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Year : 2018  |  Volume : 12  |  Issue : 1  |  Page : 59-61

Emphysematous pyelonephritis in a renal allograft

Department of Nephrology and Renal Transplantation, Asian Institute of Nephrology and Urology, Hyderabad, Telangana, India

Date of Web Publication29-Mar-2018

Correspondence Address:
Dr. Praveen Kumar Etta
Asian Institute of Nephrology and Urology, Hyderabad - 500 082, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_66_17

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Emphysematous pyelonephritis (EPN) is a rare gas forming, necrotizing infection of the renal parenchyma. It is potentially lethal, if not recognized and treated promptly. EPN-affecting renal allografts has been reported infrequently. We report a case of 34-year-old male renal allograft recipient presented with urosepsis and acute graft dysfunction, found to have EPN. He was treated conservatively with antibiotics and ureteral stenting along with reduction of immunosuppression, with complete recovery.

Keywords: Emphysematous pyelonephritis, renal allograft, urosepsis

How to cite this article:
Etta PK, Rao M V. Emphysematous pyelonephritis in a renal allograft. Indian J Transplant 2018;12:59-61

How to cite this URL:
Etta PK, Rao M V. Emphysematous pyelonephritis in a renal allograft. Indian J Transplant [serial online] 2018 [cited 2022 Aug 14];12:59-61. Available from: https://www.ijtonline.in/text.asp?2018/12/1/59/228932

  Introduction Top

Emphysematous pyelonephritis (EPN) is an acute, severe necrotizing infection of the renal parenchyma, caused by gas producing microbes. Most of the EPN cases reported in literature belong to infection of the native kidneys. EPN in renal allograft recipients is rarely reported. Till now, only 29 cases of EPN-affecting renal allografts have been reported in literature globally. The clinical course of EPN can be severe and life-threatening if not managed aggressively. We report herein a case of 34-year-old man, live-related renal allograft recipient with normal graft function, diagnosed to have EPN with acute graft dysfunction, successfully treated with conservative approach.

  Case Report Top

A 34-year-old man, hypertensive for the past 5 years, presented 18 months following live donor renal transplantation with high-grade fever, dysuria, nausea and anorexia. He had no history of urinary catheterization or instrumentation. His native kidney disease was presumed as chronic interstitial nephritis. He did not receive induction and was continuing triple drug immunosuppression, with normal graft function. He was diagnosed with posttransplant diabetes mellitus at 6 months after transplantation and was started on oral hypoglycemic agents with good glycemic control. He was under regular follow-up with no other complications following transplantation. His trough level of tacrolimus was optimal. On examination, he was febrile with tachycardia, low normal blood pressure (118/78 mmHg), and tenderness over graft site. The rest of the systemic examination was unremarkable.

The laboratory findings revealed hemoglobin of 10.0 g/dl, total leukocyte count of 16,000/mm 3, blood sugar of 250 mg/dl, and serum creatinine of 3.2 mg/dl. His urine examination showed trace albumin, 4–6 erythrocytes/hpf and 8–10 pus cells/hpf. Ultrasonography and Doppler revealed multiple echogenic areas in the graft kidney with dirty shadowing, with no perigraft collection. Computed tomography (CT) imaging confirmed the presence of multiple air pockets in the graft parenchyma and pelvicalyceal system with prominent calyces [Figure 1]. Urine culture revealed significant growth of Escherichia coli.
Figure 1: Noncontrast computed tomography showing gas pockets in graft kidney (arrows)

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He was immediately started on broad spectrum antibiotics, later modified after culture and sensitivity report. His immunosuppression was reduced. As he was in severe sepsis, a double J (DJ) ureteral stent was placed in the graft kidney. Over the next 2 weeks, his graft function recovered to baseline creatinine of 0.9 mg/dl and DJ stent was removed after 3 weeks from insertion. The patient remained asymptomatic at 3 months of follow-up after discharge.

