Int Urol Nephrol (2011) 43:925–928 DOI 10.1007/s11255-011-0019-6 NEPHROLOGY – CASE REPORT Acute kidney injury from pyelonephritis in an elderly man: case report Sayed Husain • Manaf Alroumoh • Prince Mohan • Gabriel El-Kass • Surya V. Seshan • Marilyn Galler Received: 27 December 2010 / Accepted: 29 April 2011 / Published online: 8 July 2011 Ó Springer Science+Business Media, B.V. 2011 Abstract Pyelonephritis is rarely considered in the differential diagnosis of acute kidney injury [1–5]. Acute non-obstructed bacterial pyelonephritis is an infrequent and rarely considered cause of rapidly progressive acute kidney injury. A diagnostic challenge thus develops as it is difficult to clinically differentiate acute kidney injury secondary to ischemic or toxic acute tubular necrosis or papillary necrosis versus acute interstitial nephritis secondary to drugs or infectious pyelonephritis. We describe a case of acute kidney injury due to suppurative pyelonephritis in an elderly immunocompetent man who presented with dysuria, vomiting, and fever and later found to have histologic and radiologic proven pyelonephritis as the cause of acute kidney injury in the absence of hypotension, nephrotoxic agents, non-steroidal analgesics, immunosuppression, urinary tract obstruction, or other structural anomalies. S. Husain (&)
P. Mohan Department of Internal Medicine, New York Hospital of Queens, NY, USA e-mail: hus9007@hotmail.com M. Alroumoh
G. El-Kass
M. Galler Department of Nephrology, New York Hospital of Queens, NY, USA S. V. Seshan Department of Pathology, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, USA The patient was managed with antimicrobial therapy, hemodialysis, and a short course of corticosteroids. Keywords Pyelonephritis
Acute kidney injury Case report A 69-year-old man presented to the emergency department of New York Hospital of Queens complaining of dysuria for 3 days with fever of 101°F/ 38.3°C, chills, intermittent lower back pain, and vomiting for 2 days with some loose bowel movements. He noted no change in his urine output, hematuria, or rash. He denied analgesic use. His past medical history included hypertension, gout, and mild intermittent asthma for which he was taking Norvasc 5 mg, Lisinopril 5 mg, and Albuterol inhaler. On admission, his blood pressure was 130/71 mm/ Hg, pulse 69/min, respiration 12/min, and oral temperature 100.2 F/37.8°C. The patient was alert and comfortable. His skin was without rashes, and mucous membranes were moist. His lungs were clear to auscultation, and heart sounds were normal sinus rhythm without murmurs or rubs audible. His abdomen was obese with normal bowel sounds, nontender with no palpable masses. No costovertebral angle tenderness was appreciated. His extremities had 1 ? peripheral edema. Initial laboratory values were as follows: hemoglobin 13 mg/dL, hematocrit 38.1%, and platelet 123 926 count 145,000/per cubic millimeter. The white cell count was 30,600 per cubic millimeter with 40.9% bands and 0% eosinophils. The metabolic panel showed a sodium of 127 mmol/L, potassium 4.2 mmol/L, chloride 91 mmol/L, bicarbonate 18 mmol/L, urea nitrogen 59 mg/dL, creatinine 5.3 mg/dL, glucose 169 mg/dL, calcium 7.3 mg/dL, albumin 2.5 g/dL, phosphorous 3.0 mg/dL, magnesium 2.2 mg/dL, lactic acid 1.3 mmol/L, AST 55 IU/L, ALT 41 IU/L, and ALP 89 IU/L. The urinalysis showed WBC of 1,529 per high power field, RBC of 50 per high power field, protein 500 mg/dL, nitrites negative, leukocyte esterase positive, pH 5.5, and specific gravity 1.015. Other laboratory findings revealed HIV, IPEP, ANA, ANCA, rheumatoid factor, and hepatitis B and C antigen and antibody to be negative and C3 and C4— within normal range. Blood and urine specimens collected on the day of admission were positive for Escherichia coli (E. coli) 105 col/ml that was sensitive to Cefepime and Levofloxacin. Random urine electrolytes were sodium 39 mmol/L, potassium 59.5 mmol/ L, chloride 24 mmol/L, osmolality 306 mosm/kg, creatinine 179 mg/dL, protein 336 mg/dL, and a urine protein creatinine ratio (UPC) of 1.0 urine. Wright stain was positive for eosinophils. A renal sonogram showed the right kidney measuring 13 cm and the left kidney 12.5 cm. There was no hydronephrosis, renal stones, or masses. A noncontrast CT of the abdomen and pelvis showed bilateral perinephric and periureteral fat stranding of uncertain significance without hydronephrosis or nephrolithiasis. The prostate gland measures 4.7 cm in transverse dimension. At the time of admission, the patient was started on aggressive hydration and Lisinopril was discontinued as prerenal azotemia was in the differential for acute kidney. Empiric antibiotic treatment with Vancomycin and Levaquin was started, and later was changed to Cefepime according to the culture and sensitivity results. Repeat urine culture on the 4th day of admission was negative and the urinalysis on the 10th day of admission showed improvement in the WBC count to 134 per high power field. Despite hydration and appropriate antibiotic therapy, the patient’s blood urea nitrogen and creatinine continued to trend upward to 158 mg/dL and 10.9 mg/dL, respectively. The patient was nonoliguric. On the 5th hospital day, he was started on hemodialysis. A renal biopsy was performed on 123 Int Urol Nephrol (2011) 43:925–928 Fig. 1 Renal cortical tissue showing diffuse, active and focal subacute inflammation, interstitial edema, and inflammatory cell casts within the tubules. Most of the tubules show evidence of tubular cell injury, focal sloughing of the lining cells. No significant changes are noted within the glomerulus (H&Ex100) the 9th day of hospitalization once his urine culture was negative. The biopsy showed diffuse active and chronic pyelonephritis, moderate to severe; minimal glomerular changes diffuse tubular injury with inflammatory cell casts, focal tubular atrophy with minimal interstitial fibrosis, and no microabscesses (Fig. 1). The findings were consistent with E. coli associated