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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 1  |  Page : 118-122
Severe renal failure in acute bacterial pyelonephritis: Do not forget corticosteroids

Department of Nephrology, AP-HP, Hopital Necker, Universite Paris V, Paris, France

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Date of Web Publication8-Jan-2010


Acute renal failure (ARF) is a rare complication of acute pyelonephritis in adult immunocompetent patients. Recovery of renal function usually occurs if antibiotics are promptly initiated. However, long-term consequences of renal scarring due to acute pyelonephritis are probably underestimated, and some patients present with prolonged renal failure despite adequate antibiotic therapy. We report two cases of severe ARF complicating bacterial pyelonephritis successfully treated with corticosteroids in association with conventional antibiotics.

How to cite this article:
Sqalli TH, Hamzaoui H, Guiard E, Noel LH, Fakhouri F. Severe renal failure in acute bacterial pyelonephritis: Do not forget corticosteroids. Saudi J Kidney Dis Transpl 2010;21:118-22

How to cite this URL:
Sqalli TH, Hamzaoui H, Guiard E, Noel LH, Fakhouri F. Severe renal failure in acute bacterial pyelonephritis: Do not forget corticosteroids. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2021 Aug 3];21:118-22. Available from: https://www.sjkdt.org/text.asp?2010/21/1/118/58785

   Introduction Top

Pyelonephritis is an ascending urinary tract infection that has reached the pelvis of the kidney. If infection is severe, the term "uro­sepsis" is used interchangeably.

The incidence of acute renal failure (ARF) as a direct consequence of acute pyelonephritis remains unknown. [1],[2],[3],[4] However, it is probably a rare complication of acute pyelonephritis as fewer than twenty cases have been reported in immunocompetent patients. Long-term compli­cations include post-pyelonephritic renal sca­rring despite antibiotic therapy.

We report two cases of severe ARF compli­cating bacterial pyelonephritis and successfully treated with corticosteroids and conventional antibiotics.

   Case Reports Top

Case 1

A 63-year-old man without any significant past medical history was admitted to our hos­pital with a two day history of nausea, and fatigue. He also reported dysuria, flank pain, and fever.

On physical examination the patient was in no acute distress with an initial blood pressure of 159/85 mmHg, a weight of 74 kg, a pulse of 72 beats/min, and a temperature of 38.4°C. Except for mild pitting edema of the lower limbs, physical examination was unremarkable.

The laboratory investigations revealed urea nitrogen level 186.7 mg/dL (31 mmol/L), crea­tinine 15.9 mg/dL (1414 μmol/L), sodium 141 mmol/L, potassium 4.1 mmol/L, bicarbonate 25 mmol/L, calcium 8.2 mg/dL (2.1 mmol/L), phos­phate 9.4 mg/dL (2.9 mmol/L), C-reactive pro­tein 135 mg/L, white blood cell count 6.4 Χ 103/μL (6.4 Χ 109 /L), hemoglobin 7.6 g/dL (76 g/L), and the platelet count was 400 Χ 103/μL (400 Χ 109/L). Urinalysis was positive for protein (1.28 g/L), blood (80/μL), and leukocytes (125/μL). Complement titers were normal and anti-streptolysin O titer (ASO), ANCA, ANA, and hepatitis B and C and HIV antibody serologies were negative. The patient required hemodialysis upon admission to the hospital.

Computed tomography (CT) scan showed an increased size of both kidneys (right kidney: 15 cm; left kidney: 16 cm) with the existence of bilateral multifocal abscesses. No stones or masses were seen. Urine and blood cultures were positive for  Escherichia More Details coli sensitive to fluoroquinolones and cephalosporins, and the patient was treated with ceftriaxon for 15 days followed by a four-week course of ciproflo­xacin. Despite adequate antibiotic therapy, there was no improvement in renal function. At that time, urine culture was negative and C-reactive protein had dropped to 15 mg/L.

A kidney biopsy was performed on day 21 of admission. On light microscopy, the examina­tion of the renal biopsy specimen revealed 10 morphologically normal glomeruli without evi­dence of proliferation or sclerosis. The peri­pheral capillary basement membranes were within normal limits. The interstitium contained diffuse and intense inflammatory infiltrate com­posed of neutrophils, lymphocytes and plasma cells [Figure 1]. The predominant cells were neutrophils. Some areas of interstitial fibrosis were observed using Masson trichome stain in addition to tubular atrophy. The arteriolar struc­tures were within normal limits. The immuno­fluorescence microscopy study was negative.