  Discussion Top

EPN is a fulminant, necrotizing, and life-threatening infection that results in the formation of gas in renal parenchyma, collecting system, or perinephric tissues.[1],[2] Various terms such as renal emphysema, pneumonephritis have been used in the past; however, EPN was suggested as the preferred term.[3] Gram-negative, facultative anaerobic bacteria such as E. coli and Klebsiella pneumoniae are the most common isolates associated with EPN. Other pathogens include P. aeruginosa, Proteus mirabilis, Enterobacter, Group D Streptococcus, coagulase negative Staphylococcus, Clostridium, and Candida. The microorganisms in presence of high levels of tissue glucose, impaired immune system, and poor vascular supply are responsible for the production of gas (carbon dioxide and hydrogen) through the fermentation of glucose and lactate.[4],[5] The common predisposing factors include uncontrolled diabetes mellitus (up to 90% of cases), urinary tract obstruction due to calculi, stricture, sloughed papillae, pelviureteric junction obstruction or malignancy, immunosuppressive state, neurogenic bladder, and anatomic anomaly of urinary tract. There is a preponderance of EPN in females; but in renal transplant patients, majority of the cases are reported in males.

EPN usually affects native kidneys. It may present as uncomplicated pyelonephritis with fever, dysuria, flank pain, and loin tenderness; but usually, it is much more aggressive with high morbidity and mortality. EPN-affecting renal allografts is very rare. In transplant recipients, presentation may be subclinical and covert due to immunosuppressive state and denervated graft. Pathogenetically, it is different from EPN of native kidneys due to anatomic differences in urinary tract such as surgical anastomosis between transplant ureter and urinary bladder and lack of barrier of Gerota's fascia, immunocompromised state, denervated graft and being a solitary functioning kidney.

CT imaging is a gold standard for diagnosis. Based on radiological findings, several classification systems for EPN of native kidneys were proposed, for prognostication and to guide therapy.[4],[5] All cases of EPN-affecting renal allograft would be considered class 4 as per Huang and Tseng classification, given the infection in solitary functioning graft kidney [Table 1]. Hence, a group of authors proposed a modified staging system for EPN in renal allograft.[6] Different management strategies have been proposed based on the stage of EPN in graft kidney [Figure 2].
Table 1: Commonly used classification systems of emphysematous pyelonephritis

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Figure 2: Management algorithm for emphysematous pyelonephritis in renal allograft.[6],[7] ¶Staging as described by Al-Geizawi et al. EPN: Emphysematous pyelonephritis, CT: Computed tomography, PCD: Percutaneous catheter drainage, MM: Medical management.

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Till date, to the best of our knowledge, only 29 cases of EPN-affecting renal allografts have been reported in English-language literature. This may be due to underdiagnosis also. In a literature review of 23 cases of EPN in transplant patients, 83% had diabetes mellitus. The disease manifested within the period from 2 weeks to 15 years after transplantation. E. coli was isolated in 56% and Klebsiella pneumoniae in 22% of patients. Totally 12 of the 23 patients underwent graft nephrectomy, and seven were treated with percutaneous catheter drainage (PCD). The remaining four patients received antibiotic therapy alone. Three patients died, and all of them underwent graft nephrectomy.[7] Among the remaining six patients who were reported recently, two received antibiotics alone, one was treated with PCD, and the remaining three underwent nephrectomy. Two patients died, among them one received antibiotics alone, and another underwent nephrectomy.[8],[9],[10],[11],[12],[13]

Poor prognostic factors include altered consciousness, shock, renal failure, thrombocytopenia, disseminated intravascular coagulation, vascular thrombosis, and type I and class 4 EPN based on Wan et al. and Huang and Tseng classifications, respectively. The management of EPN has been a subject of controversy; emergency nephrectomy was traditionally considered the treatment of choice. EPN was associated with a very high mortality rate (up to 75%) until three decades ago, primarily attributable to septic complications. Over the last two decades, with early diagnosis and improvement in management techniques, mortality rates have been reduced to <15%, and there has been a gradual shift toward nephron-sparing approaches such as PCD, percutaneous nephrostomy, and DJ stenting. Medical management includes early initiation of parenteral antibiotics, optimization of hemodynamic status, glycemic control, correction of fluid, and acid-base and electrolyte imbalance. Recent meta-analyses showed that medical management with PCD had the lowest mortality compared to medical management alone or emergency nephrectomy.[14],[15] Conservative approach with antibiotics ± intervention has thus become the standard of care in most of the cases, and nephrectomy is considered the last resort. Urinary tract obstruction, if present should always be relieved irrespective of severity of illness.