urinary tract infection with involvement of the renal parenchyma. After three hemodialysis treatment sessions, the interdialytic urea nitrogen and creatinine levels began to decline indicating improvement in his endogenous renal function. Hemodialysis was discontinued on day 11 when his creatinine level was stable at 6.3 mg/dL. Three days after the last hemodiaylsis treatment, the patient developed an attack of Gout and was started on a course of prednisone 60 mg/day for a total of 3 days. His urea nitrogen and creatinine continued to slowly improve and on the day of discharge, day 19 of his hospitalization, his urea nitrogen was 66 mg/dL and creatinine 3.73 mg/dL. The patient was prescribed an outpatient course of Cefepime 500 mg IV BID for 1 week followed with Levaquin 250 mg PO QD for 7 days per ID recommendation. Three weeks post discharge, he was seen in follow up at which time he was well, afebrile, without dysuria, back pain, or associated constitutional symptoms. His urea nitrogen level was 34 mg/dL and creatinine of 2.9 mg/dL. Six weeks postdischarge, his urea nitrogen level was Int Urol Nephrol (2011) 43:925–928 31 mg/dL and creatinine 1.8 mg/dL, and 8 months postdischarge, his creatinine improved to 1.4 mg/dL. Discussion Acute bacterial pyelonephritis is a rare and unusual cause of acute kidney injury in patients without any evidence of anatomical anomaly or other predisposing factors. It has been described more often in the pediatric population [6] but less frequently seen in the adult population, reported at an incidence of 2–3% [6, 7]. Most of the patients had some predisposing conditions such as the presence of an indwelling catheter, use of immunosuppressives, pregnancy, renal stones, solitary kidney, or non-steroidal analgesic use. A review of the literature showed 16 cases of biopsy proven acute kidney injury secondary to acute bacterial pyelonephritis. Most patients showed interstitial and peritubular inflammation with polymorph neutrophils and microabcesses. There was no evidence of obstructive uropathy or vasculitic changes. In some of the cases, toxicity was associated with non steroidal anti-inflammatory drugs (NSAIDS) and alcohol (ETOH) use. Both chronic and acute moderate alcohol use can increase host susceptibility to infections caused by bacterial pathogens due to impairment of host defense and cellular immune responses [8]. Of the 16 cases, 13 were due to E. coli and two due to Klebsiella pneumoniae. Only one patient showed no growth on culture. Prompt diagnosis with antibiotic coverage had a favorable effect on the prognosis of pyelonephritis-induced acute kidney injury in most of the patients. However, three died from pyelonephritis and two required hemodialysis [9–19]. A severe form of pyelonephritis, emphysematous pyelonephritis, is characterized by gas within the renal parenchyma and/or the collecting ducts. Khair et al. described 19 cases of emphysematous pyelonephritis and noted that diabetes, female gender, and poor glycemic control were risk factors for this disease. Eighteen of 19 patients required dialysis, and 13 of the 15 patients who survived had renal recovery and dialysis discontinuation. No renal pathology was described [20]. Xanthogranulomatous pyelonephritis is a rare chronic inflammatory condition that is characterized by destruction and replacement of renal parenchyma with lipid laden macrophages causing poor functioning 927 or non-function of the affected kidney. Patients can present with typical symptoms of bacterial pyelonephritis and renal impairment beyond expected with one diseased non-functioning kidney [21]. This case was a diagnostic challenge to the renal team as there was no history of prior renal dysfunction, radiologic evidence for Xanthogranulomatous or Emphysematous pyelonephritis, urologic anatomical abnormalities, nephrotoxic agent exposure, or hypotension, and was occurring in an immunocompetent host with a negative serological work up and positive blood and urine cultures for E. coli. Despite prompt treatment with hydration, discontinuation of the angiotensin converting enzyme inhibitors (ACEI) and appropriate antibiotics, the patient’s renal function continued to worsen necessitating the initiation of hemodialysis. Due to the unusual severity of the renal impairment and the prolonged course of acute kidney injury, a renal biopsy was performed for diagnosis and treatment confirmation. It was possible that acute tubular necrosis secondary to a gram negative infection without hypotension caused the acute kidney injury secondary to cytokine and endotoxins stimulation leading to vasoconstriction and mesangial cell contraction. However, the biopsy report was more compatible with acute bacterial pyelonephritis. Gradual recovery of our patient’s renal function occurred over weeks with appropriate antibiotic therapy. The infection was cleared as evident by urine and blood culture negativity and improvement of the urinalysis. Several reports have shown more complete recovery of renal function and decreased renal scarring in severe acute pyelonephritis when steroids were added to the anti-microbial therapy. We do not think that the incidental addition of prednisone in our patient contributed to the renal recovery. The patient’s renal function began to recover and dialysis was discontinued prior to the initiation of only 3 days of steroid therapy. Furthermore, postdiscontinuation of steroids, his renal function continued to improve. This case report emphasizes that physicians should consider acute bacterial pyelonephritis in the differential diagnosis of acute renal failure. Since this disease entity may cause permanent renal damage, it is crucial to promptly begin appropriate and adequate anti-microbial treatment to prevent the long-term consequences of renal scarring. 123 928 References 1. Baker LRI, Cattell WR, Fry IKF, Mallinson WJW (1979) Acute renal failure due to bacterial pyelonephritis. 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