By week five of hospitalization, the patient was afebrile with sterile urine and normalized inflammatory parameters. Nevertheless, he was still dialysis-dependant, and steroid therapy (pred­nisolone ΍ mg/kg/day) was started and gra­dually tapered over four weeks. Dialysis was stopped ten days after steroid therapy and the serum creatinine level decreased to 3.7 mg/dL (329 μmol/L) by the third week [Figure 2]. After discharge from the hospital, the patient was subsequently lost to follow-up.

Case 2

An 83-year-old woman was referred to our hospital with a 24-hour history of renal colic, anuria and fever. Her past medical history included a right renal autotransplantation for idiopathic retroperitoneal fibrosis. She also ex­perienced a left nephrectomy four years ago for recurrent pyelonephritis. Six months prior to admission, her serum creatinine level was 1.6 mg/dL (142μmol/L). The patient denied the use of any nonsteroidal anti-inflammatory drugs use.

Her blood pressure was 160/77 mmHg, pulse 67 beats/min, and temperature 38.6°C. The re­mainders of the physical examination findings were unremarkable.

On admission, the laboratory investigations showed a blood urea nitrogen 163 mg/dL (27 mmol/L), creatinine 5.3 mg/dL (474 μmol/L), calcium 7.8 mg/dL (1.95 mmol/L), serum phos­phate 5.5 mg/dL (1.77 mmol/L), C-reactive pro­tein 122 mg/L, white blood cell count 7.4 Χ 103/μL (15.7 Χ 109/L), hemoglobin 10 g/dL (100 g/L), and platelet count of 189 Χ 103/μL (189 Χ 109/L).

Ultrasonography showed a uniquely enlarged kidney with mildly dilated cavities. The patient underwent urgent J-J stent placement. After urine was drawn for culture, intravenous Oflo­xacin was empirically administered. Urine cul­ture revealed Proteus mirabilis.

After 10 days of antibiotics, the urine culture became negative and CRP dropped to 14 mg/L. However, the renal function worsened. A deci­sion was made to empirically administer corti­costeroids [Figure 3]. Administration of 25 mg per day of oral prednisolone dramatically im­proved her clinical condition and serum creati­nine level decreased to 2.0 mg/dL (180 μmol/L) 10 days later. Six months later, the patient's serum creatinine decreased to 1.8 mg/dL.

   Discussion Top

Acute renal impairment in the setting of acute pyelonephritis is often associated with preg­nancy, solitary kidney, indwelling catheter, im­munocompromised status or use of nonsteroi­dal anti-inflammatory drugs. [5],[6] The kidneys are usually swollen by an interstitial infiltrate and edema, and white cell tubular casts and micro­abscesses may be present. Recovery of renal function usually occurs if antibiotics are prompt­ly instituted. However, some patients present with prolonged ARF despite adequate antibio­tic therapy. Moreover, long-term consequences of renal scarring due to acute pyelonephritis are probably underestimated. For instance, in renal allograft recipients, acute allograft injury secondary to urinary tract infection has been reported and acute pyelonephritis may be asso­ciated with an enduring decrease in renal graft function. [7],[8]

Ultrasonographic and microscopic findings suggest that inflammatory infiltrate plays a major role in the onset of ARF secondary to pyelonephritis. [9] Local and systemic cytokine expression profiles during acute pyelonephritis and after urethral obstruction have been studied in several animal models. Of particular interest was the marked kidney cell expression of mRNA for TGF-beta, presumed to be important both for obstructive and post-infectious renal scarring. [10] Thus, if one could successfully mo­dulate the inflammatory response then post­pyelonephritic renal scarring might be lessened.

In our two reported cases of severe ARF complicating bacterial pyelonephritis, we suc­cessfully treated the inflammation with corti­costeroids in association with conventional an­tibiotics. In both cases, renal function did not recover after appropriate antibiotic therapy des­pite a negative urine culture and a dramatic improvement in inflammatory parameters. Fol­lowing steroid treatment, the renal function improved remarkably.

