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. 2023 Sep 17;8(12):2833-2837.
doi: 10.1016/j.ekir.2023.09.016. eCollection 2023 Dec.

Pyelonephritis is an Underrecognized Cause of CKD in Patients With Orthotopic Ileal Neobladder Substitution

Qiyu Wang  1 , Rituvanthikaa Seethapathy  1 , Tianqi Ouyang  1 , Ian A Strohbehn  1 , Nurit Katz-Agranov  1 , Paul Hanna  1 , Mohit Madken  1 , Harish Seethapathy  1 , Shruti Gupta  2   3 , Howard M Heller  4 , Matthew Wszolek  5 , David Steele  1 , Veronica E Klepeis  6 , Helmut Rennke  7 , Meghan E Sise  1
Affiliations

Pyelonephritis is an Underrecognized Cause of CKD in Patients With Orthotopic Ileal Neobladder Substitution

Qiyu Wang et al. Kidney Int Rep. .
No abstract available

Keywords: asymptomatic bacteriuria; bladder cancer; chronic kidney disease; ileal neobladder; pyelonephritis; urinary diversion.

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Figures

Figure 1
Figure 1
Kidney pathology in patients with biopsy-proven pyelonephritis. Kidney pathology of patient 1 is shown in in Figure 1a and 1b whose clinical course is described in Figure 2a. 1a shows diffuse interstitial inflammation (low power, H&E) and 1b shows neutrophil cast characteristic of acute pyelonephritis (high power, H&E). Patient 2 is shown in in Figure 1c and 1d whose clinical course is described in Figure 2b: 1c shows abrupt transition of preserved renal parenchyma to tubular atrophy and interstitial fibrosis from left side of the core to the right (low power, H&E), and 1d shows global sclerosis of the glomeruli (arrows) with predominantly lymphocytic infiltrate (high power, H&E). Patient 3 is shown in Figure 1e and 1f whose clinical course is described in 2c: 1e shows renal cortex with preserved parenchyma and minimal nonspecific focal tubular atrophy (top core, low power, PAS), whereas the bottom core reveals a chronic active inflammatory infiltrate that has resulted in extensive tubular atrophy and early interstitial fibrosis (bottom core, low power, PAS). 1f shows cortical tissue with several distended tubules that contain necrotic debris and degenerated neutrophils (neutrophil casts, black arrows); the interstitium is occupied predominantly by mononuclear cells (lymphocytes and plasma cells) with isolated neutrophils (high power, H&E). The focal nature of the processes (indicated by 1c and 1e) was highly suggestive of bacterial infection due to urinary reflux. H&E, hematoxylin and eosin; PAS, periodic acid-schiff.
Figure 2
Figure 2
Clinical course in patients with biopsy-proven pyelonephritis. Creatinine trend, clinical course, and urine culture results in patients with biopsy-proven pyelonephritis. Color scheme at the bottom of each graph represents urine bacterial colonization at different time-periods. ESR/CRP trend during extended follow-up of patient 1 was shown in Supplementary Figure S4. ESR/CRP was not trended in patient 2 and patient 3. In patient 3, immune checkpoint inhibitor-associated interstitial nephritis was initially diagnosed in the context of atezolizumab (anti-PDL1) use, and steroid treatment was started; however, given the lack of sustained improvement in kidney function after approximately 4 weeks of high dose steroids, and careful reexamination of the biopsy demonstrating neutrophil casts (Figure 1e), focal inflammation alternating with normal interstitium (Figure 1f), and positive urine culture for E. Coli, the diagnosis of pyelonephritis was favored and treatment with high dose ciprofloxacin (500 mg twice daily) began. The patient’s kidney function stabilized with cessation of atezolizumab, corticosteroids, and antibiotic treatment, though did not show a significant improvement. ESR, erythrocyte sediment rate; CRP, C-reactive protein; TMP/SMZ, trimethoprim/sulfamethoxazole; K. pneumo, Klebsiella pneumonia; E. Coli, Escherichia coli, WBC, white blood cell count, ND, not done.
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