There is a paucity of literature regarding EPN in transplant patients. It can be associated with higher mortality, graft loss, and permanent dialysis. Majority of the reported cases have undergone graft nephrectomy. Optimal role and timing of nephrectomy is still not clear. However, it is wise to treat by a more conservative approach as far as possible aimed toward graft preservation. High degree of suspicion, prompt diagnosis, and early administration of antibiotics ± nephron-sparing intervention with serial follow-up imaging will help in greater preservation of renal allografts, even in severe grades of the disease. Reduction of immunosuppression is required in most of the cases. Further studies are required to establish treatment guidelines in this group of patients.

In our case of EPN in renal allograft, the patient presented with severe sepsis and acute graft dysfunction. He was managed conservatively with antibiotics, reduction of immunosuppression, and urinary tract stenting with subsequent complete cure, including recovery of graft function.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Michaeli J, Mogle P, Perlberg S, Heiman S, Caine M. Emphysematous pyelonephritis. J Urol 1984;131:203-8.  Back to cited text no. 1
Pontin AR, Barnes RD, Joffe J, Kahn D. Emphysematous pyelonephritis in diabetic patients. Br J Urol 1995;75:71-4.  Back to cited text no. 2
Schultz EH Jr., Klorfein EH. Emphysematous pyelonephritis. J Urol 1962;87:762-6.  Back to cited text no. 3
Wan YL, Lee TY, Bullard MJ, Tsai CC. Acute gas-producing bacterial renal infection: Correlation between imaging findings and clinical outcome. Radiology 1996;198:433-8.  Back to cited text no. 4
Huang JJ, Tseng CC. Emphysematous pyelonephritis: Clinicoradiological classification, management, prognosis, and pathogenesis. Arch Intern Med 2000;160:797-805.  Back to cited text no. 5
Al-Geizawi SM, Farney AC, Rogers J, Assimos D, Requarth JA, Doares W, et al. Renal allograft failure due to emphysematous pyelonephritis: Successful non-operative management and proposed new classification scheme based on literature review. Transpl Infect Dis 2010;12:543-50.  Back to cited text no. 6
Agreda Castañeda F, Lorente D, Trilla Herrera E, Gasanz Serrano C, Servian Vives P, Iztueta Saavedra I, et al. Extensive emphysematous pyelonephritis in a renal allograft: Case report and review of literature. Transpl Infect Dis 2014;16:642-7.  Back to cited text no. 7
Piracha KJ, Darras F, Nord EP, Wadhwa NK. Emphysematous pyelonephritis in a renal transplant patient. Open J Nephrol 2014;4:86-91.  Back to cited text no. 8
Tienza A, Hevia M, Merino I, Velis JM, Algarra R, Pascual JI, et al. Case of emphysematous pyelonephritis in kidney allograft: Conservative treatment. Can Urol Assoc J 2014;8:E256-9.  Back to cited text no. 9
Alhajjaj FS, Pasha F. Emphysematous pyelonephritis in renal allograft – A case report. Int J Health Sci (Qassim) 2016;10:311-3.  Back to cited text no. 10
Narcisse D, Agarwal M, Hancock M, Wells D, Sands C. A rare case of emphysematous pyelonephritis in a renal transplant patient. Ther Adv Infect Dis 2016;3:141-4.  Back to cited text no. 11
Oliveira CC, Garcia PD, Viero RM. Emphysematous pyelonephritis in a transplanted kidney. Autops Case Rep 2016;6:41-7.  Back to cited text no. 12
Crouter AJ, Abraham MK, Wilkerson RG. Emphysematous pyelonephritis in a renal allograft. Am J Emerg Med 2017;35:520.e1-0.  Back to cited text no. 13
Somani BK, Nabi G, Thorpe P, Hussey J, Cook J, N'Dow J, et al. Is percutaneous drainage the new gold standard in the management of emphysematous pyelonephritis? Evidence from a systematic review. J Urol 2008;179:1844-9.  Back to cited text no. 14
Aboumarzouk OM, Hughes O, Narahari K, Coulthard R, Kynaston H, Chlosta P, et al. Emphysematous pyelonephritis: Time for a management plan with an evidence-based approach. Arab J Urol 2014;12:106-15.  Back to cited text no. 15


  [Figure 1], [Figure 2]

  [Table 1]

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