Few studies have investigated the use of ad­junctive glucocorticoids in the treatment of acute pyelonephritis. Furthermore, the antimic­robial agent is believed to be effective only in eliminating bacteria, not in preventing scar for­mation. In animal models, steroids added to antibiotic therapy accelerate the clearance of inflammatory infiltrates and decrease renal scar formation resulting from pyelonephritis in ani­mals even when treatment is delayed. [11],[12],[13] Using a piglet model of reflux and acute experimen­tal pyelonephritis, Pohl and al investigated the efficacy of antibiotics combined with cortico­steroid in diminishing post-pyelonephritic renal scarring compared to standard antibiotic the­rapy. [11] They demonstrated that the risk of renal scarring is greatest after severe acute pyelo­nephritis involving greater than 66% of a renal zone. Adjunctive oral prednisolone appears to be effective in diminishing renal scarring in severely affected kidneys. However, in kidneys with mild and moderate acute pyelonephritis antibiotics alone appear to be equally effective in preventing scarring. [11]

Recovery of acute pyelonephritis-associated ARF with the use of antibiotics and steroids combination in adults has not been previously documented in the literature. Given the present cases, however, this approach should be con­sidered if ARF due to pyelonephritis that does not rapidly improve upon antibiotic therapy.

   References Top

1.Greenhill AH, Norma ME, Cornfeld D, et al. Acute renal failure secondary to acute pyelo­nephritis. Clin Nephrol 1977;8:400-3.  Back to cited text no. 1      
2.Olsson PJ, Black JR, Gaffney E, et al. Rever­sible acute renal failure secondary to acute pye­lonephritis. South Med J 1980;73:374-6.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Thompson C, Verani R, Evanoff G, et al. Sup­purative bacterial pyelonephritis as a cause of reversible acute renal failure. Am J Kidney Dis 1986;8:271-3.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Nunez JE, Perez E, Gunasekaran S, et al. Acute renal failure secondary to acute bacterial pye­lonephritis. Nephron 1991;62:240-1.  Back to cited text no. 4      
5.Nahar A, Akom M, Hanes D, Briglia A, Drachenberg CB, Weinman EJ. Pyelonephritis and acute renal failure. Am J Med Sci 2004; 328(2):121-3.  Back to cited text no. 5      
6.Jones SR. Acute renal failure in adults with uncomplicated acute pyelonephritis: Case re­ports and review. Clin Infect Dis 1992;14:243­-6.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Pelle G, Vimont S, Levy PP, et al. Acute pyelo­nephritis represents a risk factor impairing long­term kidney graft function. Am J Transplant 2007;7(4):899-907.  Back to cited text no. 7      
8.Rice JC, Peng T, Kuo YF, et al. Renal allograft injury is associated with urinary tract infection caused by Escherichia coli bearing adherence factors. Am J Transplant 2006;6(10):2375-83.  Back to cited text no. 8      
9.Kooman JP, Barendregt JN, van der Sande FM, van Suylen RJ. Acute pyelonephritis: A cause of acute renal failure? Neth J Med 2000; 57(5):185-9.  Back to cited text no. 9      
10.Khalil A, Brauner A, Bakhiet M, et al. Cyto­kine gene expression during experimental Esche­richia coli pyelonephritis in mice. J Urol 1997; 158(4):1576-80.  Back to cited text no. 10      
11.Pohl HG, Rushton HG, Park JS, Chandra R, Majd M. Adjunctive oral corticosteroids re­duce renal scarring: The piglet model of reflux and acute experimental pyelonephritis. J Urol 1999;162(3 Pt 1):815-20.  Back to cited text no. 11      
12.Haraoka M, Matsumoto T, Takahashi K, Kubo S, Tanaka M, Kumazawa J. Suppression of renal scarring by prednisolone combined with ciprofloxacin in ascending pyelonephritis in rats. J Urol 1994;151(4):1078-80.  Back to cited text no. 12      
13.Haraoka M, Matsumoto T, Mizunoe Y, et al. Effect of prednisolone on renal scarring in rats following infection with Serratia marcescens. Ren Fail 1993;15(5):567-71.  Back to cited text no. 13      

Correspondence Address:
Tarik Houssaini Sqalli
Lotissement Oulladia II, No B13 Km 8, Souissi, Rabat, Morocco

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PMID: 20061705

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