standard diagnostic modality. Aggressive resuscitation and prompt surgical exploration are key factors for optimized recipient and graft outcomes. For many years, graft nephrectomy has been considered the default treatment. However, current literature supports first-line salvage attempts. As confirmed by our experience, suture-free surgical techniques offer an easy and reproducible repair option, with excellent results and no impact on post-transplant long-term management.

ACKNOWLEDGEMENTS

We thank Cesina Tamburri for logistical support.